川金丝猴源柯萨奇B3病毒的分子特征及其致病性初步研究
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摘要
近年来,随着自然生态环境和人工圈养繁殖条件的不断改善,已被列入濒危动物的金丝猴种群数量有所增多,同时又不断有其感染疾病死亡的案例发生。除外伤和天敌等因素外,多种病原菌感染是导致金丝猴死亡的一个重要原因,但未见有病毒感染致死的相关资料。本研究对临床送检的死亡川金丝猴进行了系统的病理学和分子生物学检测,根据临床症状和实验室诊断结果综合分析,揭示该金丝猴的死亡可能与柯萨奇B组病毒感染有关,而且病理特征以病毒性心肌炎为主,并伴发有多个脏器的损伤。进而应用Vero细胞从该猴的心肌组织中成功分离获得一株病毒,对所分离的病毒进行系统的形态学、理化学、动物回归试验和RT-PCR等方法鉴定,确定其为柯萨奇B3病毒(CVB3),将其初步命名为川金丝猴源柯萨奇B3病毒(SSM-CVB3)。经SSM-CVB3免疫家兔制备的抗体用于免疫荧光化学检测结果显示,在金丝猴的心肌、肾等组织的细胞胞浆内呈病毒感染的强阳性反应。从而确诊该猴死于SSM-CVB3感染,这是国内外首次有病毒感染死亡金丝猴的报道。应用5’RACE和3’RACE试剂盒,以及设计合成的5对引物完成了该毒株的全基因组测序,获得其全长基因组共7397bp的序列,并提交GenBank(登录号为GU109481)。对SSM-CVB3的全长基因组序列进行系统的分子特征分析,发现其与GenBank中公布的另外12株CVB3相比在VP2区域有3个核苷酸缺失,导致相应位置的1个氨基酸缺失,同时该区域对应的编码氨基酸也由其他CVB3毒株的LGRTG变为SSM-CVB3毒株独有的WSDW,这一特征性变化可以作为SSM-CVB3毒株的遗传特征。另外,分别位于VP2和2A区域的氨基酸序列AAKEFAGEPI和RNKHFPVS可作为CVB3中国分离株的两个遗传标志。序列比对结果显示,SSM-CVB3的5’-NTR与CVB3F及CVB3B同源性最高,其编码区和3’-NTR均与广州分离株CVB3G的同源性最高,由此推测SSM-CVB3可能为CVB3G和CVB3F或CVB3B重组后的一个新的变种。为了进一步明确该毒株的致病特性,将SSM-CVB3通过腹腔注射途径接种猕猴,从临床病理学和病理形态学等方面进行了系统的分析。从感染后第2天开始,猕猴出现体温升高、一过性的精神沉郁和粥样粪便,其他症状不明显。不同时间点的尿常规检测发现可检出血尿和蛋白尿,其他指标变化不明显。血常规检测结果显示,其白细胞总数和红细胞总数的检测值偏低,在临床检测时有一定的参考价值。血清中的各项酶学指标检测结果证实,在感染的初期CK和CK-MB值均显著升高;第1周内ALT值显著升高,之后下降至正常水平;AMY在感染初期升高,后期下降至正常水平;CRE和BUN值无明显改变。分别于接种病毒后15天和30天剖杀猕猴进行病理学组织学观察,其病变以病毒性心肌炎、间质性肾炎、神经系统的非化脓性炎症及肝脏汇管区有细胞增生性反应为主要特征,其他组织器官也有不同程度的病理变化。说明SSM-CVB3感染猕猴可造成多系统的损伤。本研究不仅为临床上金丝猴疾病的诊断和防治提供参考,为我国流行CVB3的遗传学背景、种系进化关系及流行病学调查和预防研究提供基础,而且为后期建立该病毒感染猕猴的实验动物模型提供依据,具有重要的比较医学意义。
The snub-nosed monkey, or golden monkey, is one of the most endangered primate species due to its dramatically shrinking distribution during the past 400 years. Populations of the snub-nosed monkey are found mainly in three isolated regions in China: Qinglin, Sichuan/Gansu, and Shennongjia. There are three species of snub-nosed monkey found in China, including the Sichuan snub-nosed monkey (Rhinopithecus roxellanae), the Yunnan snub-nosed monkey (Rhinopithecus bieti) and the Guizhou snub-nosed monkey (Rhinopithecus brelichi). There is also one species of snub-nosed monkey (Rhinopithecus avunculus) found in Vietnam. The snub-nosed monkey species are all under first-class state protection in China, and the International Union for Natural Conservation (IUCN) has formally recognized them as vulnerable or endangered species. Because of these designations, snub-nosed monkeys have drawn a lot of attention from various conservation efforts. In recent years, the population of the Sichuan snub-nosed monkey has increased by more than 10,000 because of improvement in the conditions of some nature conservation areas and also by artificial propagation. However, many diseases that threaten the snub-nosed monkey have developed because of multitude of factors. There are reports that Sichuan snub-nosed monkeys have died from septicemia due to infection with pneumoniae Diplococcus or Escherichia coli and Klebsiella, from acute pyelonephritis attributed to infected with Escherichia coli and Proteus mirabilis, from unspecified parenchymatous hepatitis, and from unspecified myocarditis. In addition, Staphylococcus aureus can cause spontaneous abortion or stillbirth in the snub-nosed monkey. Since 2001, five Sichuan snub-nosed monkeys had been living in the zoological garden in Changchun in the Jilin province of China. Four of them died between 2003 and 2004. The causes of death were unknown, but they all showed the homoplastic clinical symptoms on lack of activity and shortness of breath before death, if they had cardiac failure, no more evidence were acquired. The final monkey of the original five, a five-year-old female, died on September 18, 2005. She had been in good health but exhibited reduced activity and showed evidence of shortness breath after movement during the previous day. No dizziness or syncope was observed. The hind limbs were slightly edematous. She had been treated using several drugs, but with no effect. No other information about her was available. In order to ascertain the cause of death of the suub-nosed monkey, and the pathogenicity and molecular characteristics of its etiological agent,systematical experiments were done in this study.
we dissected the died Sichuan snub-nosed monkey by the common practice and recorded its pathological changes, and then made manufacture pathological section. Pathology of the organs of the suub-nosed monkey appeared septicaemia. Cardiac pericardium, epicardium, and endocardium appeared bleeding point and ecchymosis; cardiac muscle appears white necrotic focus; lungs were swollen and congestive. Histopathologic examination showed that cardiac muscle fiber were abound with inflammatory cell infiltrate; part of them broke, degenerated, and the heart appears typical myocarditis symptom; blood capillary of alveolar wall highly stretched and congested; Other tissues appeared various degree legions. The viruses (Picornaviridae-like morphous) were found in the cardiac muscle tissue homogenate from the suub-nosed monkey by transmission electron microscope after negative staining. The animal regression test showed that the viruses isolates could make mouse died and it showed the similar pathologic symptoms with the suub-nosed monkey. The reverse transcriptase polymerase chain reaction (RT-PCR) performed on an extract of cardiac muscle tissue revealed a DNA sequence specific for Coxsackievirus B. According to the clinical symptom, pathologic histology character and results of pathogen detection, we could conclude that the myocarditis caused by the viruses was the immediate cause of the suub-nosed monkey’s death.
The tissues homogenates with PBS were centrifuged and the supernatants were treated with 100 U/ml penicillin, 0.1 g/l streptomycin, and 1 mg/l Fungizone. After centrifugation, the supernatant was added to duplicate monolayers of African green monkey kidney cells (Vero), porcine kidney cells (PK-15), and baby hamster kidney cells (BHK-21) in cell culture flasks in an attempt to isolate viruses. Five blind passages were performed at 5-day intervals, the viruses was successfully isolated from cardiac muscle tissue homogenates of the died monkey following inoculation of Vero. The viruses’property consistented with CVB by morphology, physicochemistry test, animal regression test and RT-PCR. Analysis of VP1 partial gene sequence of virus and detecting of mice specific serum IgG by virus were performing, the results showed that the strain isolated was a coxsackievirus B3. It was the first CVB3 case discovered in Sichuan snbu-nosed monkey in world and The virus was designated provisionally Sichuan snub-nosed monkey-origin coxsackievirus B3 (SSM-CVB3). Selected paraffin sections were examined for the presence of SSM-CVB3 antigens by immunofluorescence using an anti-CVB3 rabbit antibody. The fluorescence was detected using confocal laser scanning microscopy. CVB3 was found in the endochylema of myocardial cells and in the glomerular capillary basement membrane and mesangial matrix. This result can confirm furtherly that the snub-nosed monkey were infected with SSM-CVB3.
Molecular cloning and sequencing of the genome of SSM-CVB3 were performed by special primers and 5’RACE kit and 3’RACE kit. From the poly (C) tract of the 5' non-translated region (NTR) to the 3' NTR, 7397 bp sequences of the whole genome were obtained by reverse transcription polymerase reaction (RT-PCR). The genome of SSM-CVB3 has been submitted to GenBank (access number: GU109481). The deduced amino acid sequences of the structural and nonstructural proteins of the SSM-CVB3 were analyzed for the sequence similarity among CVB3 strains. Comparison between SSM-CVB3 and other 12 strains indicates that overall the number of amino acids appears an amino acid deletion in VP2 region of capsid proteins, and corresponding amino acid sequences has changed from LGRTG to WSDW, and WSDW sequence can be think as a hereditary feature of SSM-CVB3. For another, the amino acid sequence AAKEFAGEPI in VP2 and RNKHFPVS in 2A can also be think as genetic mark of CVB3 that from China. There are high homology between SSM-CVB3 and CVB3F, CVB3B in 5’-NTR, and between SSM-CVB3 and CVB3G in 3’-NTR and coding region, thus, suggesting that SSM-CVB3 evolved with minor difference from domestic strains, and may be recombinate from CVB3G and CVB3F, CVB3B, but with major difference from the standard strains CVB3N (Nancy-CVB3). Molecular studies suggest that the agent of Sichuan snub-nosed monkey is a highly variant novel CVB3.
Inoculate the SSM-CVB3 in healthy macaques by peritoneal injection, observe the pathogenicity to macaque. The macaque show hige body temperature, temple lack of activity, blood urine and albuminuria from 2 days post-inoculation. No other clinical symptoms were observed. Total white blood cells and neutrophil in blood decreased in some days post-inoculation. The myocardial enzyme, liver duty enzyme, kidney duty enzyme, amylopsin and blood sugar in serum were detected, the results showed that CK, CK-MB, ALT and AMY had different extent changing characteristic, but CRE and BUN no obviously change. Macaques were mercy killed and the representative tissues were divided into two portions: one was fixed in 10% neutral buffered formalin solution and processed for histology and immunofluorescence staining, and the other was stored at -80℃. Microscopically, the main lesion were mild extensive infiltration of lymphocytes in the heart, cells productive reaction in the Kiernan's space of liver, relatively severe infiltration of lymphocytes in the interstitial substance of kidney, and nerves cell degeneration, necrosis, and neuronophagia in the spinal cord and brain. Congestion, hyperaemia and oedema were found in most tissues, which indicated macaque infected with the SSM-CVB3 Strain can cause most organ damage. For most tissues, CVB3 antigens were detected by RT-PCR. Especially for the kidney, spleen, lung and liver of the monkey, CVB3 antigens in the cytoplasm of infected cells could be detected by immunofluorescence with a specific anti-CVB3 rabbit hyperimmune serum.
In this study, the dead snub-nosed monkey infected with CVB3 were final diagnosis, the molecular characteristics of SSM-CVB3 were analysis systematically, and pathopoiesis were studied to macaque infected with SSM-CVB3 according to clinical pathology and pathologic histology. These results not only can provide the reference for the diagnosis and prevention and cure of snub-nosed monkey disease in clinic, know the genetic background and germline evolution relation of CVB3 in China, but also settle the grounding for further construct animal model of macaque infected with SSM-CVB3, it is very significant for the comparative medicine.
The snub-nosed monkey, or golden monkey, is one of the most endangered primate species due to its dramatically shrinking distribution during the past 400 years. Populations of the snub-nosed monkey are found mainly in three isolated regions in China: Qinglin, Sichuan/Gansu, and Shennongjia. There are three species of snub-nosed monkey found in China, including the Sichuan snub-nosed monkey (Rhinopithecus roxellanae), the Yunnan snub-nosed monkey (Rhinopithecus bieti) and the Guizhou snub-nosed monkey (Rhinopithecus brelichi). There is also one species of snub-nosed monkey (Rhinopithecus avunculus) found in Vietnam. The snub-nosed monkey species are all under first-class state protection in China, and the International Union for Natural Conservation (IUCN) has formally recognized them as vulnerable or endangered species. Because of these designations, snub-nosed monkeys have drawn a lot of attention from various conservation efforts. In recent years, the population of the Sichuan snub-nosed monkey has increased by more than 10,000 because of improvement in the conditions of some nature conservation areas and also by artificial propagation. However, many diseases that threaten the snub-nosed monkey have developed because of multitude of factors. There are reports that Sichuan snub-nosed monkeys have died from septicemia due to infection with pneumoniae Diplococcus or Escherichia coli and Klebsiella, from acute pyelonephritis attributed to infected with Escherichia coli and Proteus mirabilis, from unspecified parenchymatous hepatitis, and from unspecified myocarditis. In addition, Staphylococcus aureus can cause spontaneous abortion or stillbirth in the snub-nosed monkey. Since 2001, five Sichuan snub-nosed monkeys had been living in the zoological garden in Changchun in the Jilin province of China. Four of them died between 2003 and 2004. The causes of death were unknown, but they all showed the homoplastic clinical symptoms on lack of activity and shortness of breath before death, if they had cardiac failure, no more evidence were acquired. The final monkey of the original five, a five-year-old female, died on September 18, 2005. She had been in good health but exhibited reduced activity and showed evidence of shortness breath after movement during the previous day. No dizziness or syncope was observed. The hind limbs were slightly edematous. She had been treated using several drugs, but with no effect. No other information about her was available. In order to ascertain the cause of death of the suub-nosed monkey, and the pathogenicity and molecular characteristics of its etiological agent,systematical experiments were done in this study.
we dissected the died Sichuan snub-nosed monkey by the common practice and recorded its pathological changes, and then made manufacture pathological section. Pathology of the organs of the suub-nosed monkey appeared septicaemia. Cardiac pericardium, epicardium, and endocardium appeared bleeding point and ecchymosis; cardiac muscle appears white necrotic focus; lungs were swollen and congestive. Histopathologic examination showed that cardiac muscle fiber were abound with inflammatory cell infiltrate; part of them broke, degenerated, and the heart appears typical myocarditis symptom; blood capillary of alveolar wall highly stretched and congested; Other tissues appeared various degree legions. The viruses (Picornaviridae-like morphous) were found in the cardiac muscle tissue homogenate from the suub-nosed monkey by transmission electron microscope after negative staining. The animal regression test showed that the viruses isolates could make mouse died and it showed the similar pathologic symptoms with the suub-nosed monkey. The reverse transcriptase polymerase chain reaction (RT-PCR) performed on an extract of cardiac muscle tissue revealed a DNA sequence specific for Coxsackievirus B. According to the clinical symptom, pathologic histology character and results of pathogen detection, we could conclude that the myocarditis caused by the viruses was the immediate cause of the suub-nosed monkey’s death.
The tissues homogenates with PBS were centrifuged and the supernatants were treated with 100 U/ml penicillin, 0.1 g/l streptomycin, and 1 mg/l Fungizone. After centrifugation, the supernatant was added to duplicate monolayers of African green monkey kidney cells (Vero), porcine kidney cells (PK-15), and baby hamster kidney cells (BHK-21) in cell culture flasks in an attempt to isolate viruses. Five blind passages were performed at 5-day intervals, the viruses was successfully isolated from cardiac muscle tissue homogenates of the died monkey following inoculation of Vero. The viruses’property consistented with CVB by morphology, physicochemistry test, animal regression test and RT-PCR. Analysis of VP1 partial gene sequence of virus and detecting of mice specific serum IgG by virus were performing, the results showed that the strain isolated was a coxsackievirus B3. It was the first CVB3 case discovered in Sichuan snbu-nosed monkey in world and The virus was designated provisionally Sichuan snub-nosed monkey-origin coxsackievirus B3 (SSM-CVB3). Selected paraffin sections were examined for the presence of SSM-CVB3 antigens by immunofluorescence using an anti-CVB3 rabbit antibody. The fluorescence was detected using confocal laser scanning microscopy. CVB3 was found in the endochylema of myocardial cells and in the glomerular capillary basement membrane and mesangial matrix. This result can confirm furtherly that the snub-nosed monkey were infected with SSM-CVB3.
Molecular cloning and sequencing of the genome of SSM-CVB3 were performed by special primers and 5’RACE kit and 3’RACE kit. From the poly (C) tract of the 5' non-translated region (NTR) to the 3' NTR, 7397 bp sequences of the whole genome were obtained by reverse transcription polymerase reaction (RT-PCR). The genome of SSM-CVB3 has been submitted to GenBank (access number: GU109481). The deduced amino acid sequences of the structural and nonstructural proteins of the SSM-CVB3 were analyzed for the sequence similarity among CVB3 strains. Comparison between SSM-CVB3 and other 12 strains indicates that overall the number of amino acids appears an amino acid deletion in VP2 region of capsid proteins, and corresponding amino acid sequences has changed from LGRTG to WSDW, and WSDW sequence can be think as a hereditary feature of SSM-CVB3. For another, the amino acid sequence AAKEFAGEPI in VP2 and RNKHFPVS in 2A can also be think as genetic mark of CVB3 that from China. There are high homology between SSM-CVB3 and CVB3F, CVB3B in 5’-NTR, and between SSM-CVB3 and CVB3G in 3’-NTR and coding region, thus, suggesting that SSM-CVB3 evolved with minor difference from domestic strains, and may be recombinate from CVB3G and CVB3F, CVB3B, but with major difference from the standard strains CVB3N (Nancy-CVB3). Molecular studies suggest that the agent of Sichuan snub-nosed monkey is a highly variant novel CVB3.
Inoculate the SSM-CVB3 in healthy macaques by peritoneal injection, observe the pathogenicity to macaque. The macaque show hige body temperature, temple lack of activity, blood urine and albuminuria from 2 days post-inoculation. No other clinical symptoms were observed. Total white blood cells and neutrophil in blood decreased in some days post-inoculation. The myocardial enzyme, liver duty enzyme, kidney duty enzyme, amylopsin and blood sugar in serum were detected, the results showed that CK, CK-MB, ALT and AMY had different extent changing characteristic, but CRE and BUN no obviously change. Macaques were mercy killed and the representative tissues were divided into two portions: one was fixed in 10% neutral buffered formalin solution and processed for histology and immunofluorescence staining, and the other was stored at -80℃. Microscopically, the main lesion were mild extensive infiltration of lymphocytes in the heart, cells productive reaction in the Kiernan's space of liver, relatively severe infiltration of lymphocytes in the interstitial substance of kidney, and nerves cell degeneration, necrosis, and neuronophagia in the spinal cord and brain. Congestion, hyperaemia and oedema were found in most tissues, which indicated macaque infected with the SSM-CVB3 Strain can cause most organ damage. For most tissues, CVB3 antigens were detected by RT-PCR. Especially for the kidney, spleen, lung and liver of the monkey, CVB3 antigens in the cytoplasm of infected cells could be detected by immunofluorescence with a specific anti-CVB3 rabbit hyperimmune serum.
In this study, the dead snub-nosed monkey infected with CVB3 were final diagnosis, the molecular characteristics of SSM-CVB3 were analysis systematically, and pathopoiesis were studied to macaque infected with SSM-CVB3 according to clinical pathology and pathologic histology. These results not only can provide the reference for the diagnosis and prevention and cure of snub-nosed monkey disease in clinic, know the genetic background and germline evolution relation of CVB3 in China, but also settle the grounding for further construct animal model of macaque infected with SSM-CVB3, it is very significant for the comparative medicine.
引文
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