猪瘟病毒感染对宿主细胞免疫应答基因的影响
|
摘要
猪瘟病毒(Classical swine fever virus,CSFV)是一种带有囊膜的单股正链RNA病毒,与牛病毒性粘膜腹泻病毒和羊边界病毒同属于黄病毒科瘟病毒属。猪瘟病毒的基因组大小约12.3kb,只含有一个开放阅读框,编码一个由3898个氨基酸残基组成的多聚蛋白,该多聚蛋白在宿主细胞蛋白酶和病毒特异的蛋白酶共同作用下裂解为4个结构蛋白和8个非结构蛋白。家猪和野猪是该病毒的唯一宿主,猪瘟病毒引起的猪瘟是一种具有高发病率和高死亡率的烈性接触性传染病,给养猪业造成巨大的经济损失,世界卫生组织OIE将其列为A类必须申报的重要动物传染病之一,我国也将猪瘟定为一类动物传染病,并从2008年起列为动物疫病强制免疫项目。
随着猪瘟疫苗的广泛使用,改变了猪瘟病毒的生态环境,猪瘟在流行特点和发病特点上发生了很大的变化,由大流行转变为地方性流行或散发,临床症状从典型转变为非典型,出现母猪繁殖障碍和新生仔猪先天感染。从精液、睾丸、扁桃体和淋巴结中检测到猪瘟病毒的存在,甚至在部分免疫了的猪体内检出猪瘟病毒,证实了猪瘟病毒存在持续感染现象。病毒要实现潜伏或持续性感染,必需逃脱宿主免疫系统的监视,突破宿主抗病毒防卫机制而获得免疫逃逸。研究猪瘟病毒与宿主之间的相互作用关系是理解病毒致病机制及其免疫应答的基础,猪瘟病毒在宿主体内或体外对靶细胞的影响正是它们相互作用的具体表现。PK-15细胞是猪瘟病毒体外感染的主要传代细胞,探索猪瘟病毒对PK-15细胞功能的影响,将有助于揭示猪瘟病毒感染的致病机制。因此,在本研究中我们应用real-time RT-PCR和Western blot方法对CSFV感染后宿主细胞的免疫应答基因表达的变化进行了研究,主要结果如下：
1.建立了检测猪免疫应答基因mRNA表达水平的real-time RT-PCR方法。
根据已知的猪源SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、 IFN-α、IFN-β、 GAPDH基因和CSFV5'UTR基因片段的mRNA序列,采用生物软件Oligo6.0和Primer5.0辅助设计并合成了11对特异性引物；以Oligo(dT)18为引物,合成第一链cDNA;以cDNA为模板,分别进行11个目的基因片段的PCR扩增；胶回收PCR产物,把它们克隆到pMD18-T载体上并测序；对提取的重组质粒进行10倍梯度稀释作为标准模板进行PCR扩增,同时对荧光定量PCR反应的引物浓度和退火温度进行优化。应用11对引物分别扩增出目的基因目的条带,大小与预期片段相符合；real-time RT-PCR反应的最佳引物浓度是202.5nmol/μl,最佳退火温度是60℃；目的基因real-time RT-PCR融解曲线均显示单一溶解峰。结果表明,本试验成功地建立了检测PK-15细胞中SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、 CD86、IFN-α、IFN-β、 GAPDH和CSFV5'UTR基因mRNA表达动态的实时荧光定量PCR方法。
2.应用real-time RT-PCR方法检测猪瘟病毒感染后不同时间段的PK-15细胞中免疫应答基因的mRNA转录情况。
在自然和实验环境下,猪瘟病毒能逃避宿主的免疫系统建立持续性感染。我们猜测,与MHC和细胞因子调控有关的一些基因卷入到免疫逃避事件中,但是具体的每一个基因在感染了CSFV后有什么变化尚不清楚。因此,我们用不同感染量猪瘟病毒Shimen毒株和GXXJ01毒株分别感染PK-15细胞,感染后1、3、12、24、36和48h应用real-time RT-PCR方法检测细胞中免疫应答基因SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、IFN-α和IFN-β的mRNA表达动态。结果显示,SLA-2、TAP1、SLA-DR、Ii、CD40、 CD80和CD86的mRNA表达呈现明显的下调,其中SLA-DR和Ii的rnRNA下调特别显著,IFN-a和IFN-β的mRNA表达没有明显变化,表明CSFV可能参与了抑制免疫应答基因表达的机制。
3.猪瘟病毒感染对宿主细胞中SLA-DR表达的影响。
PK-15细胞感染猪瘟病毒Shimen毒株后,细胞内SLA-DR蛋白表达呈现明显的下调,在病毒感染后的24和36h检测不到SLA-DR蛋白,在感染后的48h检测到少量的SLA-DR蛋白。为了探讨猪瘟病毒诱导的SLA-DR的分子机制,从猪瘟病毒Shimen毒株中扩增出C、Npro和E2基因,将其与真核表达载体pcDNA3.0连接,成功构建了P-C、P-Npro和P-E2重组真核表达质粒。构建成功的3个真核表达质粒应用脂质体介导的转染方法进行体外细胞表达,转染后的1、3、12、24、36和48h检测细胞中SLA-DR的表达情况。结果显示,分别转染真核表达质粒P-E2和P-C后,PK-15细胞中SLA-DR的转录水平有所升高；转染真核表达质粒P-Npro后,PK-15细胞中SLA-DR的表达在3-24h显示升高,24h后开始下降,36h后恢复到与对照组一致的水平;在蛋白质水平对PK-15细胞中SLA-DR蛋白表达进行了检测,发现分别转染或共转染P-C、P-E2和P-C/P-E2后,细胞中SLA-DR蛋白的表达有比较明显的提高；转染P-C/P-Npro/P-E2后,细胞中SLA-DR蛋白的表达量稍有上升；分别转染或共转染P-Npro、P-C/P-Npro、P-Npro/P-E2后,PK-15细胞中SLA-DR蛋白的表达明显下降。表明猪瘟病毒E2和C两个基因单独或协同作用对宿主细胞SLA-DR的下调表达没有显著影响,Npro基因对PK-15细胞中SLA-DR的表达有一定的抑制作用。研究认为,病毒病的发生、发展是多基因、多步骤、多阶段参与的过程,猪瘟病毒的不同基因在抑制宿主细胞SLA-DR表达过程中的作用有待于进一步研究。
Classical swine fever virus (CSFV), which is an enveloped, single-and positive-stranded RNA virus, with bovine viral diarrhea virus and border disease virus, belongs to the members of the Pestivirus genus within the family of Flaviviridae. The genome of CSFV is approximately12.3kb and contains a single large open reading frame encoding a polyprotein of3898amino acid, which undergoes co-and posttranslational processing and maturation into four structural and eight nonstructural proteins by viral proteases and host proteases. Domestic pigs and wild boars are the unique host of CSFV. CSFV causes a highly contagious infectious disease with high morbidity and mortality in pigs, resulting in substantial economic losses to the pig industry worldwide. Classical swine fever (CSF) is therefore classified as a List A disease by the Office International des Epizooties (OIE). In China, CSF is also listed as one of the severe animal epidemic disease and the State practices a system of immunization planning for execution of compulsory immunization against animal epidemics since2008.
After implementation of strict immunization measures, ecological environment of CSFV were changed. CSF obviously presented changing in epidemiological forms and clinical signs. The large-scale CSF has rarely outbroken but sporadic epizootics still frequently occurred every year, and the clinical signs are dominated by typical to atypical forms of the disease, such as reproductive failures in pregnant sows and congenital infections in newborn piglets were observed. Virus is detected in semen, gonads, tonsil and lymph node even in certain vaccinated pigs, which confirmed CSFV have been established as persistent infection. Virus has to invade host defense mechanism and immune response and then establishes life-long, persistent infections. Therefore, the study on the interaction between host and CSFV is critical for understanding viral pathogenesis and immunity. For realizing the status of the cellular genes relative to immune response in vitro, PK-15cells were offered as a feasible model to investigate transcriptional changes during CSFV infection. The study may provide some useful data of insight into the interaction between CSFV and swine. In this study, real-time RT-PCR and Western blot approaches was applied to monitor the expression of immune response genes of host cells following CSFV infection. The results are mainly showed as follows. Experiment1. Development of the method for determination of several immune response genes mRNA levels in PK-15cells by real-time RT-PCR.
According to the GenBank data, mRNA sequences of SLA-2, TAP1, SLA-DR, Ii, CD40, CD80, CD86, IFN-a, IFN-p, GAPDH and5'-UTR of CSFV genes were downloaded, eleven pairs of specific primers were designed by biological Oligo6.0/Primer5.0software and synthesized. Oligo(dT)18were used as primer and first strand cDNA was synthesized from total RNA, which was isolated from swine lymphocytes. Using the synthesized cDNAs as template, eleven target fragments were amplified by polymerase chain reaction (PCR), respectively. The PCR products were electrophoresed on2%agarose gels and extracted. The extracted PCR products were cloned into pMD18-T Vector and sequenced. The extracted plasmids were diluted with series10-folds and were used as standard templates, and real-time PCRs were performed. In addition, the primer concentration and annealing temperature for each pair of specific primers was optimized, respectively. The results showed that each gene was amplified using specific primer pair. The optimal primer concentration was202.5nmol/μl and annealing temperatures for eleven primer pairs was60℃. The melting curve showed the unique peak for each PCR product, indicating that the method for determination SLA-2, TAP1, SLA-DR, Ii, CD40, CD80, CD86, IFN-a, IFN-p and5'-UTR of CSFV mRNA levels in PK-15cells by real-time RT-PCR is successfully established.
Experiment2. Transcriptional abundance of several immune response genes of PK-15cells following CSFV infection in vitro using real-time RT-PCR.
CSFV evade the immune response and establish persistent infection under natural and experimental conditions. As we know, some genes relative to MHC and cytokine regulation are involved in persistent infection, but the extent of each gene responds to CSFV infection is unclear. In our study, nine immune response genes including SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、 IFN-a and IFN-β were detected using real-time RT-PCR after the PK-15cells were infected with0.1Moi or1.0Moi Shimen or GXXJ01strain of CSFV, respectively. The results showed that these immune response genes basically presented down-regulation during CSFV infection, except IFN-a and IFN-β transcriptional levels of mRNA in CSFV-infected cells did not change significantly. The SLA-2, SLA-DR, and Ii genes were notably decreased. Our experiments concluded that CSFV maybe involved in the inhibition of immune response genes.
Experiment3. Effects of classical swine fever virus infection on expression of SLA-DR gene in PK-15cells.
Following Shimen strain of CSFV infection, the expression of SLA-DR presented down-regulation. SLA-DR is inhibited at24and36hpi and its expression restained in48hpi. In order to further exploration of the regulation between CSFV and SLA-DR, eukaryotic recombination expression plasmids P-C, P-Npro and P-E2were generated. The C, Npro and E2genes from Shimen strain of CSFV were cloned, then inserted into the expression vector pcDNA3.0. The eukaryotic recombination expression plasmids P-C, P-Npro and P-E2were constructed and transfected into PK-15cells with liposome infection protocol. The SLA-DR expression was detected by real-time RT-PCR and western blot. The results showed that SLA-DR mRNA expression showed a significantly up-regulation following P-C or P-E2transfection. SLA-DR presented up-regulation after transfection3to24hours, but in24hour SLA-DR become down-regulated, the SLA-DR mRNA expression was similar to controls in36and48hours. Western blot showed that SLA-DR expression presented an obviously up-regulation following P-C or P-E2transfection or P-C/P-E2co-transfection into PK-15cells. The co-transfection of three recombination vectors P-C/P-Npro/P-E2were carried out, SLA-DR expression presented slight up-regulated. However, SLA-DR expression showed an obviously down-regulation during P-Npro or P-C/P-Npro or P-Npro/P-E2co-transfection into PK-15cells. The results suggested that C or E2alone or synergistic did not showed significantly effect on the down-regulation of SLA-DR, Npro alone or synergistic showed slight effect on the down-regulation of SLA-DR. Current studies suggest that the incidence and development of virus disease is a multi-gene, multi-stage process participation, in which the relationship between CSFV and SLA-DR need to be further studied.
随着猪瘟疫苗的广泛使用,改变了猪瘟病毒的生态环境,猪瘟在流行特点和发病特点上发生了很大的变化,由大流行转变为地方性流行或散发,临床症状从典型转变为非典型,出现母猪繁殖障碍和新生仔猪先天感染。从精液、睾丸、扁桃体和淋巴结中检测到猪瘟病毒的存在,甚至在部分免疫了的猪体内检出猪瘟病毒,证实了猪瘟病毒存在持续感染现象。病毒要实现潜伏或持续性感染,必需逃脱宿主免疫系统的监视,突破宿主抗病毒防卫机制而获得免疫逃逸。研究猪瘟病毒与宿主之间的相互作用关系是理解病毒致病机制及其免疫应答的基础,猪瘟病毒在宿主体内或体外对靶细胞的影响正是它们相互作用的具体表现。PK-15细胞是猪瘟病毒体外感染的主要传代细胞,探索猪瘟病毒对PK-15细胞功能的影响,将有助于揭示猪瘟病毒感染的致病机制。因此,在本研究中我们应用real-time RT-PCR和Western blot方法对CSFV感染后宿主细胞的免疫应答基因表达的变化进行了研究,主要结果如下：
1.建立了检测猪免疫应答基因mRNA表达水平的real-time RT-PCR方法。
根据已知的猪源SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、 IFN-α、IFN-β、 GAPDH基因和CSFV5'UTR基因片段的mRNA序列,采用生物软件Oligo6.0和Primer5.0辅助设计并合成了11对特异性引物；以Oligo(dT)18为引物,合成第一链cDNA;以cDNA为模板,分别进行11个目的基因片段的PCR扩增；胶回收PCR产物,把它们克隆到pMD18-T载体上并测序；对提取的重组质粒进行10倍梯度稀释作为标准模板进行PCR扩增,同时对荧光定量PCR反应的引物浓度和退火温度进行优化。应用11对引物分别扩增出目的基因目的条带,大小与预期片段相符合；real-time RT-PCR反应的最佳引物浓度是202.5nmol/μl,最佳退火温度是60℃；目的基因real-time RT-PCR融解曲线均显示单一溶解峰。结果表明,本试验成功地建立了检测PK-15细胞中SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、 CD86、IFN-α、IFN-β、 GAPDH和CSFV5'UTR基因mRNA表达动态的实时荧光定量PCR方法。
2.应用real-time RT-PCR方法检测猪瘟病毒感染后不同时间段的PK-15细胞中免疫应答基因的mRNA转录情况。
在自然和实验环境下,猪瘟病毒能逃避宿主的免疫系统建立持续性感染。我们猜测,与MHC和细胞因子调控有关的一些基因卷入到免疫逃避事件中,但是具体的每一个基因在感染了CSFV后有什么变化尚不清楚。因此,我们用不同感染量猪瘟病毒Shimen毒株和GXXJ01毒株分别感染PK-15细胞,感染后1、3、12、24、36和48h应用real-time RT-PCR方法检测细胞中免疫应答基因SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、IFN-α和IFN-β的mRNA表达动态。结果显示,SLA-2、TAP1、SLA-DR、Ii、CD40、 CD80和CD86的mRNA表达呈现明显的下调,其中SLA-DR和Ii的rnRNA下调特别显著,IFN-a和IFN-β的mRNA表达没有明显变化,表明CSFV可能参与了抑制免疫应答基因表达的机制。
3.猪瘟病毒感染对宿主细胞中SLA-DR表达的影响。
PK-15细胞感染猪瘟病毒Shimen毒株后,细胞内SLA-DR蛋白表达呈现明显的下调,在病毒感染后的24和36h检测不到SLA-DR蛋白,在感染后的48h检测到少量的SLA-DR蛋白。为了探讨猪瘟病毒诱导的SLA-DR的分子机制,从猪瘟病毒Shimen毒株中扩增出C、Npro和E2基因,将其与真核表达载体pcDNA3.0连接,成功构建了P-C、P-Npro和P-E2重组真核表达质粒。构建成功的3个真核表达质粒应用脂质体介导的转染方法进行体外细胞表达,转染后的1、3、12、24、36和48h检测细胞中SLA-DR的表达情况。结果显示,分别转染真核表达质粒P-E2和P-C后,PK-15细胞中SLA-DR的转录水平有所升高；转染真核表达质粒P-Npro后,PK-15细胞中SLA-DR的表达在3-24h显示升高,24h后开始下降,36h后恢复到与对照组一致的水平;在蛋白质水平对PK-15细胞中SLA-DR蛋白表达进行了检测,发现分别转染或共转染P-C、P-E2和P-C/P-E2后,细胞中SLA-DR蛋白的表达有比较明显的提高；转染P-C/P-Npro/P-E2后,细胞中SLA-DR蛋白的表达量稍有上升；分别转染或共转染P-Npro、P-C/P-Npro、P-Npro/P-E2后,PK-15细胞中SLA-DR蛋白的表达明显下降。表明猪瘟病毒E2和C两个基因单独或协同作用对宿主细胞SLA-DR的下调表达没有显著影响,Npro基因对PK-15细胞中SLA-DR的表达有一定的抑制作用。研究认为,病毒病的发生、发展是多基因、多步骤、多阶段参与的过程,猪瘟病毒的不同基因在抑制宿主细胞SLA-DR表达过程中的作用有待于进一步研究。
Classical swine fever virus (CSFV), which is an enveloped, single-and positive-stranded RNA virus, with bovine viral diarrhea virus and border disease virus, belongs to the members of the Pestivirus genus within the family of Flaviviridae. The genome of CSFV is approximately12.3kb and contains a single large open reading frame encoding a polyprotein of3898amino acid, which undergoes co-and posttranslational processing and maturation into four structural and eight nonstructural proteins by viral proteases and host proteases. Domestic pigs and wild boars are the unique host of CSFV. CSFV causes a highly contagious infectious disease with high morbidity and mortality in pigs, resulting in substantial economic losses to the pig industry worldwide. Classical swine fever (CSF) is therefore classified as a List A disease by the Office International des Epizooties (OIE). In China, CSF is also listed as one of the severe animal epidemic disease and the State practices a system of immunization planning for execution of compulsory immunization against animal epidemics since2008.
After implementation of strict immunization measures, ecological environment of CSFV were changed. CSF obviously presented changing in epidemiological forms and clinical signs. The large-scale CSF has rarely outbroken but sporadic epizootics still frequently occurred every year, and the clinical signs are dominated by typical to atypical forms of the disease, such as reproductive failures in pregnant sows and congenital infections in newborn piglets were observed. Virus is detected in semen, gonads, tonsil and lymph node even in certain vaccinated pigs, which confirmed CSFV have been established as persistent infection. Virus has to invade host defense mechanism and immune response and then establishes life-long, persistent infections. Therefore, the study on the interaction between host and CSFV is critical for understanding viral pathogenesis and immunity. For realizing the status of the cellular genes relative to immune response in vitro, PK-15cells were offered as a feasible model to investigate transcriptional changes during CSFV infection. The study may provide some useful data of insight into the interaction between CSFV and swine. In this study, real-time RT-PCR and Western blot approaches was applied to monitor the expression of immune response genes of host cells following CSFV infection. The results are mainly showed as follows. Experiment1. Development of the method for determination of several immune response genes mRNA levels in PK-15cells by real-time RT-PCR.
According to the GenBank data, mRNA sequences of SLA-2, TAP1, SLA-DR, Ii, CD40, CD80, CD86, IFN-a, IFN-p, GAPDH and5'-UTR of CSFV genes were downloaded, eleven pairs of specific primers were designed by biological Oligo6.0/Primer5.0software and synthesized. Oligo(dT)18were used as primer and first strand cDNA was synthesized from total RNA, which was isolated from swine lymphocytes. Using the synthesized cDNAs as template, eleven target fragments were amplified by polymerase chain reaction (PCR), respectively. The PCR products were electrophoresed on2%agarose gels and extracted. The extracted PCR products were cloned into pMD18-T Vector and sequenced. The extracted plasmids were diluted with series10-folds and were used as standard templates, and real-time PCRs were performed. In addition, the primer concentration and annealing temperature for each pair of specific primers was optimized, respectively. The results showed that each gene was amplified using specific primer pair. The optimal primer concentration was202.5nmol/μl and annealing temperatures for eleven primer pairs was60℃. The melting curve showed the unique peak for each PCR product, indicating that the method for determination SLA-2, TAP1, SLA-DR, Ii, CD40, CD80, CD86, IFN-a, IFN-p and5'-UTR of CSFV mRNA levels in PK-15cells by real-time RT-PCR is successfully established.
Experiment2. Transcriptional abundance of several immune response genes of PK-15cells following CSFV infection in vitro using real-time RT-PCR.
CSFV evade the immune response and establish persistent infection under natural and experimental conditions. As we know, some genes relative to MHC and cytokine regulation are involved in persistent infection, but the extent of each gene responds to CSFV infection is unclear. In our study, nine immune response genes including SLA-2、TAP1、SLA-DR、Ii、CD40、CD80、CD86、 IFN-a and IFN-β were detected using real-time RT-PCR after the PK-15cells were infected with0.1Moi or1.0Moi Shimen or GXXJ01strain of CSFV, respectively. The results showed that these immune response genes basically presented down-regulation during CSFV infection, except IFN-a and IFN-β transcriptional levels of mRNA in CSFV-infected cells did not change significantly. The SLA-2, SLA-DR, and Ii genes were notably decreased. Our experiments concluded that CSFV maybe involved in the inhibition of immune response genes.
Experiment3. Effects of classical swine fever virus infection on expression of SLA-DR gene in PK-15cells.
Following Shimen strain of CSFV infection, the expression of SLA-DR presented down-regulation. SLA-DR is inhibited at24and36hpi and its expression restained in48hpi. In order to further exploration of the regulation between CSFV and SLA-DR, eukaryotic recombination expression plasmids P-C, P-Npro and P-E2were generated. The C, Npro and E2genes from Shimen strain of CSFV were cloned, then inserted into the expression vector pcDNA3.0. The eukaryotic recombination expression plasmids P-C, P-Npro and P-E2were constructed and transfected into PK-15cells with liposome infection protocol. The SLA-DR expression was detected by real-time RT-PCR and western blot. The results showed that SLA-DR mRNA expression showed a significantly up-regulation following P-C or P-E2transfection. SLA-DR presented up-regulation after transfection3to24hours, but in24hour SLA-DR become down-regulated, the SLA-DR mRNA expression was similar to controls in36and48hours. Western blot showed that SLA-DR expression presented an obviously up-regulation following P-C or P-E2transfection or P-C/P-E2co-transfection into PK-15cells. The co-transfection of three recombination vectors P-C/P-Npro/P-E2were carried out, SLA-DR expression presented slight up-regulated. However, SLA-DR expression showed an obviously down-regulation during P-Npro or P-C/P-Npro or P-Npro/P-E2co-transfection into PK-15cells. The results suggested that C or E2alone or synergistic did not showed significantly effect on the down-regulation of SLA-DR, Npro alone or synergistic showed slight effect on the down-regulation of SLA-DR. Current studies suggest that the incidence and development of virus disease is a multi-gene, multi-stage process participation, in which the relationship between CSFV and SLA-DR need to be further studied.
引文
1. Moennig, V. Plagemann, P. G. W. The pestiviruses. Adv Virus Res.1992,41:53-98.
2. Thiel, H. J., Plagemann, P. G. W., Moennig, V. Pestiviruses. In Fields Virology,3rd edn, vol.1. Edited by B. N. Fields, D. M. Knipe & P. M. Howley. Philadelphia & New York:Lippincott-Raven.1996, 1059-1073.
3. Weesendorp, E., Stegeman, A., Loeffen, W. Dynamics of virus excretion via different routes in pigs experimentally infected with classical swine fever virus strains of high, moderate or low virulence. Vet Microbiol.2009,133(1-2):9-22.
4. Weesendorp, E., Stegeman, A., Loeffen, W. Quantification of classical swine fever virus in aerosols originating from pigs infected with strains of high, moderate or low virulence. Vet Microbiol.2009, 135(3-4):222-230.
5. Hennecken, M., Stegeman, J. A., Elbers, A. R., et al. Transmission of classical swine fever virus by artificial insemination during the 1997-1998 epidemic in The Netherlands:a descriptive epidemiological study. Vet Q.2000,22(4):228-233.
6. Edwards, S., Fukusho, A., Lefevre, P. C., et al. Classical swine fever:the global situation. Vet Microbiol.2000,73:103-119.
7. Moenning, V., Floegel-Niesmann, G., Greiser-Wilke, I. Clinical signs and epidemiology of classical swine fever:a review of new knowledge. Vet J.2003,165:11-20.
8. Terpstra C. Hog cholera:an update of present knowledge. Br Vet J.,1991; 147:397-406.
9. Moennig, V. Introduction to classical swine fever virus, disease and control policy. Vet Microbiol. 2000,73(2-3):93-102.
10.吕宗吉,涂长春,余若龙.等.我国猪瘟的流行病学现状分析.畜牧市场.2009,12：10～12.
11.陈丽颖,王自振,李春玲,等.河南省的猪瘟流行特点与防治.中国兽医杂志.2003,11：22～23.
12.陶海静.河南省猪瘟流行情况调查.安徽农业科学.2007,35(25)：7842-7843,7845.
13.吴健敏,蒋冬福,韦志峰,等.广西猪瘟流行现状的调查分析.2002,2：16～18.
14.舒相华,宋春莲,刘旭川,等.云南省部分猪场猪瘟流行情况调查.中国畜牧兽医.2009,5：166～167.
15.蒋毅立,韦柳青,郭冬,等.从母猪白细胞检出猪瘟病毒.广西畜牧兽医.2008,5：261～264.
16. Carbrey, E. A., Stewart, W. C., Kresse, J. I., et al. Natural infection of pigs with bovine viral diarrhea virus and its differential diagnosis from hog cholera. J Am Vet Med Assoc.1976,169:1217-1219.
17. Moenning, V. Pestiviruses:a review. Vet Microbiol.1990,23:35-54.
18. Meyers, G., Rumenapf, T., Thiel, H. J. Molecular cloning and nucleotide sequence of the genome of hog cholera virus. Virology.1989,171:555-567.
19. Moormann, R. J., Warmerdam, P. A., van der Meer, B., et al. Molecular cloning and nucleotide sequence of hog cholera virus strain Brescia and mapping of the genomic region encoding envelope protein E1. Virology.1990,177(1):184-198.
20. Poole, T. L., Wang, C., Popp, R. A., et al. Pestivirus translation occurs by internal ribosome entry. Virology.1995,206:750-754.
21. Pestova, T. V., Shatsky, I. N., Fletcher, S. P., et al. A prokaryotic-like mode of cytoplasmic eukaryotic ribosome binding to the initiation codon during internal translation initiation of hepatitis C and_. classical swine fever virus RNAs. Genes Dev.1998,12:67-83.
22. Deng, R., Brock, K. V.5'and 3'untranslated regions of pestivirus genome:primary and secondary structure analyses. Nucleic Acids Res.1993,21:1949-1957.
23. Yu, H., Grassmann, C. W., Behrens, S.-E. Sequence and structural elements at the 3'terminus of bovine viral diarrhea virus genomic RNA:functional role during RNA replication. J. Virol.1999,73:^ 3638-3648.
24. Pankraz, A., Thiel, H. J., Becher, P. Essential and nonessential elements in the 3'nontranslated region of bovine viral diarrhea virus. J Virol.2005,79:9119-9127.
25. Isken, O., Grassmann, C. W., Sarisky, R. T., et al. Members of the NF90/NFAR protein group are involved in the life cycle of a positive-strand RNA virus. EMBO J.2003,22:5655-5665.
26. Xiao, M., Gao, J., Wang, W., et al. Specific interaction between the classical swine fever virus NS5B protein and the viral genome. Eur J Biochem.2004,271:3888-3896.
27. Fletcher, S. P., Jackson, R. J. Pestivirus internal ribosome entry site (IRES) structure and function: elements in the 59 untranslated region important for IRES function. J Virol.2002,76:5024-5033.
28. Heinz, F. X., Collett, M. S., Purcell, R. H., et al (Eds.) Family flaviridae. Virus taxonomy. Eighth report of the international committee on taxonomy of virus. San Diego, Academic Press.2004: 981-998.
29. Rumenapf, T., Unger, G., Strauss, J. H.. et al. Processing of the envelope glycoproteins of pestiviruses. J Virol.1993,67:3288-3294.
30. Poole, T. L., Wang, C, Popp, R. A., et al. Pestivirus translation initiation occurs by internal ribosome entry. Virology.1995,206:750-754.
31. Pestova, T. V., Shatsky, I. N., Fletcher, S. P., et al. A prokaryotic-like mode of cytoplasmic eukaryotic ribosome binding to the initiation codon during internal translation initiation of hepatitis C and classical swine fever virus RNAs. Genes Dev.1998,12:67-83.
32. Fletcher, S. P., Ali,1. K., Kaminski, A., et al. The influence of viral coding sequences on pestivirus IRES activity reveals further parallels with translation initiation in prokaryotes. RNA.2002,8(12): 1558-1571.
33. Sizova, D. V., Kolupaeva, V. G., Pestova, T. A., et al. Specific interaction of eukaryotic translation initiation factor 3 with the 5'nontranslated regions of hepatitis C virus and classical swine fever virus RNAs. J Virol.1998,72:4775-4782.
34. Fletcher, S. P., Jackson, R. J. Pestivirus internal ribosome entry site (IRES) structure and function: elements in the 5'untranslated region important for IRES function. J Virol.2002,76:5024-5033.
35. Reusken, C. B., Dalebout, T. J., Eerligh, P., et al. Analysis of hepatitis C virus/classical swine fever virus chimeric 5'NTRs:sequences within the hepatitis C virus IRES are required for viral RNA replication. J Gen Virol.2003,84(Pt 7):1761-1769.
36. Rijnbrand, R., van der Straaten, T., Van Rijn, P. A., et al. Internal entry of ribosomes is directed by the 5'noncoding region of classical swine fever virus and is dependent on the presence of an RNA pseudoknot upstream of the initiation codon. J Virol.1997,71:451-457.
37. Stark, R., Meyers, G., Rumenapf, T., et al. Processing of Pestivirus Polyprotein:Cleavage Site between Autoprotease and Nucleocapsid Protein of Classical Swine Fever Virus. J Virol.1993,67:7088-7095.
38. Rumenapf, T., Stark, R., Heimann, M., et al. N-terminal protease of pestiviruses:identification of putative catalytic residues by site-directed mutagenesis. J Virol.1998,72(3):2544-2547.
39. Wiskerchen, M., Belzer, S. K., Collett, M. S. Pestivirus gene expression:the first protein product of the bovine viral diarrhea virus large open reading frame, p20, possesses proteolytic activity. J Virol. 1991,65:4508-4514.
40. Thiel, H-J., Stark, R., Weiland, E., et al. Hog cholera virus:molecular compositions of virions from a Pestivirus. J Virol.1991,65:4705-4712.
41. Rumenapf,T.,Stark. R., Heimann, M., et al. N-terminal protease of pestiviruses:identification of putative catalytic residues by site-directed mutagenesis. J Virol.1998.72:2544-2547.
42. Tratschin,J. D.,Moser. C.,Ruggli,N., et al. Classical Swine Fever Virus Leader Proteinase Npro Is Not Required for Viral Replication in Cell Culture. J Virol.1998.72(9):7681-7684.
43. Ruggli,N., Tratschin, J. D.,Schweizer. M., et al. Classical swine fever virus interferes with cellular antiviral defense:evidence for a novel function of Npro. J Virol.2003.77(13):7645-54.
44. Mayer, D., Hofmann, M. A., Tratschin, J.-D. Attenuation of classical swine fever virus by deletion of the viral Npr0 gene. Vaccine.2004,22:317-328.
45. Doceul, V., Charleston, B., Crooke, H., et al. The Npro product of classical swine fever virus interacts with IkappaBalpha, the NF-kappaB inhibitor. J Gen Virol.2008,89(Pt 8):1881-1889.
46. Pahl, H. L. Activators and target genes of Rel/NF-kappaB transcription factors. Oncogene.1999,22, 18(49):6853-6866.
47. La Rocca, S. A., Herbert, R. J., Crooke, H., et al. Loss of interferon regulatory factor 3 in cells infected with classical swine fever virus involves the N-terminal protease, Npro. J Virol.2005,79:7239-7247.
48. Ruggli, N., Bird, B. H., Liu, L., et al. Npro of classical swine fever virus is an antagonist of double-stranded RNA-mediated apoptosis and IFN-a/β induction. Virology.2005,340:265-279.
49. Bauhofer, O., Summerfield. A., Sakoda. Y., et al. Classical swine fever virus Npro interacts with interferon regulatory factor 3 and induces its proteasomal degradation. J Virol.2007,81:3087-3096.
50. Seago, J., Hilton, L., Reid, E., et al. The Npro product of classical swine fever virus and bovine viral diarrhea virus uses a conserved mechanism to target interferon regulatory factor-3. J Gen Virol.2007, 88:3002-3006.
51. Szymanski, M. R., Fiebach, A. R., Tratschin. J. D., et al. Zinc binding in pestivirus Npro is required for interferon regulatory factor 3 interaction and degradation. J Mol Biol.2009,391(2):438-449.
52. Ruggli, N., Summerfield,A.,Fiebach. A. R., et al. Classical swine fever virus can remain virulent after specific elimination of the interferon regulatory factor 3-degrading function of Npro.J Virol.2009.83: 817-829.
53. Heimann, M.,Roman-Sosa. G.,Martoglio. B., et al. Core protein of pestiviruses is processed at the C terminus by signal peptide peptidase. J Virol.2006,80:1915-1921.
54. Liu. J. J., Wong, M. L., Chang. T. J. The recombinant nucleocapsid protein of classical swine fever virus can act as a transcriptional regulator. Virus Res.1998.53:75-80.
55. Rumenapf, T., Unger, G., Strauss, J. H., et al. Processing of the envelope glycoproteins of pestiviruses. J Virol.1993,67(6):3288-3294.
56. Fetzer, C., Tews, B. A., Meyers, G. The carboxy-terminal sequence of the pestivirus glycoprotein Ems represents an unusual type of membrane anchor. J Virol.2005,79:11901-11913.
57. Tews, B. A., Meyers, G. The pestivirus glycoprotein Erns is anchored in plane in the membrane via an amphipathic helix. J Biol Chem.2007,282(45):32730-32741.
58. Hausmann, Y., Roman-Sosa, G., Thiel, H. J., et al. Classical swine fever virus glycoprotein Erns is an endoribonuclease with an unusual base specificity. J Virol.2004,78(10):5507-5512.
59. Meyers, G., Saalmuller, A., Buttner, M. Mutations abrogating the RNase activity in glycoprotein Erns of the pestivirus classical swine fever virus lead to virus attenuation. J Virol.1999,73:10224-10235.
60. Moormann, R. J., Warmerdam, P. A., van der Meer, B., et al. Nucleotide sequence of hog cholera virus RNA:properties of the polyprotein encoded by the open reading frame spanning the viral genomic RNA. Vet Microbiol.1990,23:185-191.
61. Ansari, I. H., Kwon, B., Osorio, F. A., et al. Influence of N-linked glycosylation of porcine reproductive and respiratory syndrome virus GP5 on virus infectivity, antigenicity, and ability to induce neutralizing antibodies. J Virol.2006,80:3994-4004.
62. Panda, A., Elankumaran, S., Krishnamurthy, S., et al. Loss of N-linked glycosylation from the hemagglutinin-neuraminidase protein alters virulence of Newcastle disease virus. J Virol.2004,78: 4965-4975.
63. Hulse, D. J., Webster, R. G., Russell, R. J., et al. Molecular determinants within the surface proteins involved in the pathogenicity of H5N1 influenza viruses in chickens. J Virol.2004,78:9954-9964.
64. Sainz, I. F., Holinka, L. G., Lu, Z. Removal of a N-linked glycosylation site of classical swine fever virus strain Brescia Erns glycoprotein affects virulence in swine. Virology.2008,370:122-129.
65. Tews, B. A., Schurmann, E. M., Meyers, G. Mutation of cysteine 171 of pestivirus Erns RNase prevents homodimer formation and leads to attenuation of classical swine fever virus. J Virol.2009, 83(10):4823-4834.
66. Weiland, E., Stark, R., Haas, B., et al. Pestivirus glycoprotein which induces neutralizing antibodies forms part of a disulfide-linked heterodimer. J Virol.1990,64:3563-3569.
67. Wang, Z., Nie, Y., Wang, P., et al. Characterization of classical swine fever virus entry by using pseudotyped viruses:El and E2 are sufficient to mediate viral entry. Virology.2004,330:332-341.
68. Risatt, G. R., Holinka. L. G., Lu. Z., et al. Mutation of E1 glycoprotein of classical swine fever virus affects viral virulence in swine. Virology.2005.343(1):116-127.
69. Fernandez-Sainz,I., Holinka. L. G., Gavrilov. B. K., et al. Alteration of the N-linked glycosylation condition in E1 glycoprotein of Classical Swine Fever Virus strain Brescia alters virulence in swine. Virology.2009.386:210-216.
70. Thiel, H. J., Stark. R., Weiland. E., et al. Hog cholera virus:molecular composition of virions from a pestivirus. J Virol.1991.65:4705-4712.
71. Wensvoort, G., Boonstra, J., Bodzinga, B. G. Immunoaffinity purification and characterization of the envelope protein E1 of hog cholera virus. J Gen Virol.1990,71(Pt3):531-540.
72. Van Gennip, H. G., Bouma, A., van Rijn, P. A., et al. Experimental non-transmissible marker vaccines for classical swine fever (CSF) by trans-complementation of E(rns) or E2 of CSFV. Vaccine.2002,20: 1544-1556.
73. Moormann. R. J., Warmerdam, P. A., van der Meer, B., et al. Nucleotide sequence of hog cholera virus RNA:properties of the polyprotein encoded by the open reading frame spanning the viral genomic RNA. Vet Microbiol.1990,23:185-191.
74. Risatti, G. R.. Holinka, L. G., Fernandez Sainz, I., et al. N-Linked Glycosylation Status of Classical Swine Fever Virus Strain Brescia E2 Glycoprotein Influences Virulence in Swine. J Virol.2007,81(2): 924-933.
75. Konig,M., Lengsfeld, T., Pauly, T., et al. Classical swine fever virus:independent induction of protective immunity by two structural glycoproteins. J Virol.1995,69:6479-6486.
76. Weiland,E., Stark, R., Haas, B., et al. Pestivirus glycoprotein which induces neutralizing antibodies forms part of a disulfide-linked heterodimer. J Virol.1990,64:3563-3569.
77. Van Rijn, P. A., Miedema,G. K., Wensvoort, G.. et al. Antigenic structure of envelope glycoprotein E2 of hog cholera virus. J Virol.1994,68:3934-3942.
78. Wensvoort, G. Topographical and functional mapping of epitopes on hog cholera virus with monoclonal antibodies. J Gen Virol.1989,70(Ptl 1):2865-2876.
79. Lin. M., Lin. F., Mallory. M., et al. Deletions of structural glycoprotein E2 of classical swine fever virus strain alfort/187 resolve a linear epitope of monoclonal antibody WH303 and the minimal N-terminal domain essential for binding immunoglobulin G antibodies of a pig hyperimmune serum. J Virol.2000.74:11619-11625.
80. Risatti, G. R., Holinka, L. G., Carrillo, C., et al. Identification of a novel virulence determinant within the E2 structural glycoprotein of classical swine fever virus. Virology.2006,355:94-101.
81. Risatti, G. R., Borca, M. V., Kutish, G. F., et al. The E2 glycoprotein of classical swine fever virus is a virulence determinant in swine. J Virol.2005,79:3787-3796.
82. Elbers, K., Tautz, N., Becher, P., et al. Processing in the pestivirus E2-NS2 region:identification of proteins P7 and E2P7. J Virol.1996,70:4131-4135.
83. Moser, C., Stettler, P., Tratschin, J. D., et al. Cytopathogenic and noncytopathogenic RNA replicons of classical swine fever virus. J Virol.1999,73:7787-7794.
84. Tang, Q. H., Zhang, Y. M., Fan, L., et al. Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress. Virol J,2010,7:4.
85. Sheng, C., Xiao, M., Geng, X., et al. Characterization of interaction of classical swine fever virus NS3 helicase with 3'untranslated region. Virus Res.2007,129(1):43-53.
86. Wen, G., Xue, J., Shen, Y., et al. Characterization of classical swine fever virus (CSFV) nonstructural protein 3 (NS3) helicase activity and its modulation by CSFV RNA-dependent RNA polymerase. Virus Res.2009,141(1):63-70.
87. Gallei, A., Orlich, M., Thiel, H. J., et al. Noncytopathogenic pestivirus strains generated by nonhomologous RNA recombination:alterations in the NS4A/NS4B coding region. J Virol.2005, 79(22):14261-14270.
88. Tautz, N., Kaiser, A., Thiel, H. J. NS3 serine protease of bovine viral diarrhea virus:characterization of active site residues, NS4A cofactor interactions. Virology.2000,273:351-363.
89. Xiao, M., Wang, Y., Zhu, Z., et al. Influence of NS5A protein of classical swine fever virus (CSFV) on CSFV internal ribosome entry site-dependent translation. J Gen Virol.2009,90 (Pt 12):2923-2928.
90. Xiao, M., Zhang, C. Y., Pan, Z. S., et al. Classical swine fever virus NS5B-GFP fusion protein possesses an RNA-dependent RNA polymerase activity. Arch Virol.2002,147:1779-1787.
91. Xiao, M., Bai, Y., Xu, H., et al. Effect of NS3 and NS5B proteins on classical swine fever virus internal ribosome entry site-mediated translation and its host cellular translation. J Gen Virol.2008, 89(Pt 4):994-999.
92. Wang, P., Wang, Y., Zhao, Y., et al. Classical swine fever virus NS3 enhances RNA-dependent RNA polymerase activity by binding to NS5B. Virus Res.2010,148(1-2):17-23.
93. Xiao, M., Chen, J., Wang, Y., et al. Sequence, necessary for initiating RNA synthesis, in the 3'-noncoding region of the classical swine fever virus genome. Mol Biol (Mosk).2004,38:343-351.
94. Yu. H.,Grassmann. C. W.. Behrens. S.-E. Sequence and structural elements at the 3'terminus of bovine viral diarrhea virus genomic RNA:functional role during RNA replication. J Virol.1999,73: 3638-3648.
95. Pankraz, A., Thiel, H. J., Becher, P. Essential and nonessential elements in the 3'nontranslated region of bovine viral diarrhea virus.J Virol.2005.79:9119-9127.
96. Isken,O.,Grassmann, C. W., Yu,H., et al. Complex signals in the genomic 3'nontranslated region of bovine viral diarrhea virus coordinate translation and replication of the viral RNA. RNA.2004,10(10): 1637-1652.
97. Xiao, M., Zhang, C. Y., Zhu, Z. Z., et al. Qualitative, quantitative and structure analysis of 3'UTR of classic swine fever virus. Chin Sci Bull.2001,46:544-550.
98. Huang, Q. H., Zhang, C. Y., Wang, J. F., et al. Molecular cloning and nucleotide sequence of classical swine fever virus strain Shimen. Wuhan Uni J Nat Sci.1998,3:504-508.
99. Xiao, M., Gao, J., Wang, Y. et al. Influence of a 12-nt insertion present in the 3'untranslated region of classical swine fever virus HCLV strain genome on RNA synthesis. Virus Res.2004a,102:191-198.
100. Rodriguez-Cerezo, E., Klein, P. G., Shaw, J. G. A determinant of disease symptom severity is located in the 3'-terminal noncoding region of the RNA of a plant virus. Proc Natl Acad Sci. U. S. A.1991,88: 9863-9867.
101. Wang Y., Wang Q., Lu X., et al.12-nt insertion in 3'untranslated region leads to attenuation of classic swine fever virus and protects host against lethal challenge. Virology.2008,10:374(2):390-398.
102. Hulst, M. M., van Gennip, H. G. P., Moormann, R. J. M. Passage of Classical Swine Fever Virus in Cultured Swine Kidney Cells Selects Virus Variants That Bind to Heparan Sulfate due to a Single Amino Acid Change in Envelope Protein Erns. J Virol.2000,74:9553-9561,
103. Hulst. M. M., vanGennip. H. G., Vlot. A. C., et al. Interaction of classical swine fever virus with membrane-associated heparan sulphate:role for virus replication in vivo and virulence. J Virol.2001. 75:9585-9595.
104. Maurer,K.,Krey,T.,Moennig, V., et al. CD46 is a cellular receptor for bovine viral diarrhea virus. J Virol.2004.78:1792-1799.
105. Krey. T., Himmelreich, A., Heimann. M., et al. Function of bovine CD46 as a cellular receptor for bovine viral diarrhea virus is determined by complement control protein 1. J Virol.2006.80: 3912-3922.
106. Hulst, M. M., Moormann, R. J. M. Inhibition of pestivirus infection in cell culture by envelope proteins Erns and E2 of classical swine fever virus:Ems and E2 interact with different receptors. J Ger virol.1997,78:2779-2787.
107. Agnello, V., Abel, G., Elfahal, M., et al. Hepatitis C virus and other flaviviridae viruses enter cells via low density lipoprotein receptor. PNAS.1999,96(22):12766-12771.
108. Cheville N. F., Mengeling, W. L. The pathogenesis of chronic hog cholera (swine fever). Histologic, immunofluorescent, and electron microscopic studies. Lab Invest.1969,20:261-274.
109. Ressang, A. A. Studies on the pathogenesis of hog cholera.Ⅱ. Virus distribution in tissue and morphology of the immune response. Zentralbl Veterinaermed Reihe B.1973,20:272-288.
110. Susa, M., Konig, M., Saalmuller, A., et al. Pathogenesis of classical swine fever:B-lymphocyte deficiency caused by hog cholera virus. J Virol.1992,66:1171-1176.
111.Thiel, H. J., Plagemann, G. W., Moennig, V. Pestiviruses. In B. N. Fields, D. M. Knipe, P. M. Howley, et al. (ed.), Fields virology. Lippincott-Raven Publishers, Philadelphia, Pa.1996,1059-1073.
112. Trautwein, G. Pathology and pathogenesis of the disease. In B. Liess (ed.), Classical swine fever and related infections. Martinus Nijhoff Publishing, Boston, Mass.1988,27-54.
113. Campos, E., Revilla, C., Chamorro, S., et al. In vitro effect of classical swine fever virus on a poricne aortic endothelial cell line. Vet Res.2004,35:625-633.
114. Summerfield, A., Knoetig, S. M., Tschudin, R. et al. Pathogenesis of granulocytopenia and bone marrow atrophy during classical swine fever involves apoptosis and necrosis of uninfected cells. Virology.2000,272:50-60.
115. Ressang, A. A. Studies on the pathogenesis of hog cholera.Ⅱ. Virus distribution in tissue and the morphology of the immune response. Zentbl Vetmed Reihe B.1973,20:272-288.
116. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Bautista, M. J., et al. Morphological and immunohistochemical changes in splenic macrophages of pigs infected with classical swine fever. J Comp Pathol.2001,125:98-109.
117. Sanchez-Cordon, P. J., Romanini, S., Salguero, F. J., et al. A histopathologic, immunohistochemical, and ultrastructural study of the intestine in pigs inoculated with classical swine fever virus. Vet Pathol. 2003,40:254-262.
118. Trautwein, G. Pathology and pathogenesis of the disease. In Classical Swine Fever and Related Infections. Edited by B. Liess. Boston:Martinus Nijhoff Publishing.1988,27-54.
119. Knoetig, S. M., Summerfield. A., Spagnuolo-Weaver. M., et al. Immunopathogenesis of classical swine fever:role of monocytic cells. Immunology.1999,97:359-366.
120. Summerfield. A., Knotigy. S. M., McCullough. K. C. Lymphocyte apoptosis during classical swine fever:implication of activation-induced cell death. J Virology.1998b.72:1853-1861.
121. Sato,M., Mikami,O.,Kobayashim. M., et al. Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus. Vet Microbiol.2000,75:1-9.
122. Summerfield, A., Hofmann, M.A., McCullough, K.C. Low density blood granulocytic cells induced during classical swine fever are targets for virus infection. Vet Immunol Immunopathol.1998a,63(3): 289-301.
123.de las Mulas, J. M., Ruiz-Villamor, E., Donoso, S., et al. Immunohistochemical detection of hog cholera viral glycoprotein 55 in paraffin-embedded tissues. J Vet Diagn Invest.1997,9(1):10-16.
124. Narita, M., Kawashima. K., Kimura, K., et al. Comparative immunohistopathology in pigs infected with highly virulent or less virulent strains of hog cholera virus. Vet Pathol.2000,37:402-408.
125. Fischer, V. U., Kaden, V., Beyer. J. Zur nachweissicherheit von schweinepestvirusantigen und zur differenzierung der feld-und vakzinevirusinfektion mit dem direkten immunfluoreszenztest an organmaterial. Munchener Veterinar Medizin.1991.46:133-136.
126. Dahle. J., Schagemann. G., Moennig, V., et al. Clinical, virological and serological findings after intranasal inoculation of pigs with bovine viral diarrhoea virus and subsequent intranasal challenge with hog cholera virus. Journal of Veterinary Medicine (Series B).1993,40:46-54.
127. Pan, I. C., Huang, T. S., Pan, C. H., et al. The skin, tongue and brain as favorable organs for hog cholera diagnosis by immunofluorescence. Archives of Virology.1993.131:475-481.
128. Martin de las Mulas. J., Ruiz-Villamor, E., Donoso, S., et al. Immunohistochemical detection of hog cholera viral glycoprotein 55 in paraffin-embedded tissues. J Vet Diagn Invest.1997,9(1):10-16.
129. Bruschke. C. J. M., Hulst. M. M., Moormann. R. J. M., et al. Glycoprotein Ems of pestiviruses induces apoptosis in lymphocytes of several species. Journal of Virology.1997.71:6692-6696.
130. Summerfield. A., Zingle,K.,Inumaru,S., et al. Induction of apoptosis in bone marrow neutrophil-lineage cells by classical swine fever virus. J Gen Virol.2001,82:1309-1318.
131. Carrasco,C. P.,Rigden. R. C., Vincent.I. E.,et al. Interaction of classical swine fever virus with dendritic cells. J Gen Virol.2004.85.1633-41.
132. Lee, W. C., Wang, C. S., Chien, M. S. Virus antigen expression and alterations in peripheral blood mononuclear cell subpopulations after classical swine fever virus infection. Vet Microbiol.1999,67(1): 17-29.
133. Carrasco, L., Ruiz-Villamor, E., Gomez-Villamandos, J. C., et al. Classical swine fever: morphological and morphometrical study of pulmonary intravascular macrophages. J Comp Pathol. 2001,125(1):1-7.
134. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Salguero, F. J., et al. Immunohistochemical and ultrastructural evidence of hog cholera virus infection of megakaryocytes in bone marrow and spleen. J Comp Pathol.1998,119(2):111-119.
135. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Bautista, M. J., et al. Pathogenesis of Classical Swine Fever:Renal Haemorrhages and Erythrodiapedesis. J Comp Path.2000,123:47-54.
136. Campos, E., Revilla, C., Chamorro, S., et al. In vitro effect of classical swine fever virus on a porcine aortic endothelial cell line. Vet Res.2004,35(6):625-633.
137. Markowska-Daniel, I., Pejsak, Z., Winnicka, A., et al. Phenotypic analysis of peripheral leukocytes in piglets infected with classical swine fever virus. Res Vet Sci.1999,67(1):53-57.
138. Summerfield, A., McNeilly, F., Walker, I., et al. Depletion of CD4+ and CD8high+ T-cells before the onset of viraemia during classical swine fever. Vet Immunol Immunopathol.2001,78(1):3-19.
139.孙金福,史子学,郭焕成,等.猪瘟病毒感染猪外周血白细胞凋亡及CD4+和CD8+T淋巴细胞亚群的变化.中国兽医科学.2008,38(04)：342～345.
140. Maudsley, D. J., Pound, J. D. Modulation of MHC antigen expression by viruses and oncogenes. Immunol Today.1991,12:429-431.
141. Rouse, B. T., Horohov, D. W. Immunosuppression in viral infections. Rev Inf Dis.1986,8:850-873.
142. Van Oirschot, J. T., De Jong, D., Huffels, N. D. N. H. J. Effect of infections with swine fever virus on immune functions I. Response of lymphocytes from blood and lymphoid organs from infected and normal pigs to anti-immunoglobulin serum and protein A. Vet Microbiol.1981,6:41-57.
143. Van Oirschot, J. T., De Jong, D.,Huffels, N. D. N. H. J. Effect of infections with swine fever virus on immune functions Ⅱ. Lymphocyte response to mitogens and enumeration of lymphocyte subpopulations. Vet Microbiol.1983,8:81-95.
144. Pauly, T., Konig, M., Thiel, H. J. et al. Infection with classical swine fever virus:effects on phenotype and immune responsiveness of porcine T lymphocytes. J Gen Virol.1998,79(Ptl):31-40.
145. Mittelholzer, C., Moser, C., Tratschin, J. D., et al. Porcine cells persistently infected with classical swine fever virus protected from pestivirus-induced cytopathic effect. J Gen Virol.1998,79: 2981-2987.
146.郑从义,童攒,应松成,等.猪瘟病毒野强毒株持续感染细胞模型的初步研究.武汉大学学报(理学版).2002,48(6)：720～724.
147.应松成,郑从义,屈三甫,等.猪瘟病毒野毒株持续性感染细胞模型的建立.中国病毒学.2002,17(1)：77～81.
148. Meyers, G., Thiel, H. J., Rumenapf, T. Classical swine fever virus:recovery of infectious viruses from cDNA constructs and generation of recombinant cytopathogenic defective interfering particles. J Virol. 1996,70:1588-1595.
149. Moser, C., Stettler, P., Tratschin, J. D., et al. Cytopathogenic and noncytopathogenic RNA replicons of Classical swine fever virus. J Virol.1999,73:7787-7794.
150. Xu, H., Hong, H. X., Zhang, Y. M., et al. Cytopathic effect of classical swine fever virus NS3 protein^ on PK-15 cells. Intervirology.2007,50(6):433-438.
151. Banchereau, J., Briere, F., Caux, C., et al. Immunobiology of dendritic cells. Annu Rev Immunol. 2000,18:767-811.
152. Steinman, R. M. The dendritic cell system and its role in immunogenicity. Annu Rev Immunol.1991T 9:271-296.
153. MacPherson, G. G., Liu, L. M. Dendritic cells and Langerhans cells in the uptake of mucosal antigens. Curr Top Microbiol Immunol.1999,236:33-53.
154. Pulendran, B., Palucka, K. Banchereau, J. Sensing pathogens and tuning immune responses. Science. 2001,293:253-256.
155. Carrasco, C. P., Rigden, R. C., Vincent, I. E., et al. Interaction of classical swine fever virus with dendritic cells. J Gen Virol.2004,85,1633-1641.
156. Fugier-Vivier, I., Servet-Delprat, C, Rivailler, P., et al. Measles virus suppresses cellmediated immunity by interfering with the survival and functions of dendritic and T cells. J Exp Med.1997,186: 813-823.
157. Cella, M., Salio, M., Sakakibara, Y., et al. Maturation, activation, and protection of dendritic cells induced by double-stranded RNA. J Exp Med.1999,189:821-829.
158. Ho, L. J., Wang, J. J., Shaio, M. F., et al. Infection of human dendritic cells by dengue virus causes cell maturation and cytokine production. J Immunol.2001,166:1499-1506.
159. Gardner, J. P., Frolov, I., Perri, S., et al. Infection of human dendritic cells by a Sindbis virus replicon vector is determined by a single amino acid substitution in the E2 glycoprotein. J Virol.2000,74: 11849-11857.
160. Bauhofer, O., Summerfield, A., McCullough, K. C., et al. Role of double-stranded RNA and Npro of classical swine fever virus in the activation of monocyte-derived dendritic cells. Virology.2005, 343(1):93-105.
161. Kawai, T., Akira, S. Innate immune recognition of viral infection. Nat Immunol.2006,7:131-137.
162. Malmgaard, L. Induction and regulation of IFNs during viral infections. J Interferon Cytokine Res. 2004,24:439-454.
163. Goodbourn, S., Didcock, L., Randall, R. E. Interferons:cell signalling, immune modulation, antiviral response and virus countermeasures. J Gen Virol.2000,81:2341-2364.
164. Haller, O., Kochs, G., Weber, F. The interferon response circuit:induction and suppression by pathogenic viruses. Virology.2006,344:119-130.
165. Hengel, H., Koszinowski, U. H., Conzelmann, K. K. Viruses know it all:new insights into IFN networks. Trends Immunol.2005,26:396-401.
166. Weber, F., Kochs, G., Haller, O. Inverse interference:how viruses fight the interferon system. Viral Immunol.2004,17:498-515.
167.Larocca, S. A., Herbert, R. J., Crooke, H., et al. Loss of Interferon Regulatory Factor 3 in Cells Infected with Classical Swine Fever Virus Involves the N-Terminal Protease, Npro. J Virol.2005,79: 7239-7247.
168. Xia, Y. H., Chen, L., Pan, Z. S., et al. A novel role of classical swine fever virus Erns glycoprotein in counteracting the newcastle disease virus (NDV)-mediated IFN-beta Induction. J Biochem Mol Biol. 2007,40(5):611-616.
169. Luo X, Pan R, Wan C, et al. Glycosylation of classical swine fever virus Erns is essential for binding double-stranded RNA and preventing interferon-beta induction. Virus Res,2009,146(1-2):135-139.
170. Luo,X., Ling, D., Li, T., et al. Classical swine fever virus Erns glycoprotein antagonizes induction of interferon-beta by double-stranded RNA. Can J Microbiol.2009,55(6):698-670.
171. Moore, K. W., Malefytr, D. W., Coffman, R. L., et al. Interleukin-10 and the interleukin-10 receptor. Annu Rev Immunol.2001,19:683-765.
172. Redpath. S.,Ghazal. P., Gascoigne. N. R. Hijacking and exploitation of IL-10 by intracellular pathogens. Trends Microbiol.2001.9(2):86-92.
173. Almonti, J. B.,Ball. T. B., Fowke. K. R. Mechanisms of CD4 T lymphocyte cell death in human immunodeficiency virus infection and AIDS. J Gen Virol.2003,84:1649-1661.
174. Dolganiuc. A., Kodys, K., Kopasz. A., et al. Hepatitis C virus core and non-structural protein 3 proteins induce pro-and anti-inflammatory cytokines and inhibit dendritic cell differentiation. J Immunol.2003.170(11):5615-5624.
175. Suradhat, S., Thanawongguwech,R., Poovorawan, Y. Upregulation of IL-10 gene expression in porcine peripheral blood mononuclear cells by porcine reproductive and respiratory syndrome virus. J Gen Virol.2003,84:453-459.
176. Suradhat, S., Sada, W., Buranapraditkun, S., et al. The kinetics of cytokine production and CD25 expression by porcine lymphocyte subpopulations following exposure to classical swine fever virus (CSFV). Vet Immunol Immunopathol.2005,106:197-208.
177. Jamin, A., Gorin, S., Cariolet, R., et al. Classical swine fever virus induces activation of plasmacytoid and conventional dendritic cells in tonsil, blood, and spleen of infected pigs.Vet Res.2008,39:07.
178. Bjorkman, P. J., Saper. M. A., Samraoui, B., et al. Structure of the human class I histocompatibility antigen, HLA-A2. Nature.1987,329:506-512.
179. O'Cormor, D. H., Mothe, B. R., Weinfurter. J. T., et al. Major histocompatibility complex class I alleles associated with slow simian immunodeficiency virus disease progression bind epitopes recognized by dominant acut-phase cytotoxic-T-lymphocyte responses. J Virol.2003.77:9029-9040.
180. Bobe, P., Benihoud. K., Kiger, N. Allogenic MHC class Ⅱ determinant(s) in MRL/lpr autoimmune disease-prone mice. Unusual expression of an L1 transposable element creates molecular mimicry. J Immunol.1993,151:2813-2819.
181.Chardon,P.,Renard, C Gaillard, C. R., et al. The porcine major histocompatibility complex and related paralogous regions. Genet Sel Evol.2000.32(2):109-128.
182. Sanz-Parra,A., Sobrinoand. F., Ley,V. Infection with foot-and-mouth disease virus results in a rapid reduction of MHC class 1 surface expression. J Gen Virol.1998.79:433-436.
183. Wang, X., Eaton,M., Mayer. M., et al. Porcine reproductive and respiratory syndrome virus productively infects monocyte-derived dendritic cells and compromises their antigen-presenting ability. Arch Virol.2007,152:289-303.
184. Johnson, D. C., Hill, A. B. Herpesvirus evasion of the immune system. Curr Top Microbiol Immunol. 1998,232:150-165.
185. Cohen, J.1. Infection of cells with varicella-zoster virus down-regulates surface expression of class I MHC antigens. J Infect Dis.1998,177:1390-1393.
186. Koppers-Lalic, D., Rijsewijk, F. A. M., Verschuren, S. B. E., et al. The UL41-encoded virion host shutoff (vhs) protein and vhs-independent mechanisms are responsible for downregulation of MHC class I molecules by bovine herpesvirus 1. J Gen Virol.2001,82:2071-2081.
187. Mellencamp, M. W., O'Brien, P. C., Stevenson, J. R. Pseudorabies virus-induced suppression of MHC class I antigen expression. J Virol.1991,65:3365-3370.
188. Rappocciolo, G., Birch, J., Ellis, S. A. Down-regulation of MHC class I expression by equine herpesvirus-1. J Gen Virol.2003,84:293-300.
189. Benz, C., Reusch, U., Muranyi, W., et al. Efficient downregulation of major histocompatibility complex class I molecules in human epithelial cells infected with cytomegalovirus. J Gen Virol.2001, 82(Pt9):2061-2070.
190. Lacayo, J., Sato, H., Kamiya, H., et al. Down-regulation of surface major histocompatibility complex class I by guinea pig cytomegalovirus. J Gen Virol.2003,84:75-81.
191.Tardif, K. D., Siddiqui, A. Cell surface expression of major histocompatibility complex class Ⅰ molecules is reduced in hepatitis C virus subgenomic replicon-expressing cells. J Virol.2003,77(21): 11644-11650.
192. Brown, J. A., Howcroft, T. K., Singer, D. S. HIV Tat protein requirements for transactivation and repression of transcription are separable. J Acquir Immune Defic Syndr Hum Retrovirol.1998,17: 9-16.
193. Kamp, W., Berk, M. B., Visser, C. J., et al. Mechanisms of HIV-1 to escape from the host immune surveillance. Eur J Clin Invest.2000,30:740-746.
194. Kanazawa, S., Okamoto, T., Peterlin, B. M. Tat competes with CⅡTA for the binding to P-TEFb and blocks the expression of MHC class Ⅱ genes in HIV infection. Immunity.2000,12:61-70.
195. Ashrafi, G. H., Tsirimonaki, E., Marchetti, B., et al. Down-regulation of MHC class I by bovine papillomavirus E5 oncoproteins. Oncogene.2002,21:248-259.
196. Ashrafi, G. H., Haghshenas, M. R., Marchetti, B., et al. E5 protein of human papillomavirus type 16 selectively downregulates surface HLA class I. Int J Cancer.2005,113:276-283.
197. Cadwell,K., Coscoy. L. Ubiquitination on nonlysine residues by a viral E3 ubiquitin ligase. Science. 2005.309:127-130.
198. Goto, E., Ishido. S., Sato, Y., et al. c-MIR. a human E3 ubiquitin ligase. is a functional homolog of herpesvirus proteins MIR1 and MIR2 and has similar activity. J Biol Chem.2003.278:14657-14668.
199. Coscoy, L., Ganem, D. Kaposi's sarcoma-associated herpesvirus encodes two proteins that block cell surface display of MHC class I chains by enhancing their endocytosis. PNAS.2000,97:8051-8056.
200. Ishido, S., Choi, J. K., Lee, B. S., et al. Inhibition of natural killer cell-mediated cytotoxicity by Kaposi's sarcoma-associated herpesvirus K5 protein. Immunity.2000.13:365-374.
201. Stevenson, P. G., Efstathiou, S., Doherty, P. C., et al. Inhibition of MHC class I-restricted antigen presentation by y 2-herpesviruses. PNAS.2000,97:8455-8460.
202. Lybarger, L., Wang, X., Harris, M., et al. Viral immune evasion molecules attack the ER peptide-loading complex and exploit ER-associated degradation pathways. Curr Opin Immunol.2005, 17:71-78.
203. Georgopoulos, N, T., Proffitt, J. L., Blair, G. E. Transcriptional regulation of the major histocompatibility complex (MHC) class I heavy chain, TAP1 and LMP2 genes by the human papillomavirus (HPV) type 6b,16 and 18 E7 oncoproteins. Oncogene.2000,19: 4930-4935.
204. Ahn, K., Gruhler, A., Galocha, B., et al. The ER-luminal domain of the HCMV glycoprotein US6 inhibits peptide translocation by TAP. Immunity.1997,6:613-621.
205. Fruh,K., Ahn,K.,Djaballah, H., et al. A viral inhibitor of peptide transporters for antigen presentation. Nature.1995,375:415-418.
206. Hengel, H., Koopmann, J. O., Flohr, T., et al. A viral ER-resident glycoprotein inactivates the MHC-encoded peptide transporter. Immunity.1997,6:623-632.
207. Hill, A.,Jugovic. P., York. I., et al. Herpes simplex virus turns off the TAP to evade host immunity. Nature.1995.375:411-415.
208. Lehner, P. J., Karttunen. J. T.. Wilkinson. G. W.. et al. The human cytomegalovirus US6 glycoprotein inhibits transporter associated with antigen processing-dependent peptide translocation. Proc Natl Acad Sci,USA.1997.94:6904-6909.
209. Ahn, K.,Meyer. T. H.,Uebel. S.,et al. Molecular mechanism and species specificity of TAP inhibition by herpes simplex virus ICP47. EMBO J.1996,15:3247-3255.
210. Tomazin, R., Hill, A. B., Jugovic, P., et al. Stable binding of the herpes simplex virus ICP47 protein to the peptide binding site of TAP. EMBO J.1996,15:3256-3266.
211. Ambagala, A. P., Hinkley, S., Srikumaran, S. An early pseudorabies virus protein down-regulates porcine MHC class I expression by inhibition of transporter associated with antigen processing (TAP). J Immunol.2000,164(1):93-99.
212. Tortorella, D., Gewurz, B. E., Furman, M. H., et al. Viral subversion of the immune system. Annu Rev Immunol.2000,18:861-926.
213. Spriggs, M. K. One step ahead of the game:viral immunomodulatory molecules. Annu Rev Immunol. 1996,14:101-130.
214. Fruh, K., Gruhler, A., Krishna, R. M., et al. A comparison of viral immune escape strategies targeting the MHC class I assembly pathway. Immunol Rev.1999,168:157-166.
215. Farrell, H. E., Davis-Poynter, N. J. From sabotage to camouflage:viral evasion of cytotoxic T lymphocyte and natural killer cell-mediated immunity. Semin Cell Dev Biol.1998,9:369-378.
216. Hengel, H., Brune, W., Koszinowski, U. H. Immune evasion by cytomegalovirus--survival strategies of a highly adapted opportunist. Trends Microbiol.1998,6(5):190-197.
217. Tomazin, R., Boname, J., Hegde, N. R., et al. Cytomegalovirus US2 destroys two components of the MHC class II pathway, preventing recognition by CD4+ T cells. Nat Med.1999,5:1039-1043.
218. Hegde, N. R., Tomazin, R. A., Wisner, T. W., et al. Inhibition of HLA-DR assembly, transport, and loading by human cytomegalovirus glycoprotein US3:a novel mechanism for evading major histocompatibility complex class Ⅱ antigen presentation. J Virol.2002,76(21):10929-10941.
219. Yao, Y., Li, P., Singh, P., et al. Vaccinia virus infection induces dendritic cell maturation but inhibits antigen presentation by MHC class Ⅱ. Cell Immunol.2007,246:92-102.
220. Rehm, K. E., Connor, R. F., Jones, G. J., et al. Vaccinia virus A35R inhibits MHC class II antigen presentation. Virology.2010,397:176-186.
221. Zhang, B., Li, P., Wang, E., et al. The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon-gamma. Virology. 2003,310:100-108.
222. Zhang, B., Wang. E. The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon gamm. Virology.2003,310: 100-108.
223. Mozdzanowska. K., Furchner. M.,Zharikova. D., et al. Roles of CD4- T-cell-Independent and-dependent antibody responses in the control of influenza virus infection:evidence for noncognate CD- T T cell activities that enhance the therapeutic activity of antiviral antibodies. J Virol.2005.79 (10):5943-5951.
224. Hussain, A., Wesley. C. Khalid. M. et al. Human immunodeficiency virus type 1 Vpu protein interacts with CD74 and modulates major histocompatibility complex class Ⅱ presentation. J Virol. 2008,82(2):893-902.
225. Ishido, S., Choi, J. K.,Lee. B. S., et al. Inhibition of natural killer cell-mediated cytotoxicity by Kaposi's sarcoma-associated herpesvirus K5 protein. Immunity.2000,13(3):365-374.
226. Coscoy, L., Ganem, D. A. viral protein that selectively downregulates ICAM-1 and B7-2 and modulates T cell costimulation. J Clin Invest.2001,107:1599-1606.
227. Barker, E., Bossart, K. N., Fujimura, S. H., et al. The role of CD80 and CD86 in enhancing CD8+ cell suppression of HIV replication. Cell Immunol.1999,196:95-103.
228. Salek-Ardakani, S., Arrand, J. R., Mackett, M. Epstein-Barr virus encoded interleukin-10 inhibits HLA-class I. ICAM21, and B7 expression on human monocytes:implications for immune evasion by EBV. Virology.2002,304(2):342-351.
229. Fuse, S., Obar, J. J., Bellfy, S., et al. CD80 and CD86 control antiviral CD8+ T-cell function and immune surveillance of murine gamma herpesvirus68. J Virol.2006,80(18):9159-9170.
230. Creery, W. D.,Diaz-Mitoma, F.,Filion. L., et al. Differential modulation of B7-1 and B7-2 isoform expression on human monocytes by cytokines which influence t he development of T helper cell phenotype. Eur J Immunol.1996,26(6):1273-1277.
231. Fiorentino, D. F., Zlotnik, A., Vieira, P., et al. IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Thl cells. J Immunol.1991,146(10):3444-3451.
232. Girard, B. M.,May, V., Bora, S. H.,et al. Regulation of neurotrophic peptide expression in sympathetic neurons:quantitative analysis using radioimmunoassay and real-time quantitative polymerase chain reaction. Regul Pept.2002.109(1-3):89-101.
233. Wickert. L., Steinkruger, S., Abiaka, M., et al. Quantitative monitoring of the mRNA expression pattern of the TGF-beta-isoforms (beta 1,beta 2. beta 3) during transdifferentiation of hepatic stellate cells using a newly developed real-time SYBR Green PCR. Biochem Biophys Res Commun.2002. 295:330-335.
234. Guang-li, Li., Roy, B., Xing-hua, Li., et al. Quantification of silkworm coactivator of MBF1 mRNA by SYBR Green I real-time RT-PCR reveals tissue-and stage-specific transcription levels. Mol Biol Rep.2009,36:1217-1223.
235. Sato, H., Ozawa, K., Yonemura, K., et al. Quantitative PCR to evaluate small amounts of BCL2 mRNA in human peripheral T cells:implication of equimolar target and competitor end products. Clin Chim Acta.2003,328(1-2):147-153.
236. Gallard, A., Foucras, G., Coureau, C., et al. racking T cell clonotypes in complex T lymphocyte populations by real-time quantitative PCR using fluorogenic complementarity-determining region-3-specific probes. J Immunol Methods.2002,270(2):269-280.
237. Deng, X., Li, H., Tang, Y. W. Cytokine expression in respiratory syncytial virus-infected mice as measured by quantitative reverse-transcriptase PCR. J Virol Methods.2003,107(2):141-146.
238. White, T. M., Mahalingam, R., Traina-Dorge, V., et al. Persistence of simian varicella virus DNA in CD4(+) and CD8(+) blood mononuclear cells for years after intratracheal inoculation of African green monkeys. Virology.2002,303(1):192-198.
239. Maeda, S., Miyauchi, T., Iemitsu, M., et al. Effects of exercise training on expression of endothelin-1 mRNA in the aorta of aged rats. Clin Sci (Lond).2002,103 Suppl 48:118S-123S.
240.李一荣,胡丽华,陈凤花,等.应用SYBR Green I实时荧光PCR法对中国汉族人群HLA-B27进行快速基因分型.临床血液学杂志.2008,21(10)：526～529.
241.王默进,周总光,王玲,等.运用TaqMan探针实时荧光PCR技术检测AKAP10基因2073A/G单核苷酸多态性.四川大学学报(医学版).2009,40(2)：275～278.
242.严冰冰,虞涛,方华红,等.应用实时荧光PCR分析apoE3、4等位基因.临床检验杂志.2008,26(3)：197～199.
243. Weise, A., Grundler, S., Zaumsegel, D., et al. Development and evaluation of a rapid and reliable method for cytochrome P450 2C8 genotyping. Clin Lab.2004,50(3-4):141-148.
244. Stamer, U. M., Bayerer, B., Wolf, S., et al. Rapid and reliable method for cytochrome P450 2D6 genotyping. Clin Chem.2002,48(9):1412-1217.
245. Sangkitporn, S. K., Wangkahat, K., Sangnoi, A., et al. Rapid diagnosis of alpha (a)-thalassemia using the relative quantitative PCR and the dissociation curve analysis.Clin Lab Haematol.2003,25(6): 359-365.
246.刘敬忠,闫梅,王立荣,等.实时荧光聚合酶链反应结合融解曲线分析在α-地中海贫血基因诊断 中的价值.中华检验医学杂志.2005,28(8)：858～861.
247.尹爱华.张祥忠.何蕴韶.等.TaqMan-MGB探针实时荧光PCR在β地中海贫血植入前诊断中的应用研究.热带医学杂志.2007,7(12)：1155-1158.
248. Zimmermann. B., Holzgreve, W.,Wenzel,F., et al. Novel real-time quantitative PCR test for trisomy 21. Clin Chem.2002.48(2):362-363.
249. Miyake, Y.,Fujiwara, Y., Ohue, M., et al. Quantification of micrometastases in lymph nodes of colorectal cancer using real-time fluorescence polymerase chain reaction. Int J Oncol.2000,16(2): 289-293.
250. Eckert, C., Landt, O., Taube, T., et al. Potential of LightCycler technology for quantification of minimal residual disease in childhood acute lymphoblastic leukemia. Leukemia.2000,14(2): 316-323.
251.赵建军,成丹,李娜,等.猪瘟病毒野毒株和兔化弱毒疫苗株复合实时荧光定量RT-P CR鉴别方法的建立.中国兽医科学.2007,37(05)：406～412.
252. Jamnikar Ciglenecki, U., Grom, J., Toplak, I., et al. Real-time RT-PCR assay for rapid and specific detection of classical swine fever virus:comparison of SYBR Green and TaqMan MGB detection methods using novel MGB probes. J Virol Methods.2008,147(2):257-264.
253. Yang, J. R.. Lo, J., Liu, J. L., et al. Rapid SYBR green I and modified probe real-time reverse transcription-PCR assays identify influenza H1N1 viruses and distinguish between pandemic and seasonal strains. J Clin Microbiol.2009,47(11):3714-3716.
254. Liu, S., Hou. G., Shu. Y.. et al. A SYBR Green I real-time RT-PCR assay for detection and differentiation of influenza A (H1N1) virus in swine populations. J Virol Methods.2009,162(1-2): 184-187.
255. Tan, S. W., Ideris, A., Omar, A. R., et al. Detection and differentiation of velogenic and lentogenic Newcastle disease viruses using SYBR Green I real-time PCR with nucleocapsid gene-specific primers. J Virol Methods.2009,160(1-2):149-156.
256. Martinez, E.,Riera. P., Sitja. M., et al. Simultaneous detection and genotyping of porcine reproductive and respiratory syndrome virus (PRRSV) by real-time RT-PCR and amplicon melting curve analysis using SYBR Green. Res Vet Sci.2008,85(1):184-193.
257. McIntosh,K. A., Tumber. A., Harding. J. C., et al. Development and validation of a SYBR green real-time PCR for the quantification of porcine circovirus type 2 in serum, buffy coat, feces, and multiple tissues. Vet Microbiol.2009,133(1-2):23-33.
258. Brunborg, I. M, Moldal, T., Jonassen, C. M. Quantitation of porcine circovirus type 2 isolated from serum/plasma and tissue samples of healthy pigs and pigs with postweaning multisystemic wasting syndrome using a TaqMan-based real-time PCR. J Virol Methods.2004,122(2):171-178.
259. Chung, W. B., Chan, W. H., Chaung, H. C., et al. Real-time PCR for quantitation of porcine reproductive and respiratory syndrome virus and porcine circovirus type 2 in naturally-infected and challenged pigs. J Virol Methods.2005,124(1-2):11-19.
260. Ladekjaer-Mikkelsen, A. S., Nielsen, J., Stadejek, T., et al. Reproduction of postweaning multisystemic wasting syndrome (PMWS) in immunostimulated and non-immunostimulated 3-week-old piglets experimentally infected with porcine circovirus type 2 (PCV2). Vet Microbiol. 2002,89(2-3):97-114.
261. Olvera, A., Sibila, M., Calsamiglia, M., et al. Comparison of porcine circovirus type 2 load in serum quantified by a real time PCR in postweaning multisystemic wasting syndrome and porcine dermatitis and nephropathy syndrome naturally affected pigs. J Virol Methods.2004,117(1):75-80.
262. Rovira, A., Balasch, M., Segales, J., et al. Experimental inoculation of conventional pigs conventional pigs with porcine reproductive and respiratory syndrome virus and porcine circovirus 2. J Virol.2002, 76(7):3232-3239.
263. Jefferies, R., Morgan, E. R., Shaw, S. E. A SYBR green real-time PCR assay for the detection of the nematode Angiostrongylus vasorum in definitive and intermediate hosts. Vet Parasitol.2009,166(1-2): 112-118.
264. Chen, S., Yee, A., Griffiths, M., et al. The evaluation of a fluorogenic polymerase chain reaction assay for the detection of Salmonella species in food commodities. Int J Food Microbiol.1997,35: 239-250.
265. Oberst, R. D., Hays, M. P., Bohra, L. K., et al. PCR-based DNA amplification and presumptive detection of Escherichia coli O157:H7 with an internal fluorogenic probe and the 5'nuclease TaqMan assay. Appl Environ Microbiol.1998,64:3389-3396.
266. Leutenegger, C. M., Pusterla, N., Mislin, C. N., et al. Molecular evidence of ticks coinfected with Borrelia burgdorferi sensu lato and the human granulocytic ehrlichiosis agent in Switzerland. J Clin Microbiol.1999.37:3390-3391.
267. Bassler, H. A., Flood, S. J. A., Livak, K. J., et al. Use of a fluorogenic probe in a PCR-based assay for the detection of Listeria monocytogenes. Appl Environ Microbiol.1995,61:3724-3728.
268. Nogva, H. K., Rudi, K., Naterstad, K., et al. Application of 5'-nuclease PCR for quantitative detection of Listeria monocytogenes in pure cultures, water, skim milk, and pasteurized whole milk. Appl Environ Microbiol.2000,66:4266-4271.
269. Lyon, W. J. TaqMan PCR for detection of Vibrio cholerae O1,0139, non-01, and non-0139 in pure cultures, raw oysters, and synthetic seawater. Appl Environ Microbiol.2001,67:4685-4693.
270. Haramotoa, E., Kitajimab, M., Katayamab, H., et al. Application of real-time PCR assays to genotyping of F-specific phages in river water and sediments in Japan. Water Research.2009,43: 3759-3764.
271. Wolf, S., Hewitt, J., Rivera-Aban, M., et al. Detection and characterization of F+RNA bacteriophages in water and shellfish:Application of a multiplex real-time reverse transcription PCR. J Viro Methods. 2008,149:123-128.
272.赵卫东,郑文杰,贺艳.荧光PCR方法定性和定量检测BT63转基因大米.食品研究与开发(检测分析).2009,30(3)：133～135.
273.张亮,杨剑波,宋丰顺,等.实时荧光PCR技术定量检测转Bt基因水稻的研究.生物学杂志.2008,25(6)：63～65.
274.吴孝槐,路勇.利用实时荧光PCR方法检测转Bt基因大米.现代食品科技.2009,25(2)：211～216.
275. Wengler, G., Bradley, D. W., Collett, M. S., Heinz, F. X., Schlesinger, R. W., Strauss, J. H. Family Flaviviridae. In F. A. Murphy,C. M. Fauquet, D. H. L. Bishop, S. A. Ghabrial, A. W. Jarvis, G. P. Martinelli,M. A. Mayo, and M. D. Summers (ed.), Classification and nomenclature of viruses. Sixth Report of the International Committee on Taxonomy of Viruses. Springer-Verlag, Berlin, Germany. 1995,415-427.
276. Fauquet, C. M., Mayo, M. A., Maniloff, J., Desselberger, U., Ball, L. A., editors. Virus taxonomy:the 8th report of the international committee on taxonomy of viruses. San Diego, CA:Elsevier Academic Press.2005.
277. Choi, C., Chae, C. Localization of classical swine fever virus in male gonads during subclinical infection. J Gen virol.2002,83(Ptl 1):2717-2721.
278. Floegel, G., Wehrend, A., Depner, K. R., et al. Detection of classical swine fever virus in semen of infected boars. Vet Microbiol.2000,77(1-2):109-116.
279. Vossen, M. T., Westerhout, E. M., Soderberg-Naucler, C., et al. Viral immune evasion:a masterpiece of evolution. Immunogenetics.2002,54:527-542.
280. Hariharan, M. J., Nataraj, C., Srikumaran, S. Down regulation of murine MHC class I expression by bovine herpesvirus 1. Viral Immunol.1993,6:273-284.
281. Koppers-Lalic. D., Verweij, M. C., Lipinska, A. D., et al. Varicellovirus UL 49.5 proteins differentially affect the function of the transporter associated with antigen processing, TAP. PLoS Pathog.2008,4(5):e1000080.
282. Nataraj, C., Eidmann, S., Hariharan, M. J., et al. Bovine herpesvirus 1 downregulates the expression of bovine MHC class I molecules. Viral Immunol.1997,10:21-34.
283. Sparks-Thissen, R. L., Enquist, L. W. Differential regulation of Dk and Kk major histocompatibility complex class I proteins on the cell surface after infection of murine cells by pseudorabies virus. J Virol.1999,73:5748-5756.
284. Hunt, H. D., Lupiani, B., Miller, M. M., et al. Marek's disease virus down-regulates surface expression of MHC (B Complex) Class Ⅰ (BF) glycoproteins during active but not latent infection of chicken cells. Virology.2001,282:198-205.
285. Bensaude, E., Turner, J. L., Wakeley, P. R., et al. Classical swine fever virus induces proinflammatory cytokines and tissue factor expression and inhibits apoptosis and interferon synthesis during the establishment of long-term infection of porcine vascular endothelia cells. J Gen Virol.2004,85(Pt4): 1029-1037.
286. Sanchez-Cordon, P. J., Romanini, S., Salguero, F. J., et al. Apoptosis of thymocytes related to cytokine expression in experimental classical swine fever. J Comp Pathol.2002,127:239-248.
287. Schweizer, M., Peterhans, E. Noncytopathic bovine viral diarrhea virus inhibits double-stranded RNA-induced apoptosis and interferons synthesis. J Virol.2001,75 (10):4692-4698.
288. Charleston, B., Fray, M. D., Baigent, S., et al., Establishment of persistent infection with non-cytopathic bovine viral diarrhea virus in cattle is associated with a failure to induce type I interferon, J Gen Virol.2001,82:1893-1897.
289. Gomez-Villamandos, J. C., Salguero, F. J., Ruiz-Villamor, E., et al. Classical swine fever:pathology of bonemarrow. Vet Pathol.2003,40:157-163.
290. Summerfield, A., Hofmann, M., McCullough, K. C. Immature granulocytic cells dominate the peripheral blood during classical swine fever and are targets for virus infection. Vet Immunol Immunopathol.1998.63:289-301.
291. Gisler,A. C.,Nardi,N. B.,Nonnig, R. B., et al. Classical swine fever virus in plasma and peripheral blood mononuclear cells of acutely infected swine. Zentralbl Veterinaermed B.1999.46:585-593.
292. Sato,M., Mikami. O.,Kobayashim. M., et al. Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus. Vet Microbiol.2000,75:1-9.
293. Choi, C., Hwang,K. K., Chae, C. Classical swine fever virus induces tumor necrosis factor-alpha and lymphocyte apoptosis. Arch Virol.2004,149 (5):875-889.
294. Sanchez-Cordon, P. J., Nunez, A., Salguero, F. J., et al. Lymphocyte Apoptosis and Thrombocytopenia in Spleen during Classical Swine Fever:Role of Macrophages and Cytokines. Vet Pathol.2005,42 (4):477-488.
295. Stark, G. R., Kerr,I. M., Williams, B. R., et al. How cells respond to interferons. Annu Rev Biochem. 1998,67:227-264.
296. Boehm, U., Klamp, T., Groot, M., et al. Cellular responses to interferon-gamma. Annu Rev Immunol. 1997.15:749-795.
297. Dallman, M. J. Cytokine gene expression:analysis using northern blotting, polymerase chain reaction and in situ hybridization. Immunol Rev.1991,119:163-180.
298. Higuchi, R., Dollinger. G., Walsh, P. S.. et al. Simulutaneous amplification and detection of specific DNA sequences. Biotechnology (NY).1992,10:413-417.
299. Ishiguro, T., Saitoh, J., Yawata, H., et al. Homogeneous quantitative assay of hepatitis C virus RNA by polymerase chain reaction in the presence of a fluorescent intercalater. Anal Biochem.1995.229(2): 207-213.
300. Tseng, S. Y., Macool. D., Elliott, V., et al. An homogeneous fluorescence polymerase chain reaction assay to identify Salmonella. Anal Biochem.1997,245(2):207-212.
301. Morrison, T. B.,Weis. J. J., Wittwer. C. T. Quantification of low-copy transcripts by continuous SYBR Green I monitoring during amplification. Biotechniques.1998,24(6):954-958,960,962.
302. Freeman. W. M, Walker,S. J, Vrana, K. E. Quantitative RT-PCR:pitfall and potential. Biotechniques. 1999,26(1):112-125.
303. Mackay,I. M.,Arden, K. E., Nitsche. A. Real-time PCR in virology. Nucleic Acids Res.2002.30 (6): 1292-1305.
304. Livak, K. J.,Schmittgen, T. D. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods.2001,25(4):402-408.
305. Van Oirschot, J. T. Description of the virus infection. In Classical Swine Fever and Related Viral Infections. Edited by B. Leiss. Boston:Martinus Nijhoff.1988,1-25.
306. Borca, M. V., Gudmundsdottir, I., Fernandez-Sainz,1. J., et al. Patterns of cellular gene expression in swine macrophages infected with highly virulent classical swine fever virus strain Brescia. Virus Res. 2008,138(1-2):89-96.
307. Shi, Z., Sun, J., Guo, H., et al. Genomic expression profiling of peripheral blood leukocytes of pigs infected with highly virulent classical swine fever virus strain Shimen. J Gen Virol.2009,90(Pt7): 1670-1680.
308. Li, J., Yu, Y. J., Feng, L., et al. Global transcriptional profiles in peripheral blood mononuclear cell during classical swine fever virus infection. Virus Res.2010,148 (1-2):60-70.
309. Graham, S. P., Everett, H. E., Johns, H. L., et al. Characterisation of virus-specific peripheral blood cell cytokine responses following vaccination or infection with classical swine fever viruses. Vet Microbiol.2010,142(1-2):34-40.
310. Sanchez-Cordon, P. J., Nunez, A., Salguero, F. J.m et al. Evolution of lymphocytes and cytokine expression in classical swine fever virus infection. J Comp Path.2005,132:249-260.
311.Shao, L., Sperber, K. Impaired regulation of HLA-DR expression in human immunodeficiency virus-infected monocytes. Clin Diagn Lab Immunol.2002,9(4):739-746.
312. Johnson, D. C., Hegde, N. R. Inhibition of the MHC class Ⅱ antigen presentation pathway by human cytomegalovirus. Curr Top Microbiol Immunol.2002,269:101-115.
313.Odeberg, J., Plachter, B., Branden, L., et al. Human cytomegalovirus protein pp65 mediates accumulation of HLA-DR in lysosomes and destruction of the HLA-DR a-chain. Immunobiology. 2003,101:4870-4877.
314. Li, Q., Turk, S. M., Hutt-Fletcher, L. M. The Epstein-Barr virus (EBV) BZLF2 gene product associates with the gH and gL homologs of EBV and carries an epitope critical to infection of B cells but not of epithelial cells. J Virol.1995,69(7):3987-3994.
315. Hulst, M. M., Westra, D. F., Wensvoort, G., et al. Glycoprotein E1 of hog cholera virus expressed in insect cells protects swine from hog cholera. J Virol.1993,67:5435-5442.
316. Van Zijl, M., Wensvoort, G., de Kluyver, E., et al. Live attenuated pseudorabies virus expressing envelope glycoprotein El of hog cholera virus protects swine against both pseudorabies and hog cholera. J Virol.1991,65:2761-2765.
317. Weiland, F., Weiland, E.,Unger, G., et al. Localization of pestiviral envelope proteins E(rns) and E2 at the cell surface and on isolated particles. J Gen Virol.1999,80(Pt):1157-1165.
318.王琴,郎洪武,王在时,等.猪瘟病毒E2基因的克隆与鉴定.畜牧兽医学报.2001,32(6)：549～555.
319.王琴,王在时,赵耘,等.12株猪瘟病毒E2基因主要抗原区域的序列差异分析.微生物学报.2000,40(6)：614～621.
320.吕宗吉,李红卫,涂长春,等.我国部分地区猪瘟病毒流行株的基因差异.中国兽医学报.2000,20(4)：313～316.
321.张永国,刘湘涛,韩雪清,等.广西猪瘟流行毒与C-株疫苗毒gp55(E2)主要抗原区DNA序列差异的比较.西北农林科技大学学报.2002,30(1)：79～84.
322.刘伯华,刘湘涛,韩雪清,等.急慢性猪瘟病毒分离株和疫苗株E2基因的序列分析.畜牧兽医学报.2001,32(6)：568～575.
323.赵耘,王在时,王琴,等.23株猪瘟病毒E2基因主要抗原编码区序列差异分析.中国兽医科技.2002,32(3)：3～6.
324.吴显实,罗廷荣,廖素环,等.广西猪瘟流行毒株全基因组的克隆与序列分析中国兽医学报.2005,25(2)：125～128.
325.孙石静,罗廷荣,吴显实,等.广西猪瘟流行毒株E2基因的序列分析.中国兽医科技.2004,325(9)：29～33.
326.廖素环,罗廷荣,吴显实,等.广西流行猪瘟病毒E2基因序列测定及分析.中国生物制品学杂志.2005,18(3)：196～199.
2. Thiel, H. J., Plagemann, P. G. W., Moennig, V. Pestiviruses. In Fields Virology,3rd edn, vol.1. Edited by B. N. Fields, D. M. Knipe & P. M. Howley. Philadelphia & New York:Lippincott-Raven.1996, 1059-1073.
3. Weesendorp, E., Stegeman, A., Loeffen, W. Dynamics of virus excretion via different routes in pigs experimentally infected with classical swine fever virus strains of high, moderate or low virulence. Vet Microbiol.2009,133(1-2):9-22.
4. Weesendorp, E., Stegeman, A., Loeffen, W. Quantification of classical swine fever virus in aerosols originating from pigs infected with strains of high, moderate or low virulence. Vet Microbiol.2009, 135(3-4):222-230.
5. Hennecken, M., Stegeman, J. A., Elbers, A. R., et al. Transmission of classical swine fever virus by artificial insemination during the 1997-1998 epidemic in The Netherlands:a descriptive epidemiological study. Vet Q.2000,22(4):228-233.
6. Edwards, S., Fukusho, A., Lefevre, P. C., et al. Classical swine fever:the global situation. Vet Microbiol.2000,73:103-119.
7. Moenning, V., Floegel-Niesmann, G., Greiser-Wilke, I. Clinical signs and epidemiology of classical swine fever:a review of new knowledge. Vet J.2003,165:11-20.
8. Terpstra C. Hog cholera:an update of present knowledge. Br Vet J.,1991; 147:397-406.
9. Moennig, V. Introduction to classical swine fever virus, disease and control policy. Vet Microbiol. 2000,73(2-3):93-102.
10.吕宗吉,涂长春,余若龙.等.我国猪瘟的流行病学现状分析.畜牧市场.2009,12：10～12.
11.陈丽颖,王自振,李春玲,等.河南省的猪瘟流行特点与防治.中国兽医杂志.2003,11：22～23.
12.陶海静.河南省猪瘟流行情况调查.安徽农业科学.2007,35(25)：7842-7843,7845.
13.吴健敏,蒋冬福,韦志峰,等.广西猪瘟流行现状的调查分析.2002,2：16～18.
14.舒相华,宋春莲,刘旭川,等.云南省部分猪场猪瘟流行情况调查.中国畜牧兽医.2009,5：166～167.
15.蒋毅立,韦柳青,郭冬,等.从母猪白细胞检出猪瘟病毒.广西畜牧兽医.2008,5：261～264.
16. Carbrey, E. A., Stewart, W. C., Kresse, J. I., et al. Natural infection of pigs with bovine viral diarrhea virus and its differential diagnosis from hog cholera. J Am Vet Med Assoc.1976,169:1217-1219.
17. Moenning, V. Pestiviruses:a review. Vet Microbiol.1990,23:35-54.
18. Meyers, G., Rumenapf, T., Thiel, H. J. Molecular cloning and nucleotide sequence of the genome of hog cholera virus. Virology.1989,171:555-567.
19. Moormann, R. J., Warmerdam, P. A., van der Meer, B., et al. Molecular cloning and nucleotide sequence of hog cholera virus strain Brescia and mapping of the genomic region encoding envelope protein E1. Virology.1990,177(1):184-198.
20. Poole, T. L., Wang, C., Popp, R. A., et al. Pestivirus translation occurs by internal ribosome entry. Virology.1995,206:750-754.
21. Pestova, T. V., Shatsky, I. N., Fletcher, S. P., et al. A prokaryotic-like mode of cytoplasmic eukaryotic ribosome binding to the initiation codon during internal translation initiation of hepatitis C and_. classical swine fever virus RNAs. Genes Dev.1998,12:67-83.
22. Deng, R., Brock, K. V.5'and 3'untranslated regions of pestivirus genome:primary and secondary structure analyses. Nucleic Acids Res.1993,21:1949-1957.
23. Yu, H., Grassmann, C. W., Behrens, S.-E. Sequence and structural elements at the 3'terminus of bovine viral diarrhea virus genomic RNA:functional role during RNA replication. J. Virol.1999,73:^ 3638-3648.
24. Pankraz, A., Thiel, H. J., Becher, P. Essential and nonessential elements in the 3'nontranslated region of bovine viral diarrhea virus. J Virol.2005,79:9119-9127.
25. Isken, O., Grassmann, C. W., Sarisky, R. T., et al. Members of the NF90/NFAR protein group are involved in the life cycle of a positive-strand RNA virus. EMBO J.2003,22:5655-5665.
26. Xiao, M., Gao, J., Wang, W., et al. Specific interaction between the classical swine fever virus NS5B protein and the viral genome. Eur J Biochem.2004,271:3888-3896.
27. Fletcher, S. P., Jackson, R. J. Pestivirus internal ribosome entry site (IRES) structure and function: elements in the 59 untranslated region important for IRES function. J Virol.2002,76:5024-5033.
28. Heinz, F. X., Collett, M. S., Purcell, R. H., et al (Eds.) Family flaviridae. Virus taxonomy. Eighth report of the international committee on taxonomy of virus. San Diego, Academic Press.2004: 981-998.
29. Rumenapf, T., Unger, G., Strauss, J. H.. et al. Processing of the envelope glycoproteins of pestiviruses. J Virol.1993,67:3288-3294.
30. Poole, T. L., Wang, C, Popp, R. A., et al. Pestivirus translation initiation occurs by internal ribosome entry. Virology.1995,206:750-754.
31. Pestova, T. V., Shatsky, I. N., Fletcher, S. P., et al. A prokaryotic-like mode of cytoplasmic eukaryotic ribosome binding to the initiation codon during internal translation initiation of hepatitis C and classical swine fever virus RNAs. Genes Dev.1998,12:67-83.
32. Fletcher, S. P., Ali,1. K., Kaminski, A., et al. The influence of viral coding sequences on pestivirus IRES activity reveals further parallels with translation initiation in prokaryotes. RNA.2002,8(12): 1558-1571.
33. Sizova, D. V., Kolupaeva, V. G., Pestova, T. A., et al. Specific interaction of eukaryotic translation initiation factor 3 with the 5'nontranslated regions of hepatitis C virus and classical swine fever virus RNAs. J Virol.1998,72:4775-4782.
34. Fletcher, S. P., Jackson, R. J. Pestivirus internal ribosome entry site (IRES) structure and function: elements in the 5'untranslated region important for IRES function. J Virol.2002,76:5024-5033.
35. Reusken, C. B., Dalebout, T. J., Eerligh, P., et al. Analysis of hepatitis C virus/classical swine fever virus chimeric 5'NTRs:sequences within the hepatitis C virus IRES are required for viral RNA replication. J Gen Virol.2003,84(Pt 7):1761-1769.
36. Rijnbrand, R., van der Straaten, T., Van Rijn, P. A., et al. Internal entry of ribosomes is directed by the 5'noncoding region of classical swine fever virus and is dependent on the presence of an RNA pseudoknot upstream of the initiation codon. J Virol.1997,71:451-457.
37. Stark, R., Meyers, G., Rumenapf, T., et al. Processing of Pestivirus Polyprotein:Cleavage Site between Autoprotease and Nucleocapsid Protein of Classical Swine Fever Virus. J Virol.1993,67:7088-7095.
38. Rumenapf, T., Stark, R., Heimann, M., et al. N-terminal protease of pestiviruses:identification of putative catalytic residues by site-directed mutagenesis. J Virol.1998,72(3):2544-2547.
39. Wiskerchen, M., Belzer, S. K., Collett, M. S. Pestivirus gene expression:the first protein product of the bovine viral diarrhea virus large open reading frame, p20, possesses proteolytic activity. J Virol. 1991,65:4508-4514.
40. Thiel, H-J., Stark, R., Weiland, E., et al. Hog cholera virus:molecular compositions of virions from a Pestivirus. J Virol.1991,65:4705-4712.
41. Rumenapf,T.,Stark. R., Heimann, M., et al. N-terminal protease of pestiviruses:identification of putative catalytic residues by site-directed mutagenesis. J Virol.1998.72:2544-2547.
42. Tratschin,J. D.,Moser. C.,Ruggli,N., et al. Classical Swine Fever Virus Leader Proteinase Npro Is Not Required for Viral Replication in Cell Culture. J Virol.1998.72(9):7681-7684.
43. Ruggli,N., Tratschin, J. D.,Schweizer. M., et al. Classical swine fever virus interferes with cellular antiviral defense:evidence for a novel function of Npro. J Virol.2003.77(13):7645-54.
44. Mayer, D., Hofmann, M. A., Tratschin, J.-D. Attenuation of classical swine fever virus by deletion of the viral Npr0 gene. Vaccine.2004,22:317-328.
45. Doceul, V., Charleston, B., Crooke, H., et al. The Npro product of classical swine fever virus interacts with IkappaBalpha, the NF-kappaB inhibitor. J Gen Virol.2008,89(Pt 8):1881-1889.
46. Pahl, H. L. Activators and target genes of Rel/NF-kappaB transcription factors. Oncogene.1999,22, 18(49):6853-6866.
47. La Rocca, S. A., Herbert, R. J., Crooke, H., et al. Loss of interferon regulatory factor 3 in cells infected with classical swine fever virus involves the N-terminal protease, Npro. J Virol.2005,79:7239-7247.
48. Ruggli, N., Bird, B. H., Liu, L., et al. Npro of classical swine fever virus is an antagonist of double-stranded RNA-mediated apoptosis and IFN-a/β induction. Virology.2005,340:265-279.
49. Bauhofer, O., Summerfield. A., Sakoda. Y., et al. Classical swine fever virus Npro interacts with interferon regulatory factor 3 and induces its proteasomal degradation. J Virol.2007,81:3087-3096.
50. Seago, J., Hilton, L., Reid, E., et al. The Npro product of classical swine fever virus and bovine viral diarrhea virus uses a conserved mechanism to target interferon regulatory factor-3. J Gen Virol.2007, 88:3002-3006.
51. Szymanski, M. R., Fiebach, A. R., Tratschin. J. D., et al. Zinc binding in pestivirus Npro is required for interferon regulatory factor 3 interaction and degradation. J Mol Biol.2009,391(2):438-449.
52. Ruggli, N., Summerfield,A.,Fiebach. A. R., et al. Classical swine fever virus can remain virulent after specific elimination of the interferon regulatory factor 3-degrading function of Npro.J Virol.2009.83: 817-829.
53. Heimann, M.,Roman-Sosa. G.,Martoglio. B., et al. Core protein of pestiviruses is processed at the C terminus by signal peptide peptidase. J Virol.2006,80:1915-1921.
54. Liu. J. J., Wong, M. L., Chang. T. J. The recombinant nucleocapsid protein of classical swine fever virus can act as a transcriptional regulator. Virus Res.1998.53:75-80.
55. Rumenapf, T., Unger, G., Strauss, J. H., et al. Processing of the envelope glycoproteins of pestiviruses. J Virol.1993,67(6):3288-3294.
56. Fetzer, C., Tews, B. A., Meyers, G. The carboxy-terminal sequence of the pestivirus glycoprotein Ems represents an unusual type of membrane anchor. J Virol.2005,79:11901-11913.
57. Tews, B. A., Meyers, G. The pestivirus glycoprotein Erns is anchored in plane in the membrane via an amphipathic helix. J Biol Chem.2007,282(45):32730-32741.
58. Hausmann, Y., Roman-Sosa, G., Thiel, H. J., et al. Classical swine fever virus glycoprotein Erns is an endoribonuclease with an unusual base specificity. J Virol.2004,78(10):5507-5512.
59. Meyers, G., Saalmuller, A., Buttner, M. Mutations abrogating the RNase activity in glycoprotein Erns of the pestivirus classical swine fever virus lead to virus attenuation. J Virol.1999,73:10224-10235.
60. Moormann, R. J., Warmerdam, P. A., van der Meer, B., et al. Nucleotide sequence of hog cholera virus RNA:properties of the polyprotein encoded by the open reading frame spanning the viral genomic RNA. Vet Microbiol.1990,23:185-191.
61. Ansari, I. H., Kwon, B., Osorio, F. A., et al. Influence of N-linked glycosylation of porcine reproductive and respiratory syndrome virus GP5 on virus infectivity, antigenicity, and ability to induce neutralizing antibodies. J Virol.2006,80:3994-4004.
62. Panda, A., Elankumaran, S., Krishnamurthy, S., et al. Loss of N-linked glycosylation from the hemagglutinin-neuraminidase protein alters virulence of Newcastle disease virus. J Virol.2004,78: 4965-4975.
63. Hulse, D. J., Webster, R. G., Russell, R. J., et al. Molecular determinants within the surface proteins involved in the pathogenicity of H5N1 influenza viruses in chickens. J Virol.2004,78:9954-9964.
64. Sainz, I. F., Holinka, L. G., Lu, Z. Removal of a N-linked glycosylation site of classical swine fever virus strain Brescia Erns glycoprotein affects virulence in swine. Virology.2008,370:122-129.
65. Tews, B. A., Schurmann, E. M., Meyers, G. Mutation of cysteine 171 of pestivirus Erns RNase prevents homodimer formation and leads to attenuation of classical swine fever virus. J Virol.2009, 83(10):4823-4834.
66. Weiland, E., Stark, R., Haas, B., et al. Pestivirus glycoprotein which induces neutralizing antibodies forms part of a disulfide-linked heterodimer. J Virol.1990,64:3563-3569.
67. Wang, Z., Nie, Y., Wang, P., et al. Characterization of classical swine fever virus entry by using pseudotyped viruses:El and E2 are sufficient to mediate viral entry. Virology.2004,330:332-341.
68. Risatt, G. R., Holinka. L. G., Lu. Z., et al. Mutation of E1 glycoprotein of classical swine fever virus affects viral virulence in swine. Virology.2005.343(1):116-127.
69. Fernandez-Sainz,I., Holinka. L. G., Gavrilov. B. K., et al. Alteration of the N-linked glycosylation condition in E1 glycoprotein of Classical Swine Fever Virus strain Brescia alters virulence in swine. Virology.2009.386:210-216.
70. Thiel, H. J., Stark. R., Weiland. E., et al. Hog cholera virus:molecular composition of virions from a pestivirus. J Virol.1991.65:4705-4712.
71. Wensvoort, G., Boonstra, J., Bodzinga, B. G. Immunoaffinity purification and characterization of the envelope protein E1 of hog cholera virus. J Gen Virol.1990,71(Pt3):531-540.
72. Van Gennip, H. G., Bouma, A., van Rijn, P. A., et al. Experimental non-transmissible marker vaccines for classical swine fever (CSF) by trans-complementation of E(rns) or E2 of CSFV. Vaccine.2002,20: 1544-1556.
73. Moormann. R. J., Warmerdam, P. A., van der Meer, B., et al. Nucleotide sequence of hog cholera virus RNA:properties of the polyprotein encoded by the open reading frame spanning the viral genomic RNA. Vet Microbiol.1990,23:185-191.
74. Risatti, G. R.. Holinka, L. G., Fernandez Sainz, I., et al. N-Linked Glycosylation Status of Classical Swine Fever Virus Strain Brescia E2 Glycoprotein Influences Virulence in Swine. J Virol.2007,81(2): 924-933.
75. Konig,M., Lengsfeld, T., Pauly, T., et al. Classical swine fever virus:independent induction of protective immunity by two structural glycoproteins. J Virol.1995,69:6479-6486.
76. Weiland,E., Stark, R., Haas, B., et al. Pestivirus glycoprotein which induces neutralizing antibodies forms part of a disulfide-linked heterodimer. J Virol.1990,64:3563-3569.
77. Van Rijn, P. A., Miedema,G. K., Wensvoort, G.. et al. Antigenic structure of envelope glycoprotein E2 of hog cholera virus. J Virol.1994,68:3934-3942.
78. Wensvoort, G. Topographical and functional mapping of epitopes on hog cholera virus with monoclonal antibodies. J Gen Virol.1989,70(Ptl 1):2865-2876.
79. Lin. M., Lin. F., Mallory. M., et al. Deletions of structural glycoprotein E2 of classical swine fever virus strain alfort/187 resolve a linear epitope of monoclonal antibody WH303 and the minimal N-terminal domain essential for binding immunoglobulin G antibodies of a pig hyperimmune serum. J Virol.2000.74:11619-11625.
80. Risatti, G. R., Holinka, L. G., Carrillo, C., et al. Identification of a novel virulence determinant within the E2 structural glycoprotein of classical swine fever virus. Virology.2006,355:94-101.
81. Risatti, G. R., Borca, M. V., Kutish, G. F., et al. The E2 glycoprotein of classical swine fever virus is a virulence determinant in swine. J Virol.2005,79:3787-3796.
82. Elbers, K., Tautz, N., Becher, P., et al. Processing in the pestivirus E2-NS2 region:identification of proteins P7 and E2P7. J Virol.1996,70:4131-4135.
83. Moser, C., Stettler, P., Tratschin, J. D., et al. Cytopathogenic and noncytopathogenic RNA replicons of classical swine fever virus. J Virol.1999,73:7787-7794.
84. Tang, Q. H., Zhang, Y. M., Fan, L., et al. Classic swine fever virus NS2 protein leads to the induction of cell cycle arrest at S-phase and endoplasmic reticulum stress. Virol J,2010,7:4.
85. Sheng, C., Xiao, M., Geng, X., et al. Characterization of interaction of classical swine fever virus NS3 helicase with 3'untranslated region. Virus Res.2007,129(1):43-53.
86. Wen, G., Xue, J., Shen, Y., et al. Characterization of classical swine fever virus (CSFV) nonstructural protein 3 (NS3) helicase activity and its modulation by CSFV RNA-dependent RNA polymerase. Virus Res.2009,141(1):63-70.
87. Gallei, A., Orlich, M., Thiel, H. J., et al. Noncytopathogenic pestivirus strains generated by nonhomologous RNA recombination:alterations in the NS4A/NS4B coding region. J Virol.2005, 79(22):14261-14270.
88. Tautz, N., Kaiser, A., Thiel, H. J. NS3 serine protease of bovine viral diarrhea virus:characterization of active site residues, NS4A cofactor interactions. Virology.2000,273:351-363.
89. Xiao, M., Wang, Y., Zhu, Z., et al. Influence of NS5A protein of classical swine fever virus (CSFV) on CSFV internal ribosome entry site-dependent translation. J Gen Virol.2009,90 (Pt 12):2923-2928.
90. Xiao, M., Zhang, C. Y., Pan, Z. S., et al. Classical swine fever virus NS5B-GFP fusion protein possesses an RNA-dependent RNA polymerase activity. Arch Virol.2002,147:1779-1787.
91. Xiao, M., Bai, Y., Xu, H., et al. Effect of NS3 and NS5B proteins on classical swine fever virus internal ribosome entry site-mediated translation and its host cellular translation. J Gen Virol.2008, 89(Pt 4):994-999.
92. Wang, P., Wang, Y., Zhao, Y., et al. Classical swine fever virus NS3 enhances RNA-dependent RNA polymerase activity by binding to NS5B. Virus Res.2010,148(1-2):17-23.
93. Xiao, M., Chen, J., Wang, Y., et al. Sequence, necessary for initiating RNA synthesis, in the 3'-noncoding region of the classical swine fever virus genome. Mol Biol (Mosk).2004,38:343-351.
94. Yu. H.,Grassmann. C. W.. Behrens. S.-E. Sequence and structural elements at the 3'terminus of bovine viral diarrhea virus genomic RNA:functional role during RNA replication. J Virol.1999,73: 3638-3648.
95. Pankraz, A., Thiel, H. J., Becher, P. Essential and nonessential elements in the 3'nontranslated region of bovine viral diarrhea virus.J Virol.2005.79:9119-9127.
96. Isken,O.,Grassmann, C. W., Yu,H., et al. Complex signals in the genomic 3'nontranslated region of bovine viral diarrhea virus coordinate translation and replication of the viral RNA. RNA.2004,10(10): 1637-1652.
97. Xiao, M., Zhang, C. Y., Zhu, Z. Z., et al. Qualitative, quantitative and structure analysis of 3'UTR of classic swine fever virus. Chin Sci Bull.2001,46:544-550.
98. Huang, Q. H., Zhang, C. Y., Wang, J. F., et al. Molecular cloning and nucleotide sequence of classical swine fever virus strain Shimen. Wuhan Uni J Nat Sci.1998,3:504-508.
99. Xiao, M., Gao, J., Wang, Y. et al. Influence of a 12-nt insertion present in the 3'untranslated region of classical swine fever virus HCLV strain genome on RNA synthesis. Virus Res.2004a,102:191-198.
100. Rodriguez-Cerezo, E., Klein, P. G., Shaw, J. G. A determinant of disease symptom severity is located in the 3'-terminal noncoding region of the RNA of a plant virus. Proc Natl Acad Sci. U. S. A.1991,88: 9863-9867.
101. Wang Y., Wang Q., Lu X., et al.12-nt insertion in 3'untranslated region leads to attenuation of classic swine fever virus and protects host against lethal challenge. Virology.2008,10:374(2):390-398.
102. Hulst, M. M., van Gennip, H. G. P., Moormann, R. J. M. Passage of Classical Swine Fever Virus in Cultured Swine Kidney Cells Selects Virus Variants That Bind to Heparan Sulfate due to a Single Amino Acid Change in Envelope Protein Erns. J Virol.2000,74:9553-9561,
103. Hulst. M. M., vanGennip. H. G., Vlot. A. C., et al. Interaction of classical swine fever virus with membrane-associated heparan sulphate:role for virus replication in vivo and virulence. J Virol.2001. 75:9585-9595.
104. Maurer,K.,Krey,T.,Moennig, V., et al. CD46 is a cellular receptor for bovine viral diarrhea virus. J Virol.2004.78:1792-1799.
105. Krey. T., Himmelreich, A., Heimann. M., et al. Function of bovine CD46 as a cellular receptor for bovine viral diarrhea virus is determined by complement control protein 1. J Virol.2006.80: 3912-3922.
106. Hulst, M. M., Moormann, R. J. M. Inhibition of pestivirus infection in cell culture by envelope proteins Erns and E2 of classical swine fever virus:Ems and E2 interact with different receptors. J Ger virol.1997,78:2779-2787.
107. Agnello, V., Abel, G., Elfahal, M., et al. Hepatitis C virus and other flaviviridae viruses enter cells via low density lipoprotein receptor. PNAS.1999,96(22):12766-12771.
108. Cheville N. F., Mengeling, W. L. The pathogenesis of chronic hog cholera (swine fever). Histologic, immunofluorescent, and electron microscopic studies. Lab Invest.1969,20:261-274.
109. Ressang, A. A. Studies on the pathogenesis of hog cholera.Ⅱ. Virus distribution in tissue and morphology of the immune response. Zentralbl Veterinaermed Reihe B.1973,20:272-288.
110. Susa, M., Konig, M., Saalmuller, A., et al. Pathogenesis of classical swine fever:B-lymphocyte deficiency caused by hog cholera virus. J Virol.1992,66:1171-1176.
111.Thiel, H. J., Plagemann, G. W., Moennig, V. Pestiviruses. In B. N. Fields, D. M. Knipe, P. M. Howley, et al. (ed.), Fields virology. Lippincott-Raven Publishers, Philadelphia, Pa.1996,1059-1073.
112. Trautwein, G. Pathology and pathogenesis of the disease. In B. Liess (ed.), Classical swine fever and related infections. Martinus Nijhoff Publishing, Boston, Mass.1988,27-54.
113. Campos, E., Revilla, C., Chamorro, S., et al. In vitro effect of classical swine fever virus on a poricne aortic endothelial cell line. Vet Res.2004,35:625-633.
114. Summerfield, A., Knoetig, S. M., Tschudin, R. et al. Pathogenesis of granulocytopenia and bone marrow atrophy during classical swine fever involves apoptosis and necrosis of uninfected cells. Virology.2000,272:50-60.
115. Ressang, A. A. Studies on the pathogenesis of hog cholera.Ⅱ. Virus distribution in tissue and the morphology of the immune response. Zentbl Vetmed Reihe B.1973,20:272-288.
116. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Bautista, M. J., et al. Morphological and immunohistochemical changes in splenic macrophages of pigs infected with classical swine fever. J Comp Pathol.2001,125:98-109.
117. Sanchez-Cordon, P. J., Romanini, S., Salguero, F. J., et al. A histopathologic, immunohistochemical, and ultrastructural study of the intestine in pigs inoculated with classical swine fever virus. Vet Pathol. 2003,40:254-262.
118. Trautwein, G. Pathology and pathogenesis of the disease. In Classical Swine Fever and Related Infections. Edited by B. Liess. Boston:Martinus Nijhoff Publishing.1988,27-54.
119. Knoetig, S. M., Summerfield. A., Spagnuolo-Weaver. M., et al. Immunopathogenesis of classical swine fever:role of monocytic cells. Immunology.1999,97:359-366.
120. Summerfield. A., Knotigy. S. M., McCullough. K. C. Lymphocyte apoptosis during classical swine fever:implication of activation-induced cell death. J Virology.1998b.72:1853-1861.
121. Sato,M., Mikami,O.,Kobayashim. M., et al. Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus. Vet Microbiol.2000,75:1-9.
122. Summerfield, A., Hofmann, M.A., McCullough, K.C. Low density blood granulocytic cells induced during classical swine fever are targets for virus infection. Vet Immunol Immunopathol.1998a,63(3): 289-301.
123.de las Mulas, J. M., Ruiz-Villamor, E., Donoso, S., et al. Immunohistochemical detection of hog cholera viral glycoprotein 55 in paraffin-embedded tissues. J Vet Diagn Invest.1997,9(1):10-16.
124. Narita, M., Kawashima. K., Kimura, K., et al. Comparative immunohistopathology in pigs infected with highly virulent or less virulent strains of hog cholera virus. Vet Pathol.2000,37:402-408.
125. Fischer, V. U., Kaden, V., Beyer. J. Zur nachweissicherheit von schweinepestvirusantigen und zur differenzierung der feld-und vakzinevirusinfektion mit dem direkten immunfluoreszenztest an organmaterial. Munchener Veterinar Medizin.1991.46:133-136.
126. Dahle. J., Schagemann. G., Moennig, V., et al. Clinical, virological and serological findings after intranasal inoculation of pigs with bovine viral diarrhoea virus and subsequent intranasal challenge with hog cholera virus. Journal of Veterinary Medicine (Series B).1993,40:46-54.
127. Pan, I. C., Huang, T. S., Pan, C. H., et al. The skin, tongue and brain as favorable organs for hog cholera diagnosis by immunofluorescence. Archives of Virology.1993.131:475-481.
128. Martin de las Mulas. J., Ruiz-Villamor, E., Donoso, S., et al. Immunohistochemical detection of hog cholera viral glycoprotein 55 in paraffin-embedded tissues. J Vet Diagn Invest.1997,9(1):10-16.
129. Bruschke. C. J. M., Hulst. M. M., Moormann. R. J. M., et al. Glycoprotein Ems of pestiviruses induces apoptosis in lymphocytes of several species. Journal of Virology.1997.71:6692-6696.
130. Summerfield. A., Zingle,K.,Inumaru,S., et al. Induction of apoptosis in bone marrow neutrophil-lineage cells by classical swine fever virus. J Gen Virol.2001,82:1309-1318.
131. Carrasco,C. P.,Rigden. R. C., Vincent.I. E.,et al. Interaction of classical swine fever virus with dendritic cells. J Gen Virol.2004.85.1633-41.
132. Lee, W. C., Wang, C. S., Chien, M. S. Virus antigen expression and alterations in peripheral blood mononuclear cell subpopulations after classical swine fever virus infection. Vet Microbiol.1999,67(1): 17-29.
133. Carrasco, L., Ruiz-Villamor, E., Gomez-Villamandos, J. C., et al. Classical swine fever: morphological and morphometrical study of pulmonary intravascular macrophages. J Comp Pathol. 2001,125(1):1-7.
134. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Salguero, F. J., et al. Immunohistochemical and ultrastructural evidence of hog cholera virus infection of megakaryocytes in bone marrow and spleen. J Comp Pathol.1998,119(2):111-119.
135. Gomez-Villamandos, J. C., Ruiz-Villamor, E., Bautista, M. J., et al. Pathogenesis of Classical Swine Fever:Renal Haemorrhages and Erythrodiapedesis. J Comp Path.2000,123:47-54.
136. Campos, E., Revilla, C., Chamorro, S., et al. In vitro effect of classical swine fever virus on a porcine aortic endothelial cell line. Vet Res.2004,35(6):625-633.
137. Markowska-Daniel, I., Pejsak, Z., Winnicka, A., et al. Phenotypic analysis of peripheral leukocytes in piglets infected with classical swine fever virus. Res Vet Sci.1999,67(1):53-57.
138. Summerfield, A., McNeilly, F., Walker, I., et al. Depletion of CD4+ and CD8high+ T-cells before the onset of viraemia during classical swine fever. Vet Immunol Immunopathol.2001,78(1):3-19.
139.孙金福,史子学,郭焕成,等.猪瘟病毒感染猪外周血白细胞凋亡及CD4+和CD8+T淋巴细胞亚群的变化.中国兽医科学.2008,38(04)：342～345.
140. Maudsley, D. J., Pound, J. D. Modulation of MHC antigen expression by viruses and oncogenes. Immunol Today.1991,12:429-431.
141. Rouse, B. T., Horohov, D. W. Immunosuppression in viral infections. Rev Inf Dis.1986,8:850-873.
142. Van Oirschot, J. T., De Jong, D., Huffels, N. D. N. H. J. Effect of infections with swine fever virus on immune functions I. Response of lymphocytes from blood and lymphoid organs from infected and normal pigs to anti-immunoglobulin serum and protein A. Vet Microbiol.1981,6:41-57.
143. Van Oirschot, J. T., De Jong, D.,Huffels, N. D. N. H. J. Effect of infections with swine fever virus on immune functions Ⅱ. Lymphocyte response to mitogens and enumeration of lymphocyte subpopulations. Vet Microbiol.1983,8:81-95.
144. Pauly, T., Konig, M., Thiel, H. J. et al. Infection with classical swine fever virus:effects on phenotype and immune responsiveness of porcine T lymphocytes. J Gen Virol.1998,79(Ptl):31-40.
145. Mittelholzer, C., Moser, C., Tratschin, J. D., et al. Porcine cells persistently infected with classical swine fever virus protected from pestivirus-induced cytopathic effect. J Gen Virol.1998,79: 2981-2987.
146.郑从义,童攒,应松成,等.猪瘟病毒野强毒株持续感染细胞模型的初步研究.武汉大学学报(理学版).2002,48(6)：720～724.
147.应松成,郑从义,屈三甫,等.猪瘟病毒野毒株持续性感染细胞模型的建立.中国病毒学.2002,17(1)：77～81.
148. Meyers, G., Thiel, H. J., Rumenapf, T. Classical swine fever virus:recovery of infectious viruses from cDNA constructs and generation of recombinant cytopathogenic defective interfering particles. J Virol. 1996,70:1588-1595.
149. Moser, C., Stettler, P., Tratschin, J. D., et al. Cytopathogenic and noncytopathogenic RNA replicons of Classical swine fever virus. J Virol.1999,73:7787-7794.
150. Xu, H., Hong, H. X., Zhang, Y. M., et al. Cytopathic effect of classical swine fever virus NS3 protein^ on PK-15 cells. Intervirology.2007,50(6):433-438.
151. Banchereau, J., Briere, F., Caux, C., et al. Immunobiology of dendritic cells. Annu Rev Immunol. 2000,18:767-811.
152. Steinman, R. M. The dendritic cell system and its role in immunogenicity. Annu Rev Immunol.1991T 9:271-296.
153. MacPherson, G. G., Liu, L. M. Dendritic cells and Langerhans cells in the uptake of mucosal antigens. Curr Top Microbiol Immunol.1999,236:33-53.
154. Pulendran, B., Palucka, K. Banchereau, J. Sensing pathogens and tuning immune responses. Science. 2001,293:253-256.
155. Carrasco, C. P., Rigden, R. C., Vincent, I. E., et al. Interaction of classical swine fever virus with dendritic cells. J Gen Virol.2004,85,1633-1641.
156. Fugier-Vivier, I., Servet-Delprat, C, Rivailler, P., et al. Measles virus suppresses cellmediated immunity by interfering with the survival and functions of dendritic and T cells. J Exp Med.1997,186: 813-823.
157. Cella, M., Salio, M., Sakakibara, Y., et al. Maturation, activation, and protection of dendritic cells induced by double-stranded RNA. J Exp Med.1999,189:821-829.
158. Ho, L. J., Wang, J. J., Shaio, M. F., et al. Infection of human dendritic cells by dengue virus causes cell maturation and cytokine production. J Immunol.2001,166:1499-1506.
159. Gardner, J. P., Frolov, I., Perri, S., et al. Infection of human dendritic cells by a Sindbis virus replicon vector is determined by a single amino acid substitution in the E2 glycoprotein. J Virol.2000,74: 11849-11857.
160. Bauhofer, O., Summerfield, A., McCullough, K. C., et al. Role of double-stranded RNA and Npro of classical swine fever virus in the activation of monocyte-derived dendritic cells. Virology.2005, 343(1):93-105.
161. Kawai, T., Akira, S. Innate immune recognition of viral infection. Nat Immunol.2006,7:131-137.
162. Malmgaard, L. Induction and regulation of IFNs during viral infections. J Interferon Cytokine Res. 2004,24:439-454.
163. Goodbourn, S., Didcock, L., Randall, R. E. Interferons:cell signalling, immune modulation, antiviral response and virus countermeasures. J Gen Virol.2000,81:2341-2364.
164. Haller, O., Kochs, G., Weber, F. The interferon response circuit:induction and suppression by pathogenic viruses. Virology.2006,344:119-130.
165. Hengel, H., Koszinowski, U. H., Conzelmann, K. K. Viruses know it all:new insights into IFN networks. Trends Immunol.2005,26:396-401.
166. Weber, F., Kochs, G., Haller, O. Inverse interference:how viruses fight the interferon system. Viral Immunol.2004,17:498-515.
167.Larocca, S. A., Herbert, R. J., Crooke, H., et al. Loss of Interferon Regulatory Factor 3 in Cells Infected with Classical Swine Fever Virus Involves the N-Terminal Protease, Npro. J Virol.2005,79: 7239-7247.
168. Xia, Y. H., Chen, L., Pan, Z. S., et al. A novel role of classical swine fever virus Erns glycoprotein in counteracting the newcastle disease virus (NDV)-mediated IFN-beta Induction. J Biochem Mol Biol. 2007,40(5):611-616.
169. Luo X, Pan R, Wan C, et al. Glycosylation of classical swine fever virus Erns is essential for binding double-stranded RNA and preventing interferon-beta induction. Virus Res,2009,146(1-2):135-139.
170. Luo,X., Ling, D., Li, T., et al. Classical swine fever virus Erns glycoprotein antagonizes induction of interferon-beta by double-stranded RNA. Can J Microbiol.2009,55(6):698-670.
171. Moore, K. W., Malefytr, D. W., Coffman, R. L., et al. Interleukin-10 and the interleukin-10 receptor. Annu Rev Immunol.2001,19:683-765.
172. Redpath. S.,Ghazal. P., Gascoigne. N. R. Hijacking and exploitation of IL-10 by intracellular pathogens. Trends Microbiol.2001.9(2):86-92.
173. Almonti, J. B.,Ball. T. B., Fowke. K. R. Mechanisms of CD4 T lymphocyte cell death in human immunodeficiency virus infection and AIDS. J Gen Virol.2003,84:1649-1661.
174. Dolganiuc. A., Kodys, K., Kopasz. A., et al. Hepatitis C virus core and non-structural protein 3 proteins induce pro-and anti-inflammatory cytokines and inhibit dendritic cell differentiation. J Immunol.2003.170(11):5615-5624.
175. Suradhat, S., Thanawongguwech,R., Poovorawan, Y. Upregulation of IL-10 gene expression in porcine peripheral blood mononuclear cells by porcine reproductive and respiratory syndrome virus. J Gen Virol.2003,84:453-459.
176. Suradhat, S., Sada, W., Buranapraditkun, S., et al. The kinetics of cytokine production and CD25 expression by porcine lymphocyte subpopulations following exposure to classical swine fever virus (CSFV). Vet Immunol Immunopathol.2005,106:197-208.
177. Jamin, A., Gorin, S., Cariolet, R., et al. Classical swine fever virus induces activation of plasmacytoid and conventional dendritic cells in tonsil, blood, and spleen of infected pigs.Vet Res.2008,39:07.
178. Bjorkman, P. J., Saper. M. A., Samraoui, B., et al. Structure of the human class I histocompatibility antigen, HLA-A2. Nature.1987,329:506-512.
179. O'Cormor, D. H., Mothe, B. R., Weinfurter. J. T., et al. Major histocompatibility complex class I alleles associated with slow simian immunodeficiency virus disease progression bind epitopes recognized by dominant acut-phase cytotoxic-T-lymphocyte responses. J Virol.2003.77:9029-9040.
180. Bobe, P., Benihoud. K., Kiger, N. Allogenic MHC class Ⅱ determinant(s) in MRL/lpr autoimmune disease-prone mice. Unusual expression of an L1 transposable element creates molecular mimicry. J Immunol.1993,151:2813-2819.
181.Chardon,P.,Renard, C Gaillard, C. R., et al. The porcine major histocompatibility complex and related paralogous regions. Genet Sel Evol.2000.32(2):109-128.
182. Sanz-Parra,A., Sobrinoand. F., Ley,V. Infection with foot-and-mouth disease virus results in a rapid reduction of MHC class 1 surface expression. J Gen Virol.1998.79:433-436.
183. Wang, X., Eaton,M., Mayer. M., et al. Porcine reproductive and respiratory syndrome virus productively infects monocyte-derived dendritic cells and compromises their antigen-presenting ability. Arch Virol.2007,152:289-303.
184. Johnson, D. C., Hill, A. B. Herpesvirus evasion of the immune system. Curr Top Microbiol Immunol. 1998,232:150-165.
185. Cohen, J.1. Infection of cells with varicella-zoster virus down-regulates surface expression of class I MHC antigens. J Infect Dis.1998,177:1390-1393.
186. Koppers-Lalic, D., Rijsewijk, F. A. M., Verschuren, S. B. E., et al. The UL41-encoded virion host shutoff (vhs) protein and vhs-independent mechanisms are responsible for downregulation of MHC class I molecules by bovine herpesvirus 1. J Gen Virol.2001,82:2071-2081.
187. Mellencamp, M. W., O'Brien, P. C., Stevenson, J. R. Pseudorabies virus-induced suppression of MHC class I antigen expression. J Virol.1991,65:3365-3370.
188. Rappocciolo, G., Birch, J., Ellis, S. A. Down-regulation of MHC class I expression by equine herpesvirus-1. J Gen Virol.2003,84:293-300.
189. Benz, C., Reusch, U., Muranyi, W., et al. Efficient downregulation of major histocompatibility complex class I molecules in human epithelial cells infected with cytomegalovirus. J Gen Virol.2001, 82(Pt9):2061-2070.
190. Lacayo, J., Sato, H., Kamiya, H., et al. Down-regulation of surface major histocompatibility complex class I by guinea pig cytomegalovirus. J Gen Virol.2003,84:75-81.
191.Tardif, K. D., Siddiqui, A. Cell surface expression of major histocompatibility complex class Ⅰ molecules is reduced in hepatitis C virus subgenomic replicon-expressing cells. J Virol.2003,77(21): 11644-11650.
192. Brown, J. A., Howcroft, T. K., Singer, D. S. HIV Tat protein requirements for transactivation and repression of transcription are separable. J Acquir Immune Defic Syndr Hum Retrovirol.1998,17: 9-16.
193. Kamp, W., Berk, M. B., Visser, C. J., et al. Mechanisms of HIV-1 to escape from the host immune surveillance. Eur J Clin Invest.2000,30:740-746.
194. Kanazawa, S., Okamoto, T., Peterlin, B. M. Tat competes with CⅡTA for the binding to P-TEFb and blocks the expression of MHC class Ⅱ genes in HIV infection. Immunity.2000,12:61-70.
195. Ashrafi, G. H., Tsirimonaki, E., Marchetti, B., et al. Down-regulation of MHC class I by bovine papillomavirus E5 oncoproteins. Oncogene.2002,21:248-259.
196. Ashrafi, G. H., Haghshenas, M. R., Marchetti, B., et al. E5 protein of human papillomavirus type 16 selectively downregulates surface HLA class I. Int J Cancer.2005,113:276-283.
197. Cadwell,K., Coscoy. L. Ubiquitination on nonlysine residues by a viral E3 ubiquitin ligase. Science. 2005.309:127-130.
198. Goto, E., Ishido. S., Sato, Y., et al. c-MIR. a human E3 ubiquitin ligase. is a functional homolog of herpesvirus proteins MIR1 and MIR2 and has similar activity. J Biol Chem.2003.278:14657-14668.
199. Coscoy, L., Ganem, D. Kaposi's sarcoma-associated herpesvirus encodes two proteins that block cell surface display of MHC class I chains by enhancing their endocytosis. PNAS.2000,97:8051-8056.
200. Ishido, S., Choi, J. K., Lee, B. S., et al. Inhibition of natural killer cell-mediated cytotoxicity by Kaposi's sarcoma-associated herpesvirus K5 protein. Immunity.2000.13:365-374.
201. Stevenson, P. G., Efstathiou, S., Doherty, P. C., et al. Inhibition of MHC class I-restricted antigen presentation by y 2-herpesviruses. PNAS.2000,97:8455-8460.
202. Lybarger, L., Wang, X., Harris, M., et al. Viral immune evasion molecules attack the ER peptide-loading complex and exploit ER-associated degradation pathways. Curr Opin Immunol.2005, 17:71-78.
203. Georgopoulos, N, T., Proffitt, J. L., Blair, G. E. Transcriptional regulation of the major histocompatibility complex (MHC) class I heavy chain, TAP1 and LMP2 genes by the human papillomavirus (HPV) type 6b,16 and 18 E7 oncoproteins. Oncogene.2000,19: 4930-4935.
204. Ahn, K., Gruhler, A., Galocha, B., et al. The ER-luminal domain of the HCMV glycoprotein US6 inhibits peptide translocation by TAP. Immunity.1997,6:613-621.
205. Fruh,K., Ahn,K.,Djaballah, H., et al. A viral inhibitor of peptide transporters for antigen presentation. Nature.1995,375:415-418.
206. Hengel, H., Koopmann, J. O., Flohr, T., et al. A viral ER-resident glycoprotein inactivates the MHC-encoded peptide transporter. Immunity.1997,6:623-632.
207. Hill, A.,Jugovic. P., York. I., et al. Herpes simplex virus turns off the TAP to evade host immunity. Nature.1995.375:411-415.
208. Lehner, P. J., Karttunen. J. T.. Wilkinson. G. W.. et al. The human cytomegalovirus US6 glycoprotein inhibits transporter associated with antigen processing-dependent peptide translocation. Proc Natl Acad Sci,USA.1997.94:6904-6909.
209. Ahn, K.,Meyer. T. H.,Uebel. S.,et al. Molecular mechanism and species specificity of TAP inhibition by herpes simplex virus ICP47. EMBO J.1996,15:3247-3255.
210. Tomazin, R., Hill, A. B., Jugovic, P., et al. Stable binding of the herpes simplex virus ICP47 protein to the peptide binding site of TAP. EMBO J.1996,15:3256-3266.
211. Ambagala, A. P., Hinkley, S., Srikumaran, S. An early pseudorabies virus protein down-regulates porcine MHC class I expression by inhibition of transporter associated with antigen processing (TAP). J Immunol.2000,164(1):93-99.
212. Tortorella, D., Gewurz, B. E., Furman, M. H., et al. Viral subversion of the immune system. Annu Rev Immunol.2000,18:861-926.
213. Spriggs, M. K. One step ahead of the game:viral immunomodulatory molecules. Annu Rev Immunol. 1996,14:101-130.
214. Fruh, K., Gruhler, A., Krishna, R. M., et al. A comparison of viral immune escape strategies targeting the MHC class I assembly pathway. Immunol Rev.1999,168:157-166.
215. Farrell, H. E., Davis-Poynter, N. J. From sabotage to camouflage:viral evasion of cytotoxic T lymphocyte and natural killer cell-mediated immunity. Semin Cell Dev Biol.1998,9:369-378.
216. Hengel, H., Brune, W., Koszinowski, U. H. Immune evasion by cytomegalovirus--survival strategies of a highly adapted opportunist. Trends Microbiol.1998,6(5):190-197.
217. Tomazin, R., Boname, J., Hegde, N. R., et al. Cytomegalovirus US2 destroys two components of the MHC class II pathway, preventing recognition by CD4+ T cells. Nat Med.1999,5:1039-1043.
218. Hegde, N. R., Tomazin, R. A., Wisner, T. W., et al. Inhibition of HLA-DR assembly, transport, and loading by human cytomegalovirus glycoprotein US3:a novel mechanism for evading major histocompatibility complex class Ⅱ antigen presentation. J Virol.2002,76(21):10929-10941.
219. Yao, Y., Li, P., Singh, P., et al. Vaccinia virus infection induces dendritic cell maturation but inhibits antigen presentation by MHC class Ⅱ. Cell Immunol.2007,246:92-102.
220. Rehm, K. E., Connor, R. F., Jones, G. J., et al. Vaccinia virus A35R inhibits MHC class II antigen presentation. Virology.2010,397:176-186.
221. Zhang, B., Li, P., Wang, E., et al. The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon-gamma. Virology. 2003,310:100-108.
222. Zhang, B., Wang. E. The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon gamm. Virology.2003,310: 100-108.
223. Mozdzanowska. K., Furchner. M.,Zharikova. D., et al. Roles of CD4- T-cell-Independent and-dependent antibody responses in the control of influenza virus infection:evidence for noncognate CD- T T cell activities that enhance the therapeutic activity of antiviral antibodies. J Virol.2005.79 (10):5943-5951.
224. Hussain, A., Wesley. C. Khalid. M. et al. Human immunodeficiency virus type 1 Vpu protein interacts with CD74 and modulates major histocompatibility complex class Ⅱ presentation. J Virol. 2008,82(2):893-902.
225. Ishido, S., Choi, J. K.,Lee. B. S., et al. Inhibition of natural killer cell-mediated cytotoxicity by Kaposi's sarcoma-associated herpesvirus K5 protein. Immunity.2000,13(3):365-374.
226. Coscoy, L., Ganem, D. A. viral protein that selectively downregulates ICAM-1 and B7-2 and modulates T cell costimulation. J Clin Invest.2001,107:1599-1606.
227. Barker, E., Bossart, K. N., Fujimura, S. H., et al. The role of CD80 and CD86 in enhancing CD8+ cell suppression of HIV replication. Cell Immunol.1999,196:95-103.
228. Salek-Ardakani, S., Arrand, J. R., Mackett, M. Epstein-Barr virus encoded interleukin-10 inhibits HLA-class I. ICAM21, and B7 expression on human monocytes:implications for immune evasion by EBV. Virology.2002,304(2):342-351.
229. Fuse, S., Obar, J. J., Bellfy, S., et al. CD80 and CD86 control antiviral CD8+ T-cell function and immune surveillance of murine gamma herpesvirus68. J Virol.2006,80(18):9159-9170.
230. Creery, W. D.,Diaz-Mitoma, F.,Filion. L., et al. Differential modulation of B7-1 and B7-2 isoform expression on human monocytes by cytokines which influence t he development of T helper cell phenotype. Eur J Immunol.1996,26(6):1273-1277.
231. Fiorentino, D. F., Zlotnik, A., Vieira, P., et al. IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Thl cells. J Immunol.1991,146(10):3444-3451.
232. Girard, B. M.,May, V., Bora, S. H.,et al. Regulation of neurotrophic peptide expression in sympathetic neurons:quantitative analysis using radioimmunoassay and real-time quantitative polymerase chain reaction. Regul Pept.2002.109(1-3):89-101.
233. Wickert. L., Steinkruger, S., Abiaka, M., et al. Quantitative monitoring of the mRNA expression pattern of the TGF-beta-isoforms (beta 1,beta 2. beta 3) during transdifferentiation of hepatic stellate cells using a newly developed real-time SYBR Green PCR. Biochem Biophys Res Commun.2002. 295:330-335.
234. Guang-li, Li., Roy, B., Xing-hua, Li., et al. Quantification of silkworm coactivator of MBF1 mRNA by SYBR Green I real-time RT-PCR reveals tissue-and stage-specific transcription levels. Mol Biol Rep.2009,36:1217-1223.
235. Sato, H., Ozawa, K., Yonemura, K., et al. Quantitative PCR to evaluate small amounts of BCL2 mRNA in human peripheral T cells:implication of equimolar target and competitor end products. Clin Chim Acta.2003,328(1-2):147-153.
236. Gallard, A., Foucras, G., Coureau, C., et al. racking T cell clonotypes in complex T lymphocyte populations by real-time quantitative PCR using fluorogenic complementarity-determining region-3-specific probes. J Immunol Methods.2002,270(2):269-280.
237. Deng, X., Li, H., Tang, Y. W. Cytokine expression in respiratory syncytial virus-infected mice as measured by quantitative reverse-transcriptase PCR. J Virol Methods.2003,107(2):141-146.
238. White, T. M., Mahalingam, R., Traina-Dorge, V., et al. Persistence of simian varicella virus DNA in CD4(+) and CD8(+) blood mononuclear cells for years after intratracheal inoculation of African green monkeys. Virology.2002,303(1):192-198.
239. Maeda, S., Miyauchi, T., Iemitsu, M., et al. Effects of exercise training on expression of endothelin-1 mRNA in the aorta of aged rats. Clin Sci (Lond).2002,103 Suppl 48:118S-123S.
240.李一荣,胡丽华,陈凤花,等.应用SYBR Green I实时荧光PCR法对中国汉族人群HLA-B27进行快速基因分型.临床血液学杂志.2008,21(10)：526～529.
241.王默进,周总光,王玲,等.运用TaqMan探针实时荧光PCR技术检测AKAP10基因2073A/G单核苷酸多态性.四川大学学报(医学版).2009,40(2)：275～278.
242.严冰冰,虞涛,方华红,等.应用实时荧光PCR分析apoE3、4等位基因.临床检验杂志.2008,26(3)：197～199.
243. Weise, A., Grundler, S., Zaumsegel, D., et al. Development and evaluation of a rapid and reliable method for cytochrome P450 2C8 genotyping. Clin Lab.2004,50(3-4):141-148.
244. Stamer, U. M., Bayerer, B., Wolf, S., et al. Rapid and reliable method for cytochrome P450 2D6 genotyping. Clin Chem.2002,48(9):1412-1217.
245. Sangkitporn, S. K., Wangkahat, K., Sangnoi, A., et al. Rapid diagnosis of alpha (a)-thalassemia using the relative quantitative PCR and the dissociation curve analysis.Clin Lab Haematol.2003,25(6): 359-365.
246.刘敬忠,闫梅,王立荣,等.实时荧光聚合酶链反应结合融解曲线分析在α-地中海贫血基因诊断 中的价值.中华检验医学杂志.2005,28(8)：858～861.
247.尹爱华.张祥忠.何蕴韶.等.TaqMan-MGB探针实时荧光PCR在β地中海贫血植入前诊断中的应用研究.热带医学杂志.2007,7(12)：1155-1158.
248. Zimmermann. B., Holzgreve, W.,Wenzel,F., et al. Novel real-time quantitative PCR test for trisomy 21. Clin Chem.2002.48(2):362-363.
249. Miyake, Y.,Fujiwara, Y., Ohue, M., et al. Quantification of micrometastases in lymph nodes of colorectal cancer using real-time fluorescence polymerase chain reaction. Int J Oncol.2000,16(2): 289-293.
250. Eckert, C., Landt, O., Taube, T., et al. Potential of LightCycler technology for quantification of minimal residual disease in childhood acute lymphoblastic leukemia. Leukemia.2000,14(2): 316-323.
251.赵建军,成丹,李娜,等.猪瘟病毒野毒株和兔化弱毒疫苗株复合实时荧光定量RT-P CR鉴别方法的建立.中国兽医科学.2007,37(05)：406～412.
252. Jamnikar Ciglenecki, U., Grom, J., Toplak, I., et al. Real-time RT-PCR assay for rapid and specific detection of classical swine fever virus:comparison of SYBR Green and TaqMan MGB detection methods using novel MGB probes. J Virol Methods.2008,147(2):257-264.
253. Yang, J. R.. Lo, J., Liu, J. L., et al. Rapid SYBR green I and modified probe real-time reverse transcription-PCR assays identify influenza H1N1 viruses and distinguish between pandemic and seasonal strains. J Clin Microbiol.2009,47(11):3714-3716.
254. Liu, S., Hou. G., Shu. Y.. et al. A SYBR Green I real-time RT-PCR assay for detection and differentiation of influenza A (H1N1) virus in swine populations. J Virol Methods.2009,162(1-2): 184-187.
255. Tan, S. W., Ideris, A., Omar, A. R., et al. Detection and differentiation of velogenic and lentogenic Newcastle disease viruses using SYBR Green I real-time PCR with nucleocapsid gene-specific primers. J Virol Methods.2009,160(1-2):149-156.
256. Martinez, E.,Riera. P., Sitja. M., et al. Simultaneous detection and genotyping of porcine reproductive and respiratory syndrome virus (PRRSV) by real-time RT-PCR and amplicon melting curve analysis using SYBR Green. Res Vet Sci.2008,85(1):184-193.
257. McIntosh,K. A., Tumber. A., Harding. J. C., et al. Development and validation of a SYBR green real-time PCR for the quantification of porcine circovirus type 2 in serum, buffy coat, feces, and multiple tissues. Vet Microbiol.2009,133(1-2):23-33.
258. Brunborg, I. M, Moldal, T., Jonassen, C. M. Quantitation of porcine circovirus type 2 isolated from serum/plasma and tissue samples of healthy pigs and pigs with postweaning multisystemic wasting syndrome using a TaqMan-based real-time PCR. J Virol Methods.2004,122(2):171-178.
259. Chung, W. B., Chan, W. H., Chaung, H. C., et al. Real-time PCR for quantitation of porcine reproductive and respiratory syndrome virus and porcine circovirus type 2 in naturally-infected and challenged pigs. J Virol Methods.2005,124(1-2):11-19.
260. Ladekjaer-Mikkelsen, A. S., Nielsen, J., Stadejek, T., et al. Reproduction of postweaning multisystemic wasting syndrome (PMWS) in immunostimulated and non-immunostimulated 3-week-old piglets experimentally infected with porcine circovirus type 2 (PCV2). Vet Microbiol. 2002,89(2-3):97-114.
261. Olvera, A., Sibila, M., Calsamiglia, M., et al. Comparison of porcine circovirus type 2 load in serum quantified by a real time PCR in postweaning multisystemic wasting syndrome and porcine dermatitis and nephropathy syndrome naturally affected pigs. J Virol Methods.2004,117(1):75-80.
262. Rovira, A., Balasch, M., Segales, J., et al. Experimental inoculation of conventional pigs conventional pigs with porcine reproductive and respiratory syndrome virus and porcine circovirus 2. J Virol.2002, 76(7):3232-3239.
263. Jefferies, R., Morgan, E. R., Shaw, S. E. A SYBR green real-time PCR assay for the detection of the nematode Angiostrongylus vasorum in definitive and intermediate hosts. Vet Parasitol.2009,166(1-2): 112-118.
264. Chen, S., Yee, A., Griffiths, M., et al. The evaluation of a fluorogenic polymerase chain reaction assay for the detection of Salmonella species in food commodities. Int J Food Microbiol.1997,35: 239-250.
265. Oberst, R. D., Hays, M. P., Bohra, L. K., et al. PCR-based DNA amplification and presumptive detection of Escherichia coli O157:H7 with an internal fluorogenic probe and the 5'nuclease TaqMan assay. Appl Environ Microbiol.1998,64:3389-3396.
266. Leutenegger, C. M., Pusterla, N., Mislin, C. N., et al. Molecular evidence of ticks coinfected with Borrelia burgdorferi sensu lato and the human granulocytic ehrlichiosis agent in Switzerland. J Clin Microbiol.1999.37:3390-3391.
267. Bassler, H. A., Flood, S. J. A., Livak, K. J., et al. Use of a fluorogenic probe in a PCR-based assay for the detection of Listeria monocytogenes. Appl Environ Microbiol.1995,61:3724-3728.
268. Nogva, H. K., Rudi, K., Naterstad, K., et al. Application of 5'-nuclease PCR for quantitative detection of Listeria monocytogenes in pure cultures, water, skim milk, and pasteurized whole milk. Appl Environ Microbiol.2000,66:4266-4271.
269. Lyon, W. J. TaqMan PCR for detection of Vibrio cholerae O1,0139, non-01, and non-0139 in pure cultures, raw oysters, and synthetic seawater. Appl Environ Microbiol.2001,67:4685-4693.
270. Haramotoa, E., Kitajimab, M., Katayamab, H., et al. Application of real-time PCR assays to genotyping of F-specific phages in river water and sediments in Japan. Water Research.2009,43: 3759-3764.
271. Wolf, S., Hewitt, J., Rivera-Aban, M., et al. Detection and characterization of F+RNA bacteriophages in water and shellfish:Application of a multiplex real-time reverse transcription PCR. J Viro Methods. 2008,149:123-128.
272.赵卫东,郑文杰,贺艳.荧光PCR方法定性和定量检测BT63转基因大米.食品研究与开发(检测分析).2009,30(3)：133～135.
273.张亮,杨剑波,宋丰顺,等.实时荧光PCR技术定量检测转Bt基因水稻的研究.生物学杂志.2008,25(6)：63～65.
274.吴孝槐,路勇.利用实时荧光PCR方法检测转Bt基因大米.现代食品科技.2009,25(2)：211～216.
275. Wengler, G., Bradley, D. W., Collett, M. S., Heinz, F. X., Schlesinger, R. W., Strauss, J. H. Family Flaviviridae. In F. A. Murphy,C. M. Fauquet, D. H. L. Bishop, S. A. Ghabrial, A. W. Jarvis, G. P. Martinelli,M. A. Mayo, and M. D. Summers (ed.), Classification and nomenclature of viruses. Sixth Report of the International Committee on Taxonomy of Viruses. Springer-Verlag, Berlin, Germany. 1995,415-427.
276. Fauquet, C. M., Mayo, M. A., Maniloff, J., Desselberger, U., Ball, L. A., editors. Virus taxonomy:the 8th report of the international committee on taxonomy of viruses. San Diego, CA:Elsevier Academic Press.2005.
277. Choi, C., Chae, C. Localization of classical swine fever virus in male gonads during subclinical infection. J Gen virol.2002,83(Ptl 1):2717-2721.
278. Floegel, G., Wehrend, A., Depner, K. R., et al. Detection of classical swine fever virus in semen of infected boars. Vet Microbiol.2000,77(1-2):109-116.
279. Vossen, M. T., Westerhout, E. M., Soderberg-Naucler, C., et al. Viral immune evasion:a masterpiece of evolution. Immunogenetics.2002,54:527-542.
280. Hariharan, M. J., Nataraj, C., Srikumaran, S. Down regulation of murine MHC class I expression by bovine herpesvirus 1. Viral Immunol.1993,6:273-284.
281. Koppers-Lalic. D., Verweij, M. C., Lipinska, A. D., et al. Varicellovirus UL 49.5 proteins differentially affect the function of the transporter associated with antigen processing, TAP. PLoS Pathog.2008,4(5):e1000080.
282. Nataraj, C., Eidmann, S., Hariharan, M. J., et al. Bovine herpesvirus 1 downregulates the expression of bovine MHC class I molecules. Viral Immunol.1997,10:21-34.
283. Sparks-Thissen, R. L., Enquist, L. W. Differential regulation of Dk and Kk major histocompatibility complex class I proteins on the cell surface after infection of murine cells by pseudorabies virus. J Virol.1999,73:5748-5756.
284. Hunt, H. D., Lupiani, B., Miller, M. M., et al. Marek's disease virus down-regulates surface expression of MHC (B Complex) Class Ⅰ (BF) glycoproteins during active but not latent infection of chicken cells. Virology.2001,282:198-205.
285. Bensaude, E., Turner, J. L., Wakeley, P. R., et al. Classical swine fever virus induces proinflammatory cytokines and tissue factor expression and inhibits apoptosis and interferon synthesis during the establishment of long-term infection of porcine vascular endothelia cells. J Gen Virol.2004,85(Pt4): 1029-1037.
286. Sanchez-Cordon, P. J., Romanini, S., Salguero, F. J., et al. Apoptosis of thymocytes related to cytokine expression in experimental classical swine fever. J Comp Pathol.2002,127:239-248.
287. Schweizer, M., Peterhans, E. Noncytopathic bovine viral diarrhea virus inhibits double-stranded RNA-induced apoptosis and interferons synthesis. J Virol.2001,75 (10):4692-4698.
288. Charleston, B., Fray, M. D., Baigent, S., et al., Establishment of persistent infection with non-cytopathic bovine viral diarrhea virus in cattle is associated with a failure to induce type I interferon, J Gen Virol.2001,82:1893-1897.
289. Gomez-Villamandos, J. C., Salguero, F. J., Ruiz-Villamor, E., et al. Classical swine fever:pathology of bonemarrow. Vet Pathol.2003,40:157-163.
290. Summerfield, A., Hofmann, M., McCullough, K. C. Immature granulocytic cells dominate the peripheral blood during classical swine fever and are targets for virus infection. Vet Immunol Immunopathol.1998.63:289-301.
291. Gisler,A. C.,Nardi,N. B.,Nonnig, R. B., et al. Classical swine fever virus in plasma and peripheral blood mononuclear cells of acutely infected swine. Zentralbl Veterinaermed B.1999.46:585-593.
292. Sato,M., Mikami. O.,Kobayashim. M., et al. Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus. Vet Microbiol.2000,75:1-9.
293. Choi, C., Hwang,K. K., Chae, C. Classical swine fever virus induces tumor necrosis factor-alpha and lymphocyte apoptosis. Arch Virol.2004,149 (5):875-889.
294. Sanchez-Cordon, P. J., Nunez, A., Salguero, F. J., et al. Lymphocyte Apoptosis and Thrombocytopenia in Spleen during Classical Swine Fever:Role of Macrophages and Cytokines. Vet Pathol.2005,42 (4):477-488.
295. Stark, G. R., Kerr,I. M., Williams, B. R., et al. How cells respond to interferons. Annu Rev Biochem. 1998,67:227-264.
296. Boehm, U., Klamp, T., Groot, M., et al. Cellular responses to interferon-gamma. Annu Rev Immunol. 1997.15:749-795.
297. Dallman, M. J. Cytokine gene expression:analysis using northern blotting, polymerase chain reaction and in situ hybridization. Immunol Rev.1991,119:163-180.
298. Higuchi, R., Dollinger. G., Walsh, P. S.. et al. Simulutaneous amplification and detection of specific DNA sequences. Biotechnology (NY).1992,10:413-417.
299. Ishiguro, T., Saitoh, J., Yawata, H., et al. Homogeneous quantitative assay of hepatitis C virus RNA by polymerase chain reaction in the presence of a fluorescent intercalater. Anal Biochem.1995.229(2): 207-213.
300. Tseng, S. Y., Macool. D., Elliott, V., et al. An homogeneous fluorescence polymerase chain reaction assay to identify Salmonella. Anal Biochem.1997,245(2):207-212.
301. Morrison, T. B.,Weis. J. J., Wittwer. C. T. Quantification of low-copy transcripts by continuous SYBR Green I monitoring during amplification. Biotechniques.1998,24(6):954-958,960,962.
302. Freeman. W. M, Walker,S. J, Vrana, K. E. Quantitative RT-PCR:pitfall and potential. Biotechniques. 1999,26(1):112-125.
303. Mackay,I. M.,Arden, K. E., Nitsche. A. Real-time PCR in virology. Nucleic Acids Res.2002.30 (6): 1292-1305.
304. Livak, K. J.,Schmittgen, T. D. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods.2001,25(4):402-408.
305. Van Oirschot, J. T. Description of the virus infection. In Classical Swine Fever and Related Viral Infections. Edited by B. Leiss. Boston:Martinus Nijhoff.1988,1-25.
306. Borca, M. V., Gudmundsdottir, I., Fernandez-Sainz,1. J., et al. Patterns of cellular gene expression in swine macrophages infected with highly virulent classical swine fever virus strain Brescia. Virus Res. 2008,138(1-2):89-96.
307. Shi, Z., Sun, J., Guo, H., et al. Genomic expression profiling of peripheral blood leukocytes of pigs infected with highly virulent classical swine fever virus strain Shimen. J Gen Virol.2009,90(Pt7): 1670-1680.
308. Li, J., Yu, Y. J., Feng, L., et al. Global transcriptional profiles in peripheral blood mononuclear cell during classical swine fever virus infection. Virus Res.2010,148 (1-2):60-70.
309. Graham, S. P., Everett, H. E., Johns, H. L., et al. Characterisation of virus-specific peripheral blood cell cytokine responses following vaccination or infection with classical swine fever viruses. Vet Microbiol.2010,142(1-2):34-40.
310. Sanchez-Cordon, P. J., Nunez, A., Salguero, F. J.m et al. Evolution of lymphocytes and cytokine expression in classical swine fever virus infection. J Comp Path.2005,132:249-260.
311.Shao, L., Sperber, K. Impaired regulation of HLA-DR expression in human immunodeficiency virus-infected monocytes. Clin Diagn Lab Immunol.2002,9(4):739-746.
312. Johnson, D. C., Hegde, N. R. Inhibition of the MHC class Ⅱ antigen presentation pathway by human cytomegalovirus. Curr Top Microbiol Immunol.2002,269:101-115.
313.Odeberg, J., Plachter, B., Branden, L., et al. Human cytomegalovirus protein pp65 mediates accumulation of HLA-DR in lysosomes and destruction of the HLA-DR a-chain. Immunobiology. 2003,101:4870-4877.
314. Li, Q., Turk, S. M., Hutt-Fletcher, L. M. The Epstein-Barr virus (EBV) BZLF2 gene product associates with the gH and gL homologs of EBV and carries an epitope critical to infection of B cells but not of epithelial cells. J Virol.1995,69(7):3987-3994.
315. Hulst, M. M., Westra, D. F., Wensvoort, G., et al. Glycoprotein E1 of hog cholera virus expressed in insect cells protects swine from hog cholera. J Virol.1993,67:5435-5442.
316. Van Zijl, M., Wensvoort, G., de Kluyver, E., et al. Live attenuated pseudorabies virus expressing envelope glycoprotein El of hog cholera virus protects swine against both pseudorabies and hog cholera. J Virol.1991,65:2761-2765.
317. Weiland, F., Weiland, E.,Unger, G., et al. Localization of pestiviral envelope proteins E(rns) and E2 at the cell surface and on isolated particles. J Gen Virol.1999,80(Pt):1157-1165.
318.王琴,郎洪武,王在时,等.猪瘟病毒E2基因的克隆与鉴定.畜牧兽医学报.2001,32(6)：549～555.
319.王琴,王在时,赵耘,等.12株猪瘟病毒E2基因主要抗原区域的序列差异分析.微生物学报.2000,40(6)：614～621.
320.吕宗吉,李红卫,涂长春,等.我国部分地区猪瘟病毒流行株的基因差异.中国兽医学报.2000,20(4)：313～316.
321.张永国,刘湘涛,韩雪清,等.广西猪瘟流行毒与C-株疫苗毒gp55(E2)主要抗原区DNA序列差异的比较.西北农林科技大学学报.2002,30(1)：79～84.
322.刘伯华,刘湘涛,韩雪清,等.急慢性猪瘟病毒分离株和疫苗株E2基因的序列分析.畜牧兽医学报.2001,32(6)：568～575.
323.赵耘,王在时,王琴,等.23株猪瘟病毒E2基因主要抗原编码区序列差异分析.中国兽医科技.2002,32(3)：3～6.
324.吴显实,罗廷荣,廖素环,等.广西猪瘟流行毒株全基因组的克隆与序列分析中国兽医学报.2005,25(2)：125～128.
325.孙石静,罗廷荣,吴显实,等.广西猪瘟流行毒株E2基因的序列分析.中国兽医科技.2004,325(9)：29～33.
326.廖素环,罗廷荣,吴显实,等.广西流行猪瘟病毒E2基因序列测定及分析.中国生物制品学杂志.2005,18(3)：196～199.