A亚群禽白血病病毒单克隆抗体的制备和不同亚群禽白血病病毒共感染相互影响的研究
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摘要
禽白血病(Avian Leukosis)是由禽白血病病毒(Avian Leukosis Virus, ALV)和禽肉瘤病毒(Avian Sarcoma Virus,ASV)群中的病毒感染引起的多种肿瘤性疾病的统称。过去十几年,ALV-J亚群病毒对肉用型鸡、蛋用型鸡和我国地方品系鸡的感染已经给养殖业造成了巨大经济损失。由于中国在过去几十年中从未对ALV采取过有效的净化措施,中国鸡群中存在其它亚型ALV感染的可能性很大,近几年病毒分离鉴定也表明,血管瘤的发生不仅由J亚群禽白血病病毒引起,同时也有由A亚群禽白血病病毒(ALV-A)和B亚群禽白血病病毒(ALV-B)感染引起。为了更好、更快、更准确地进行病毒的分离、鉴定以及临床检测,探讨ALV-A和ALV-J共感染SPF鸡后抗体反应和带毒排毒的规律,本研究克隆与表达ALV-A-SDAU09C1毒株gp85蛋白,用纯化的gp85蛋白研制抗ALV-A单克隆抗体(Monoclonal antibody;McAb),进而研究了其与ALV-J共感染SPF鸡病毒血症和抗体反应相互影响。
1. ALV-A-SDAU09C1 gp85基因的克隆与表达
以感染本研究室分离保存的ALV-A-SDAU09C1(GenBank:HM452339)株的细胞基因组DNA为模板,采用PCR扩增技术,扩增出1017bp大小的env-gp85基因片段,并将其克隆到原核表达性载体pET-32a (+)中,构建成重组质粒pET-SDAU09C1-gp85。经测序鉴定结果显示,成功构建了重组质粒pET-SDAU09C1-gp85。将重组质粒转化到大肠杆菌BL21中培养并用IPTG诱导后,其菌体的超声波裂解物用SDS-PAGE电泳分离蛋白质,在经考马斯亮蓝染色的SDS-PAGE凝胶中与非重组载体pET-32a (+)的转化菌裂解物相比,重组质粒pET-SDAU09C1-gp85出现了1条相对分子量为53kD左右的条带,结果显示,env基因在大肠杆菌中进行了高效表达。Western-blot分析结果能从重组质粒pET-SDAU09C1-gp85的转化菌中特异性地识别出该53kD的蛋白条带,而与天然非重组载体pET-32a(+)的转化菌不发生反应。结果证明,能被gp85蛋白高免阳性血清识别的相对分子质量为53kD的蛋白质,确实为pET-SDAU09C1-gp85蛋白。
2. A亚群禽白血病病毒单克隆抗体的研制及其部分生物学特性的研究
2.1间接ELISA检测方法的建立
用纯化的gp85蛋白为包被抗原,建立了检测抗ALV-A抗体的间接ELISA。经对ELISA的最佳工作条件测定结果表明,抗原最佳包被浓度为2μg/ml、血清的最佳稀释度为1:1000,二抗的最佳稀释度为1:2000,最佳包被液为PBS Buffer(pH7.4),最佳显色时间为15min。经重复性试验、特异性试验结果显示,建立ELISA方法有良好的可重复性;与鸡NDV、REV、IBDV、MDV等病毒阳性抗体均无交叉反应。
2.2抗ALV-A单克隆抗体的制备及纯化表达的env-gp85蛋白经纯化复性后免疫8-10周龄Balb/c小白鼠,经2-3次免疫后,取小白鼠血清进行检测,当抗体效价超过105后,取小白鼠脾脏细胞与骨髓瘤细胞Sp2/0在PEG1450作用下进行细胞融合,经建立间接ELISA法进行检测筛选阳性杂交瘤细胞株,经有限稀释法亚克隆2-3次,共获得了3株(A6D1株,A5C1株,A4C8株)分泌抗ALV-A独特型抗体的杂交瘤细胞株,并进行了单抗腹水的大量制备,经过饱和硫酸铵沉淀,经过蛋G亲和纯化后得到的单克隆抗体浓度别为A6D1,1.575mg/ml;A5C1,0.903 mg/ml;A4C8,0.758 mg/ml。
2.3抗ALV-A单克隆抗体特性研究
2.3.1单抗的效价测定
用已经建立的ELISA方法对三株单抗的效价测定结果分别为:A6D1 210; A5C1 28;A4C8 27。
2.3.2抗体分泌稳定性
将获得的3株单克隆抗体细胞株冻存后,隔3、6、9、12个月后,复苏培养,至少传代3次以上,用建立的间接ELISA方法进行检测。结果表明,获得的单克隆抗体细胞株经冻存复苏后,抗体分泌能力没有任何下降,其具有较高的分泌抗体水平的能力。
2.3.3单抗的Western blotting分析
取10ul纯化的表达蛋白,用等量的2×上样缓冲液处理后,进行SDS-PAGE,然后转到NC膜上,经封闭,单抗200倍稀释液孵育后,加入酶标羊抗鼠IgG孵育后,加底物显色,于NC膜上出现一条清晰的条带,该带与标准分子量比较,其大小约为53kD,说明这株单抗与所表达的gp85蛋白发生特异性结合。
2.3.4间接免疫荧光分析
用IFA对试验所获得的A6D1、A5C1、A4C8株单克隆抗体的特异性进行了鉴定。结果证明,单抗A5C1、A4C8是特异性抗ALV-A的单克隆抗体,它们均与试验的所有ALV-A分离株发生反应,而不与试验的ALV-B和ALV-J亚群的毒株发生反应。值得注意的是单抗A6D1,它不仅能与所试验的ALV-A毒株发生反应,而且还能与所试验的ALV-B亚群的毒株发生反应,但不与ALV-J亚群的毒株发生反应,这说明单抗A5C1、A4C8是特异性抗ALV-A的单克隆抗体,而A6D1是特异性抗ALV-AB的单克隆抗体,3株单克隆抗体均能与病毒正常分泌的天然蛋白发生特异反应。
3. ALV-A与ALV-J共感染对SPF鸡病毒血症及抗体反应的相互影响
1日龄SPF鸡200只随机分成4组,平均每组50只。2日龄时,4个组每只鸡分别腹腔接种:第一组接种0.2ml ALV-A和ALV-J感染细胞培养上清混合液(比例1:1);第二组接种ALV-A0.2ml感染细胞培养上清;第三组接种ALV-J0.2ml感染细胞培养上清;第四组接种灭菌Hank’s液0.2ml作为阴性对照;常规程序进行免疫;攻毒后在1周龄、2周龄、3周龄、5周龄、7周龄、8周龄时从各组中分别随机取出6只鸡,编号。其中6只无菌采集加抗凝剂的新鲜血液用于病毒血症检测,其余鸡常规采血,分离血清供抗体检测;病毒血症的检测采用IFA法,同时用ELISA检测鸡群的抗体水平。
实验结果表明:
3.1病毒血症检测结果
单独感染ALV-A组的病毒血症水平从2周龄开始检测到,随后一直持续增高,从从第3周到第7周增长较缓慢,到第7周龄时的病毒血症水平达到最高为3.72 PFU/ml,第8周龄病毒血症水平有所下降为3.01 PFU/ml。单独感染ALV-J组的病毒血症水平从1周龄开始检测到,随后一直呈升高趋势,第8周龄时为3.71 PFU/ml;
ALV-A+ALV-J共感染组与单独感染ALV-A组相比,也在7周龄时达到最高,为3.74 PFU/ml;8周龄也有所下降,在7周龄以前病毒血症水平始终高于ALV-A组,但两组的病毒血症水平变化趋势大体相同,在整个实验过程中病毒血症水平总体差异不显著(p>0.05);
2周龄时ALV-A +ALV-J共感染组的病毒血症还未出现,与单独感染ALV-J组相比差异显著(P<0.05),随后病毒血症水平逐渐升高,直到7周龄时达到最高,8周龄时已有所降低;而单独感染ALV-J组在整个检测过程中病毒血症水平一直在升高,但
3周龄、5周龄、7周龄及8周龄的病毒血症水平与ALV-A +ALV-J共感染组相比差异不显著(p>0.05)。
3.2共感染对特异性抗体反应的影响
3.2.1 ALV-J共感染时对ALV-A特异性抗体的影响无论是ALV-A+ALV-J共感染组,还是单独感染ALV-A组在2周龄时血清中ALV-A特异性抗体的阳性率均为0;在3周龄时,ALV-A+ALV-J共感染组和单独感染ALV-A组中均只有部分鸡产生ALV-A特异性抗体,不过ALV-A+ALV-J共感染组ALV-A特异性抗体阳性率明显低于单独感染ALV-A组。而在5周龄、7周龄时,两组鸡中ALV-A特异性抗体阳性率基本相同,表明在本实验中ALV-J共感染对ALV-A感染诱发的抗体反应的影响不明显。
3.2.2 ALV-A共感染时对ALV-J特异性抗体的影响
在2周龄、3周龄时,ALV-A+ALV-J共感染组和单独感染ALV-J组中均没有出现ALV-J特异性抗体。在5周龄、7周龄时,ALV-A+ALV-J共感染组仍无阳性样品,单独感染ALV-J组的阳性率也仅为20.00%和13.33%。可见ALV-J特异性抗体较ALV-A特异性抗体产生得晚,在2日龄感染ALV-J后鸡群的耐受性感染程度比ALV-A更严重。特别是ALV-A+ALV-J共感染组,在8周龄之前一直未出现阳性样品,显然,ALV-A共感染显著减弱了鸡体对ALV-J感染诱导的特异性抗体反应。
3.2.3病毒血症及相应抗体反应的相关性
将被检测的不同鸡的病毒血症和抗体反应表现一一对应,ALV-A+ALV-J共感染组及单独感染ALV-A组在2周龄时没有出现病毒血症,抗体反应均为阴性;3周龄时ALV-A+ALV-J共感组1/6( 6.25%)和单独感染ALV-A组2/6(33.33%)都出现了部分鸡病毒血症和抗体反应均为阳性, ALV-A+ALV-J共感组5周时有4/6(50%)都出现了部分鸡病毒血症和抗体反应均为阳性,直到7周龄这种现象还持续存在;单独感染ALV-A组5周时有4/6(66.67%)都出现了部分鸡病毒血症和抗体反应均为阳性,到7周龄有所下降3/6(50%);
在ALV-A+ALV-J共感染组和单独感染ALV-J组的被检鸡只中病毒血症和抗体反应均为阳性的数量明显较少,仅见于ALV-J组中(5周龄为1/6(6.25%)和7周龄为2/6(33.33% )),可见ALV-J感染后鸡体血液当中ALV-J和相应抗体共同存在的几率很小,而ALV-A的共感染更降低了这种几率。
Avian leukosis is a variety of tumor diseases caused by avian leukosis virus and avian sarcoma virus. In last ten years, leukemia / hemangioma cases increased significantly in layers breeder industry again. avian leukemia become a serious disease,which does severely harm to layer industry in China. Isolation and identification of virus showed that the vascular tumors was causednot only by the subgroup J avian leukemia virusbut also by the subgroup A and B. In order to greatly enhance the diagnosis and treatment of clinical diseases, the monoclonal antibodies (Mabs) to ALV–A were prepared and characterization of monoclonal antibodies to subgroup A avian leukosis virus were tudied in this study. To understand the dynamics of viremia, virus shedding and antibody responses in chickens inoculated with ALV-A and ALV-J and provide essential epidemiological data for prevention and eradicationo of ALV-A and ALV-J infection.
1. Cloning and expression of gp85 gene of ALV-A-SDAU09C1
The env-gp85 gene of ALV-A-SDAU09C1(GenBank:HM452339)was amplified by PCR and then subcloned into the prokaryotic expressing vector pET32a and recombinant vector pET32a-SDAU09C1-gp85 was further transformed into Escherichia coli strain BL21 for expression under the induction of IPTG.. After IPTG induction, there was a new protein band about Mr 53kD on SDS-PAGE. Western blot analysis also showed that a protein band with a molecular weight of about 53 kD was detected. Then the protein were purified and stored.
2. Development and characterization of monoclonal antibodies to subgroup A avian leukosis virus
2.1 Establishment of the Indirect ELISA
An alternative indirect enzyme- linked immunosorbent assay (ELISA) for detection of ALV antibody was developed using a truncated envelop glycoprotein(env)-gp85 protein of ALV produced in Escherichia coli.The results show that the appropriate testing condition is as follows: 2μg/ml antigen used to coat ELISA plate with PBS Buffe(rpH7.4), 1:1000 of sera as detecting samples, The working concentration of HRP-labelled sheep antichicken IgG was 1:2000 and the reaction time was 10 min. Cross-reactivity assay showed that this assay was not cross-react with REV、NDV、IBDVet al, this demonstrated it has good specifity. It showed that the ELISA had good repeativity, high specifity and high sensitivity.
2.2 Development of monoclonal antibodies to subgroup A avian leukosis virus
Six adult female Balb/c mice, 8–10 weeks old, were subcutaneously injected with purified recombinant myocilinemulsified in a 1:1 ratio with complete Freund’s adjuvant. Two booster doses, again in 50% emulsion with Freund's incomplete adjuvant, were given at 2 weeks intervals. The mouse with the highest antibody titer tested by ELISA was boosted intraperitoneally with 100μg protein without adjuvant 3 days before the cell fusion. Feeder layer cells were prepared 1 day prior to fusion. Splenocytes from mice with the highest ELISA antibody titers were fused with murine myeloma cells Sp2/0 following standard procedures. Three strains (A6D1,A5C1,A4C8) were selected for subcloning. For the production of MAbs, BALB/c mice (4-6 weeks old) were injected intraperitoneally with 106 hybridoma cells per mouse. Ten days later, the ascitic fluid was further purified by using protein A agarose columns (Bio-Rad Laboratories). The concentration of three Mabs was : A6D1,1.575mg/ml;A5C1,0.903 mg/ml;A4C8,0.758 mg/ml. The purified ascitic fluids were used for further characterization.
2.3 Characterization of monoclonal antibodies to subgroup A avian leukosis virus
2.3.1 Titera of obtained McAbs
The titera of obtained McAbs from the mouse ascetic fluid were 210 (A6D1)、28 (A5C1)、27(A4C8), respectively, in indirect ELISA.
2.3.2 Antibody secreting stabilities of hybridoma cell strains
Three primary hybridoma cell strains secreting McAb were resuscitated and cloned. After the cloning positive ratereached 100%, the 3 strains were passaged for 3, 6,9,12 months, and the antibody secreting stabilities of them were monitored by indirect ELISA. The results showed that the property of three strains secreting McAb was stable after long culture and cry preservation.
2.3.3 Western blot analysis
The purified protein was analysed by means of SDS polyacrylamide gel electrophoresis (SDS PAGE) and followed by Western blotting. The purified protein with a band of molecular mass 53 kDa were got in SDS-PAGE, and it bind specifically to McAbs in Western-blot and ELISA assay. The Western blot analysis showed the 3 strains McAbs were all specific to ALV env gp 85 protein.
2.3.4 IFA analysis
Three strains of monoclonal antibodies (McAbs) against ALV-A were obtained by using hybridoma technique and their characteristics were studied by IFA . The results showed that three MAbs (A5C1 and A4C8) reacted with ALV-A but not with subgroups B, or J of ALV. MAb A6D1 reacted with subgroups A and B of ALV but not with ALV-J.
3. Dynamics of viremia and antibody responses in chickens Co-infected with ALV-A and ALV-J
In order to discuss the interference of viremia and antibody caused by avian leucosis virus of subgroup A(ALV-A) and avian leucosis virus of subgroup J(ALV-J), 200 SPF chickens are divided into 4 groups randomly at 1d: one is injected by 0.2ml cell culture supernatant of ALV-A(containing 103.01 TCID50 of 0.1ml infected cell culture supernatant), the other is ALV-J, the third is ALV-A+ALV-J and the fourth is Hank’s liquid as negative control at 2d separately; the chickens are immuned as usual; on 14d, 21d, 35d and 49d, 30 chickens are taken out from these groups and the serial numbers are given contemporarily. The fresh blood containing anticoagulant are collected without any bacterias from 6 of the 30 chickens to test the viremia; the other blood are collected in the normal way to test antibodies; the viremia are detected by IFA and the level of antibody are detected by ELISA.
3.1 Dynamics of viremia in chickens Co-infected with ALV-A and ALV-J
Viremia was detected from the 2nd week after inoculation with ALV-A at 2-day-old and was increasing gradually from the 3nd week to 7nd week; The viremia was 3.72 PFU/ml at 7-week-old(reach to peak and was decreased at 8week-old (3.01 PFU/ml);
Viremia was detected from the 1nd week after inoculation with ALV-A at 2-day-old and was increasing gradually from the 3nd week to 8nd week; The viremia was 3.71 PFU/ml at 8-week-old;
The coinfection of ALV-A can interfere the dynamic viremia level of ALV-J obviously(P<0.05)on 2w, but the coinfection of ALV-J can’t interfere the dynamic viremia level of ALV-A(P>0.05).
3.2 Dynamics of antibody responses in chickens Co-infected with ALV-J
3.2.1 Iinfluence of coinfection with ALV-J on antibody to ALV-A
The antibody is 0 in ALV-A group and ALV-A+ALV-J group on 2w; Only some chicken produced specific antibodies to ALV-A on 3w, the antibody positive rates of in ALV-A group was significantly lower than that in ALV-A+ALV-J group (P<0.05), increasing with age. The antibody positive rates of in ALV-A group and ALV-A+ALV-J group was basically the same on 5w and 7w. The results showed that coinfection with ALV-J has no significantly influence on ALV-A antibody produce.
3.2.2 Iinfluence of coinfection with ALV-A on antibody to ALV-J
The antibody positive rates of was 0 in ALV-J group and ALV-A+ALV-J group on 2w and 3w ; The antibody also was 0 ALV-A+ALV-J group on 5w and 7w; the antibody positive rates of in ALV-J group only was 20.00% on on 5w and 13.33% on 7w. The results showed that the emerge of antibody of ALV-J was inhibitated because of coinfection of ALV-A, although the coinfection of ALV-J don’t affect the emerge of antibody of ALV-A.
3.2.3 Interaction of Virema and Antibody in Chickens Coinfected with ALV-A and ALV-J
Compared the dynamic viremia level and the level of antibody at the same time, the rate of coexistance of ALV and its antibody positive rates of is 0 in ALV group and ALV-A+ALV-J group on 2w and there is coexistance of ALV and its antibody positive rates of in ALV-A(33.33%) group and ALV-A+ALV-J group on 3w ( 6.25%) ; the antibody positive rates of ALV-A +ALV-J group was 50.00% on 5w, this phenomena lasts until 7w; the antibody positive rates of ALV-A group was 66.67%% on 5w, and 50% on 7w.
The antibody in ALV-J group ALV-A +ALV-J group was 6.25% on 5w and 33.33% on 7w. The results showed that there isn’t coexistance of ALV-J and its antibody at all in the whole test processa nd the rate declines obviously after coinfected ALV-A .
1. ALV-A-SDAU09C1 gp85基因的克隆与表达
以感染本研究室分离保存的ALV-A-SDAU09C1(GenBank:HM452339)株的细胞基因组DNA为模板,采用PCR扩增技术,扩增出1017bp大小的env-gp85基因片段,并将其克隆到原核表达性载体pET-32a (+)中,构建成重组质粒pET-SDAU09C1-gp85。经测序鉴定结果显示,成功构建了重组质粒pET-SDAU09C1-gp85。将重组质粒转化到大肠杆菌BL21中培养并用IPTG诱导后,其菌体的超声波裂解物用SDS-PAGE电泳分离蛋白质,在经考马斯亮蓝染色的SDS-PAGE凝胶中与非重组载体pET-32a (+)的转化菌裂解物相比,重组质粒pET-SDAU09C1-gp85出现了1条相对分子量为53kD左右的条带,结果显示,env基因在大肠杆菌中进行了高效表达。Western-blot分析结果能从重组质粒pET-SDAU09C1-gp85的转化菌中特异性地识别出该53kD的蛋白条带,而与天然非重组载体pET-32a(+)的转化菌不发生反应。结果证明,能被gp85蛋白高免阳性血清识别的相对分子质量为53kD的蛋白质,确实为pET-SDAU09C1-gp85蛋白。
2. A亚群禽白血病病毒单克隆抗体的研制及其部分生物学特性的研究
2.1间接ELISA检测方法的建立
用纯化的gp85蛋白为包被抗原,建立了检测抗ALV-A抗体的间接ELISA。经对ELISA的最佳工作条件测定结果表明,抗原最佳包被浓度为2μg/ml、血清的最佳稀释度为1:1000,二抗的最佳稀释度为1:2000,最佳包被液为PBS Buffer(pH7.4),最佳显色时间为15min。经重复性试验、特异性试验结果显示,建立ELISA方法有良好的可重复性;与鸡NDV、REV、IBDV、MDV等病毒阳性抗体均无交叉反应。
2.2抗ALV-A单克隆抗体的制备及纯化表达的env-gp85蛋白经纯化复性后免疫8-10周龄Balb/c小白鼠,经2-3次免疫后,取小白鼠血清进行检测,当抗体效价超过105后,取小白鼠脾脏细胞与骨髓瘤细胞Sp2/0在PEG1450作用下进行细胞融合,经建立间接ELISA法进行检测筛选阳性杂交瘤细胞株,经有限稀释法亚克隆2-3次,共获得了3株(A6D1株,A5C1株,A4C8株)分泌抗ALV-A独特型抗体的杂交瘤细胞株,并进行了单抗腹水的大量制备,经过饱和硫酸铵沉淀,经过蛋G亲和纯化后得到的单克隆抗体浓度别为A6D1,1.575mg/ml;A5C1,0.903 mg/ml;A4C8,0.758 mg/ml。
2.3抗ALV-A单克隆抗体特性研究
2.3.1单抗的效价测定
用已经建立的ELISA方法对三株单抗的效价测定结果分别为:A6D1 210; A5C1 28;A4C8 27。
2.3.2抗体分泌稳定性
将获得的3株单克隆抗体细胞株冻存后,隔3、6、9、12个月后,复苏培养,至少传代3次以上,用建立的间接ELISA方法进行检测。结果表明,获得的单克隆抗体细胞株经冻存复苏后,抗体分泌能力没有任何下降,其具有较高的分泌抗体水平的能力。
2.3.3单抗的Western blotting分析
取10ul纯化的表达蛋白,用等量的2×上样缓冲液处理后,进行SDS-PAGE,然后转到NC膜上,经封闭,单抗200倍稀释液孵育后,加入酶标羊抗鼠IgG孵育后,加底物显色,于NC膜上出现一条清晰的条带,该带与标准分子量比较,其大小约为53kD,说明这株单抗与所表达的gp85蛋白发生特异性结合。
2.3.4间接免疫荧光分析
用IFA对试验所获得的A6D1、A5C1、A4C8株单克隆抗体的特异性进行了鉴定。结果证明,单抗A5C1、A4C8是特异性抗ALV-A的单克隆抗体,它们均与试验的所有ALV-A分离株发生反应,而不与试验的ALV-B和ALV-J亚群的毒株发生反应。值得注意的是单抗A6D1,它不仅能与所试验的ALV-A毒株发生反应,而且还能与所试验的ALV-B亚群的毒株发生反应,但不与ALV-J亚群的毒株发生反应,这说明单抗A5C1、A4C8是特异性抗ALV-A的单克隆抗体,而A6D1是特异性抗ALV-AB的单克隆抗体,3株单克隆抗体均能与病毒正常分泌的天然蛋白发生特异反应。
3. ALV-A与ALV-J共感染对SPF鸡病毒血症及抗体反应的相互影响
1日龄SPF鸡200只随机分成4组,平均每组50只。2日龄时,4个组每只鸡分别腹腔接种:第一组接种0.2ml ALV-A和ALV-J感染细胞培养上清混合液(比例1:1);第二组接种ALV-A0.2ml感染细胞培养上清;第三组接种ALV-J0.2ml感染细胞培养上清;第四组接种灭菌Hank’s液0.2ml作为阴性对照;常规程序进行免疫;攻毒后在1周龄、2周龄、3周龄、5周龄、7周龄、8周龄时从各组中分别随机取出6只鸡,编号。其中6只无菌采集加抗凝剂的新鲜血液用于病毒血症检测,其余鸡常规采血,分离血清供抗体检测;病毒血症的检测采用IFA法,同时用ELISA检测鸡群的抗体水平。
实验结果表明:
3.1病毒血症检测结果
单独感染ALV-A组的病毒血症水平从2周龄开始检测到,随后一直持续增高,从从第3周到第7周增长较缓慢,到第7周龄时的病毒血症水平达到最高为3.72 PFU/ml,第8周龄病毒血症水平有所下降为3.01 PFU/ml。单独感染ALV-J组的病毒血症水平从1周龄开始检测到,随后一直呈升高趋势,第8周龄时为3.71 PFU/ml;
ALV-A+ALV-J共感染组与单独感染ALV-A组相比,也在7周龄时达到最高,为3.74 PFU/ml;8周龄也有所下降,在7周龄以前病毒血症水平始终高于ALV-A组,但两组的病毒血症水平变化趋势大体相同,在整个实验过程中病毒血症水平总体差异不显著(p>0.05);
2周龄时ALV-A +ALV-J共感染组的病毒血症还未出现,与单独感染ALV-J组相比差异显著(P<0.05),随后病毒血症水平逐渐升高,直到7周龄时达到最高,8周龄时已有所降低;而单独感染ALV-J组在整个检测过程中病毒血症水平一直在升高,但
3周龄、5周龄、7周龄及8周龄的病毒血症水平与ALV-A +ALV-J共感染组相比差异不显著(p>0.05)。
3.2共感染对特异性抗体反应的影响
3.2.1 ALV-J共感染时对ALV-A特异性抗体的影响无论是ALV-A+ALV-J共感染组,还是单独感染ALV-A组在2周龄时血清中ALV-A特异性抗体的阳性率均为0;在3周龄时,ALV-A+ALV-J共感染组和单独感染ALV-A组中均只有部分鸡产生ALV-A特异性抗体,不过ALV-A+ALV-J共感染组ALV-A特异性抗体阳性率明显低于单独感染ALV-A组。而在5周龄、7周龄时,两组鸡中ALV-A特异性抗体阳性率基本相同,表明在本实验中ALV-J共感染对ALV-A感染诱发的抗体反应的影响不明显。
3.2.2 ALV-A共感染时对ALV-J特异性抗体的影响
在2周龄、3周龄时,ALV-A+ALV-J共感染组和单独感染ALV-J组中均没有出现ALV-J特异性抗体。在5周龄、7周龄时,ALV-A+ALV-J共感染组仍无阳性样品,单独感染ALV-J组的阳性率也仅为20.00%和13.33%。可见ALV-J特异性抗体较ALV-A特异性抗体产生得晚,在2日龄感染ALV-J后鸡群的耐受性感染程度比ALV-A更严重。特别是ALV-A+ALV-J共感染组,在8周龄之前一直未出现阳性样品,显然,ALV-A共感染显著减弱了鸡体对ALV-J感染诱导的特异性抗体反应。
3.2.3病毒血症及相应抗体反应的相关性
将被检测的不同鸡的病毒血症和抗体反应表现一一对应,ALV-A+ALV-J共感染组及单独感染ALV-A组在2周龄时没有出现病毒血症,抗体反应均为阴性;3周龄时ALV-A+ALV-J共感组1/6( 6.25%)和单独感染ALV-A组2/6(33.33%)都出现了部分鸡病毒血症和抗体反应均为阳性, ALV-A+ALV-J共感组5周时有4/6(50%)都出现了部分鸡病毒血症和抗体反应均为阳性,直到7周龄这种现象还持续存在;单独感染ALV-A组5周时有4/6(66.67%)都出现了部分鸡病毒血症和抗体反应均为阳性,到7周龄有所下降3/6(50%);
在ALV-A+ALV-J共感染组和单独感染ALV-J组的被检鸡只中病毒血症和抗体反应均为阳性的数量明显较少,仅见于ALV-J组中(5周龄为1/6(6.25%)和7周龄为2/6(33.33% )),可见ALV-J感染后鸡体血液当中ALV-J和相应抗体共同存在的几率很小,而ALV-A的共感染更降低了这种几率。
Avian leukosis is a variety of tumor diseases caused by avian leukosis virus and avian sarcoma virus. In last ten years, leukemia / hemangioma cases increased significantly in layers breeder industry again. avian leukemia become a serious disease,which does severely harm to layer industry in China. Isolation and identification of virus showed that the vascular tumors was causednot only by the subgroup J avian leukemia virusbut also by the subgroup A and B. In order to greatly enhance the diagnosis and treatment of clinical diseases, the monoclonal antibodies (Mabs) to ALV–A were prepared and characterization of monoclonal antibodies to subgroup A avian leukosis virus were tudied in this study. To understand the dynamics of viremia, virus shedding and antibody responses in chickens inoculated with ALV-A and ALV-J and provide essential epidemiological data for prevention and eradicationo of ALV-A and ALV-J infection.
1. Cloning and expression of gp85 gene of ALV-A-SDAU09C1
The env-gp85 gene of ALV-A-SDAU09C1(GenBank:HM452339)was amplified by PCR and then subcloned into the prokaryotic expressing vector pET32a and recombinant vector pET32a-SDAU09C1-gp85 was further transformed into Escherichia coli strain BL21 for expression under the induction of IPTG.. After IPTG induction, there was a new protein band about Mr 53kD on SDS-PAGE. Western blot analysis also showed that a protein band with a molecular weight of about 53 kD was detected. Then the protein were purified and stored.
2. Development and characterization of monoclonal antibodies to subgroup A avian leukosis virus
2.1 Establishment of the Indirect ELISA
An alternative indirect enzyme- linked immunosorbent assay (ELISA) for detection of ALV antibody was developed using a truncated envelop glycoprotein(env)-gp85 protein of ALV produced in Escherichia coli.The results show that the appropriate testing condition is as follows: 2μg/ml antigen used to coat ELISA plate with PBS Buffe(rpH7.4), 1:1000 of sera as detecting samples, The working concentration of HRP-labelled sheep antichicken IgG was 1:2000 and the reaction time was 10 min. Cross-reactivity assay showed that this assay was not cross-react with REV、NDV、IBDVet al, this demonstrated it has good specifity. It showed that the ELISA had good repeativity, high specifity and high sensitivity.
2.2 Development of monoclonal antibodies to subgroup A avian leukosis virus
Six adult female Balb/c mice, 8–10 weeks old, were subcutaneously injected with purified recombinant myocilinemulsified in a 1:1 ratio with complete Freund’s adjuvant. Two booster doses, again in 50% emulsion with Freund's incomplete adjuvant, were given at 2 weeks intervals. The mouse with the highest antibody titer tested by ELISA was boosted intraperitoneally with 100μg protein without adjuvant 3 days before the cell fusion. Feeder layer cells were prepared 1 day prior to fusion. Splenocytes from mice with the highest ELISA antibody titers were fused with murine myeloma cells Sp2/0 following standard procedures. Three strains (A6D1,A5C1,A4C8) were selected for subcloning. For the production of MAbs, BALB/c mice (4-6 weeks old) were injected intraperitoneally with 106 hybridoma cells per mouse. Ten days later, the ascitic fluid was further purified by using protein A agarose columns (Bio-Rad Laboratories). The concentration of three Mabs was : A6D1,1.575mg/ml;A5C1,0.903 mg/ml;A4C8,0.758 mg/ml. The purified ascitic fluids were used for further characterization.
2.3 Characterization of monoclonal antibodies to subgroup A avian leukosis virus
2.3.1 Titera of obtained McAbs
The titera of obtained McAbs from the mouse ascetic fluid were 210 (A6D1)、28 (A5C1)、27(A4C8), respectively, in indirect ELISA.
2.3.2 Antibody secreting stabilities of hybridoma cell strains
Three primary hybridoma cell strains secreting McAb were resuscitated and cloned. After the cloning positive ratereached 100%, the 3 strains were passaged for 3, 6,9,12 months, and the antibody secreting stabilities of them were monitored by indirect ELISA. The results showed that the property of three strains secreting McAb was stable after long culture and cry preservation.
2.3.3 Western blot analysis
The purified protein was analysed by means of SDS polyacrylamide gel electrophoresis (SDS PAGE) and followed by Western blotting. The purified protein with a band of molecular mass 53 kDa were got in SDS-PAGE, and it bind specifically to McAbs in Western-blot and ELISA assay. The Western blot analysis showed the 3 strains McAbs were all specific to ALV env gp 85 protein.
2.3.4 IFA analysis
Three strains of monoclonal antibodies (McAbs) against ALV-A were obtained by using hybridoma technique and their characteristics were studied by IFA . The results showed that three MAbs (A5C1 and A4C8) reacted with ALV-A but not with subgroups B, or J of ALV. MAb A6D1 reacted with subgroups A and B of ALV but not with ALV-J.
3. Dynamics of viremia and antibody responses in chickens Co-infected with ALV-A and ALV-J
In order to discuss the interference of viremia and antibody caused by avian leucosis virus of subgroup A(ALV-A) and avian leucosis virus of subgroup J(ALV-J), 200 SPF chickens are divided into 4 groups randomly at 1d: one is injected by 0.2ml cell culture supernatant of ALV-A(containing 103.01 TCID50 of 0.1ml infected cell culture supernatant), the other is ALV-J, the third is ALV-A+ALV-J and the fourth is Hank’s liquid as negative control at 2d separately; the chickens are immuned as usual; on 14d, 21d, 35d and 49d, 30 chickens are taken out from these groups and the serial numbers are given contemporarily. The fresh blood containing anticoagulant are collected without any bacterias from 6 of the 30 chickens to test the viremia; the other blood are collected in the normal way to test antibodies; the viremia are detected by IFA and the level of antibody are detected by ELISA.
3.1 Dynamics of viremia in chickens Co-infected with ALV-A and ALV-J
Viremia was detected from the 2nd week after inoculation with ALV-A at 2-day-old and was increasing gradually from the 3nd week to 7nd week; The viremia was 3.72 PFU/ml at 7-week-old(reach to peak and was decreased at 8week-old (3.01 PFU/ml);
Viremia was detected from the 1nd week after inoculation with ALV-A at 2-day-old and was increasing gradually from the 3nd week to 8nd week; The viremia was 3.71 PFU/ml at 8-week-old;
The coinfection of ALV-A can interfere the dynamic viremia level of ALV-J obviously(P<0.05)on 2w, but the coinfection of ALV-J can’t interfere the dynamic viremia level of ALV-A(P>0.05).
3.2 Dynamics of antibody responses in chickens Co-infected with ALV-J
3.2.1 Iinfluence of coinfection with ALV-J on antibody to ALV-A
The antibody is 0 in ALV-A group and ALV-A+ALV-J group on 2w; Only some chicken produced specific antibodies to ALV-A on 3w, the antibody positive rates of in ALV-A group was significantly lower than that in ALV-A+ALV-J group (P<0.05), increasing with age. The antibody positive rates of in ALV-A group and ALV-A+ALV-J group was basically the same on 5w and 7w. The results showed that coinfection with ALV-J has no significantly influence on ALV-A antibody produce.
3.2.2 Iinfluence of coinfection with ALV-A on antibody to ALV-J
The antibody positive rates of was 0 in ALV-J group and ALV-A+ALV-J group on 2w and 3w ; The antibody also was 0 ALV-A+ALV-J group on 5w and 7w; the antibody positive rates of in ALV-J group only was 20.00% on on 5w and 13.33% on 7w. The results showed that the emerge of antibody of ALV-J was inhibitated because of coinfection of ALV-A, although the coinfection of ALV-J don’t affect the emerge of antibody of ALV-A.
3.2.3 Interaction of Virema and Antibody in Chickens Coinfected with ALV-A and ALV-J
Compared the dynamic viremia level and the level of antibody at the same time, the rate of coexistance of ALV and its antibody positive rates of is 0 in ALV group and ALV-A+ALV-J group on 2w and there is coexistance of ALV and its antibody positive rates of in ALV-A(33.33%) group and ALV-A+ALV-J group on 3w ( 6.25%) ; the antibody positive rates of ALV-A +ALV-J group was 50.00% on 5w, this phenomena lasts until 7w; the antibody positive rates of ALV-A group was 66.67%% on 5w, and 50% on 7w.
The antibody in ALV-J group ALV-A +ALV-J group was 6.25% on 5w and 33.33% on 7w. The results showed that there isn’t coexistance of ALV-J and its antibody at all in the whole test processa nd the rate declines obviously after coinfected ALV-A .
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