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为了解禽白血病病毒在广西鸡群中流行情况,采用DF-1细胞接种、细胞培养上清p27抗原检测、PCR扩增,对临床血管瘤型禽白血病的三黄鸡病料进行了病毒分离,并对分离病毒gp85基因进行测序和序列比较。结果表明,从1只病鸡同时分离到了一株A亚群禽白血病病毒(ALV-A)与一株J亚群禽白血病病毒(ALV-J),分别命名为HG01-A株和HG01-J株。ALV-A gp85与7株A亚群氨基酸同源性为85.8%~87.5%,与A亚群美国株MQNCSU同源性最高为87.5%,与A亚群原型株RSA同源性为86.9%。而ALV-J gp85与7株毒株核酸序列同源性为84.0%~93.8%,与广东株XX2-08以及四川株SCSM01同源性最高为93.8%,与英国原型株HPRS103同源性为90.2%。进化分析进一步表明,HG01-A与各参考株亲缘关系较远,HG01-J与SCSM01亲缘关系最近。本研究首次从同一只广西三黄鸡中同时分离到ALV-A及ALV-J,进一步完善了我国地方品种鸡群中禽白血病的流行病学信息。 相似文献
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从山东省某海兰褐鸡场祖代、父母代种鸡和商品代蛋鸡中获得疑似血管瘤型禽白血病(Avian leukosis,AL)病料.采用病理剖检、IFA、分子生物学检测,确定为J亚群禽白血病.从祖代、父母代病料中各分离到1株J亚群禽白血病病毒(J subgroup of avian leukosis virus,ALV-J),从商品代蛋鸡中分离到4株ALV-J.根据原型毒株HPRS103设计1对gp85基因引物,获得gp85基因序列.获得的gp85基因序列与各亚群参考毒株序列核苷酸同源性比对,结果显示:分离自商品代蛋鸡的Commercial03株、Commercial04株、Commercial06株和父母代分离株Parent02株位于同一分支,同源性在97.2％～97.9％,与HPRS103株同源性94.7％～95.2％;Commercial05株与祖代分离株Grandparent01株在同一分支,与HPRS103株同源性为98.3％,4株分离自商品代的ALV-J同源性为95.0％～99.9％.表明商品代蛋鸡中的ALV-J可能来自父母代或祖代种鸡的垂直传播,也可能来自于其他来源的水平传播.从同一鸡场祖代、父母代及商品代鸡中分离得到ALV-J,这在我国还是首次.对后续研究其基因突变、致瘤机制等奠定了良好的基础. 相似文献
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不同地区海兰褐蛋鸡中J亚群-禽白血病病毒株gp85基因的分子演化分析 总被引：1，自引：0，他引：1
本研究通过对不同地区海兰褐蛋鸡群中分离的5株J亚群-禽白血病病毒(ALV-J)的囊膜糖蛋白基因(gp85)进行同源性分析,阐述了不同海兰褐鸡群中存在的ALV-J的分子演化规律。对2008-2009年分别从北京、陕西、山东泰安、济阳、曲阜等不同地区饲养的海兰褐鸡分离到的5株ALV-J,用PCR方法克隆gp85基因、测序,并与国内外已发表的14株ALV-Jgp85基因进行同源性比较。结果表明,5株ALV-J与来自白羽肉鸡的HPRS-103株的同源性最近,平均为96.6%(96.4%～96.8%);与来自国内海兰灰蛋鸡的SD07LK1株的同源性平均仅为89.6%(89.3%～89.9%);而5株ALV-J间的同源性高达98.1%以上(98.1%～100%)。本研究发现,不同地区的海兰褐蛋鸡中广泛存在的ALV-J可能有一个共同的来源,即国外的白羽肉鸡。 相似文献
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2018年以来,某进口品种肉种鸡发生疑似禽白血病病例,流行范围广,危害严重,为确定该次疫情的病原,本研究从辽宁、山东等地发病鸡场采集55份疑似禽白血病病料样品。病理组织切片观察显示,病料样品肝脏和脾脏均有髓细胞样肿瘤细胞增生。针对禽白血病病毒(ALV)、鸡马立克氏病病毒(MDV)和网状内皮组织增生症病毒(REV)的特异性PCR检测结果显示,55份病料样品中ALV阳性样品12份(21.8%),MDV阳性样品1份(1.82%),REV均为阴性。将12份ALV阳性病料样品经处理后接种DF-1细胞进行病毒分离,ELISA检测结果显示有8份ALV群特异性抗原阳性。ALV多重PCR检测结果表明,8个分离株均为J亚群ALV(ALV-J),测序结果显示,8个分离株之间核苷酸序列同源性为99.5%~100%,与A、B、C、D、E亚群ALV的同源性仅为56.5%~58.8%,与ALV-J的同源性为90.7%~96.6%,进一步表明所有分离株均为ALV-J。上述结果表明,引起该次进口白羽父母代肉种鸡发生禽白血病的病原主要以ALV-J为主,该研究结果为疫情的溯源和有效防控奠定了基础。 相似文献
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817肉杂鸡肉瘤组织分离出A、J亚型禽白血病病毒 总被引：5，自引：1，他引：4
山东某地饲养的36日龄817肉杂鸡生长迟缓并发生颈部肉瘤。取肉瘤组织上清液接种CEF,培养12d,用IFA试验进行病毒鉴定。检测结果表明,从该肉瘤组织分离到A亚型与J亚型禽白血病病毒(ALV-A、ALV-J),命名为SD1005株。取肉瘤组织上清液人工感染817肉杂鸡与SPF鸡进行动物回归试验,结果复制出同样肉瘤。用复制出的新鲜肉瘤分别制备肉瘤细胞与肉瘤组织触片,IFA试验再次验证出ALV-A与ALV-J均为阳性,而且发现ALV-A与ALV-J分别共感染同一个组织细胞。同时,通过PCR方法用针对ALV-A、ALV-J的2对引物扩增并鉴定出肉瘤组织中含有ALV-A、ALV-J。对扩增的ALV-J囊膜糖蛋白(env)基因1 710bp片段进行的遗传变异分析结果显示,SD1005株与14株国内外参考株之间的同源性为88.5%～94.0%,其中与来自白羽肉鸡的美国参考株0661(AF247566)、ADOL-Hc1(AF097731)的同源性最高,分别为94.0%、93.8%。本研究显示,来自817肉杂鸡的肉瘤组织上清液接种鸡可诱发急性肉瘤,其中既检出ALV-A,又检出ALV-J,但急性肉瘤由单个病毒诱发还是与共感染... 相似文献
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山东不同品系蛋鸡禽白血病流行病学调查 总被引：4，自引：1，他引：3
为了解山东不同品系蛋鸡白血病流行情况,作者采集了山东各地区主要引进品系及地方品种鸡的血清3882份、棉拭子2428份和疑似病例41例,对采集样品分别进行了血清学、病理学及病原学检测.结果表明:包括祖代鸡在内的各品系蛋鸡群P27抗原阳性率为19.36%;ALV-A/B亚型抗体阳性率9.29%、ALV-J亚型抗体阳性率5.18%、REV抗体阳性率13.77%;发病鸡群主要是商品鸡群和父母代鸡群,海兰褐祖代鸡群也有发病;病理学诊断证明肿瘤类型主要为髓细胞瘤(27/41)、血管瘤或血管内皮细胞瘤(7/41)、纤维肉瘤(2/41)、平滑肌肉瘤(2/41)及马立克氏病(5/41);PCR检测结果显示,41份病料中有33份为ALV-J阳性(80.49%);22份为MDV阳性(53.66%);两者共感染率高达43.9%;从疑似病例分离到的17株ALV-J病毒gp85基因的同源性为94.0%～100%,与ALV-J原型株HPRS-103 gp85基因同源性为94.3%～98.7%;与其它已发表的分离毒株ALV-J gp85基因的同源性较低(84.4%～96.8%).调查结果表明,目前山东各品系蛋鸡群均存在ALV感染,其中以ALV-J为主,ALV-A和ALV-B同时存在,且存在与MDV、REV的混合感染,病鸡主要表现髓细胞瘤和血管瘤. 相似文献
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为分析我国J亚群禽白血病病毒(ALV-J)蛋鸡分离株的进化关系,本研究将山东省某鸡场采集的蛋鸡病料样品接种DF-1细胞系,利用ELISA群特异性抗原检测以及亚群特异性间接免疫荧光方法,分离鉴定得到一株ALV-J,命名为SD1009,并对其进行全基因组测序,将该序列与其他ALV-J代表性病毒株序列进行比较。结果表明:SD1009分离株的gag和pol基因相对保守,与各参考病毒株的同源性为95%～99%,env基因的同源性为91%～95%;在其5'UTR中出现了连续19 bp的插入突变,与TW-3577、SDAU09C3、JS09GY6、JS09GY3蛋鸡分离株的5'UTR基本一致,提示19 bp的插入现象可能是近年来蛋鸡ALV-J的进化趋势;此外,其3'UTR的rTM和DR区出现部分缺失现象,该缺失部分也可能与ALV-J进化相关。 相似文献
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<正>1病原学临床表现为腺胃炎的病例,其病原学非常复杂,因分离到的病原难以复制出临床典型病例,故真正病原尚未定论。我国学者朱国强等从江苏腺胃肿大的病鸡中分离到H95病毒,认为与传染性支气管炎病毒有密切的血清学关系;王玉东等从患腺胃肿大病鸡中分离到冠状病毒,认为是传染性支气管炎病毒(IBV)的变异株。 相似文献
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为研究引起我国部分地区进口白羽肉种鸡发生禽白血病疫情的病毒来源及其变异趋势,本研究对从进口白羽肉种鸡分离的8株J亚群禽白血病病毒(ALV-J)的全基因组序列进行测序分析。8株ALV-Jgp85氨基酸遗传演化分析显示,其与ALV-J肉鸡分离株(包括ALV-J原型病毒株HPRS-103、美国肉鸡ALV-J分离株、国内肉鸡分离株)及蛋鸡分离株氨基酸序列同源性均低于92.5%,而与国内2014年父母代白羽肉种鸡ALV-J分离株GD14J2同源性较高,为93.5%~95.1%,处于同一分支。8株ALV-J的3'非编码区(3'UTR)在rTM区缺失203bp,DR-1区缺失7bp,E元件位置缺失125bp,仅保留了22个碱基,这一缺失特征与GD14J2一致。8株ALV-J的3'LTRU3区序列与ALV-J肉鸡分离株及蛋鸡分离株的相应基因序列同源性均低于91.5%,而与GD14J2病毒株的同源性较高,为94.3%~96.3%。序列分析发现U3区存在连续11bp缺失和164位碱基突变(C/T),该突变形成2个新的转录调控元件AIBREP1、AIBREP2。综合gp85、3'UTR和U3区序列特征,推测引起本次进口白羽肉种鸡禽白血病的ALV-J与国内2014年父母代白羽肉种鸡ALV-J分离株GD14J2为同一来源。但本次分离到的ALV-J病毒株也有新的变异趋势,这些变异是否与ALV-J致病性相关,还需进一步研究。本研究为ALV-J有效防控和净化提供数据支持。 相似文献
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Response of white leghorn chickens of various genetic lines to infection with avian leukosis virus subgroup J 总被引：2，自引：0，他引：2
In Experiment 1, chickens from various white leghorn experimental lines were inoculated with strain ADOL-Hcl of subgroup J avian leukosis virus (ALV-J) either as embryos or at 1 day of age. At various ages, chickens were tested for ALV-J induced viremia, antibody, and packed cell volume (PCV). Also, at 4 and 10 wk of age, bursal tissues were examined for avian leukosis virus (ALV)-induced preneoplastic lesions with the methyl green-pyronine (MGP) stain. In Experiment 2, chickens harboring or lacking endogenous virus 21 (EV21) were inoculated with strain ADOL-Hcl of ALV-J at hatch. All embryo-inoculated chickens in Experiment 1 tested positive for ALV-J and lacked antibody throughout the experimental period of 30 wk and were considered viremic tolerant, regardless of line of chickens. By 10 wk of age, the incidence of ALV-J viremia in chickens inoculated with virus at hatch varied from 0 (line 0 chickens) to 97% (line 1515); no influence of ALV-J infection was noted on PCV. Results from microscopic examination of MGP-stained bursal tissues indicate that ALV-J can induce typical ALV-induced transformation in bursal follicles of white leghorn chickens. Lymphoid leukosis and hemangiomas were the most common ALV-J-induced tumors noted in chickens in Experiment 1. At termination of Experiment 2 (31 wk of age), 54% of chickens harboring EV21 were viremic tolerant compared with 5% of chickens lacking EV21 after inoculation with ALV-J at hatch. The data indicate that genetic differences among lines of white leghorn chickens, including the presence or absence of EV21, can influence response of chickens to infection with ALV-J. 相似文献
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Several subgroup J-like avian leukosis viruses (ALV-Js) were isolated from broiler breeder (BB) and commercial broiler flocks experiencing myeloid leukosis (ML) at 4 wk of age or older. In all cases, diagnosis of ML was based on the presence of typical gross and microscopic lesions in affected tissues. The isolates were classified as ALV-J by 1) their ability to propagate in chicken embryo fibroblasts (CEF) that are resistant to avian leukosis virus (ALV) subgroups A and E (C/AE) and 2) positive reaction in a polymerase chain reaction with primers specific for ALV-J. The prototype strain of these isolates, an isolate termed ADOL-Hc1, was obtained from an adult BB flock that had a history of ML. The ADOL-Hc1 was isolated and propagated on C/AE CEF and was distinct antigenically from ALV of subgroups A, B, C, D, and E, as determined by virus neutralization tests. Antibody to ADOL-Hc1 neutralized strain HPRS-103, the prototype of ALV-J isolated from meat-type chickens in the United Kingdom, but antibody to HPRS-103 did not neutralize strain ADOL-Hc1. On the basis of both viremia and antibody, prevalence of ALV-J infection in affected flocks was as high as 87%. Viremia in day-old chicks of three different hatches from a BB flock naturally infected with ALV-J varied from 4% to 25%; in two of the three hatches, 100% of chicks that tested negative for virus at hatch had evidence of viremia by 8 wk of age. The data document the isolation of ALV-J from meat-type chickens experiencing ML as young as 4 wk of age. The data also suggest that strain ADOL-Hc1 is antigenically related, but not identical, to strain HPRS-103 and that contact transmission of ALV-J is efficient and can lead to tolerant infection. 相似文献
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从安徽省的黄羽肉鸡和罗曼蛋鸡中各分离鉴定出1株J亚群禽白血病病毒,克隆获得了2条相应的gp85基因序列,并与参考毒株进行序列比对。结果表明,两分离毒株与J亚群参考毒株同源性为82.1%~99.4%,分离毒株之间同源性为85.4%。其中肉鸡分离毒株与J亚群原型毒株HPRS-103同源性为97.1%,与J亚群国内毒株SD09TA04、SDYC02J同源性均为99.4%;蛋鸡分离毒株与HPRS-103的同源性为89.0%,与SD09TA04和SDYC02J同源性仅为88.6%。两分离毒株的gp85氨基酸序列出现突变和缺失,在高变区hr1、hr2变异明显。进化分析进一步表明,2个分离毒株亲缘关系较远,可能来源于不同的原始病毒株。 相似文献
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In Experiment 1, a monoclonal antibody against the envelope glycoprotein (gp85) of subgroup J avian leukosis virus (ALV-J) was used to study the distribution of ALV-J in various tissues of White Leghorn chickens inoculated as embryos with the strain ADOL-Hcl of ALV-J. At 2 and 6 wk of age, various tissues from infected and control uninfected chickens were tested for the presence of ALV-J gp85 by immunohistochemistry. In Experiment 2, using the methyl green-pyronine (MGP) stain, sections of bursa of Fabricius (BF) from chickens of line 15I5 x 7(1), inoculated with ALV-J or Rous-associated virus-1 (RAV-1), a subgroup A ALV, at hatch were examined for transformation of bursal follicles at 4 and 10 wk of age. In Experiment 1, specific staining indicative of the presence of ALV-J gp85 was noted at both 2 and 6 wk of age in the adrenal gland, bursa, gonads, heart, kidney, liver, bone marrow, nerve, pancreas, proventriculus, spleen, and thymus. In Experiment 2, by 10 wk of age, transformed bursal follicles were detected in MGP-stained sections of BF in only one of five (20%) chickens inoculated with ALV-J at hatch, compared with five of five (100%) chickens inoculated with RAV-1. The data demonstrate distribution of ALV-J gp85 in various tissues of White Leghorn chickens experimentally inoculated as embryos with the virus. The data also confirm our previous observation that ALV-J is capable of inducing transformation of bursal follicles, albeit the incidence is less frequent than that induced by subgroup A ALV. 相似文献
15.
从J亚群禽白血病肿瘤中检测出禽网状内皮组织增生症病毒 总被引：35，自引：4，他引：35
将表现为典型 J亚群禽白血病肿瘤的病料分别接种于鸡胚成纤维细胞和 DF1细胞 ,采用间接荧光抗体试验(IFA)和 PCR方法 ,从这些肿瘤病料中分离和鉴定出 8株 J亚群禽白血病病毒 (AL V- J)。对证明感染了 AL V- J的细胞继续培养 ,并用禽网状内皮组织增生症病毒 (REV)的特异性单抗及引物做 IFA和 PCR,在 8株 AL V- J中 ,有 3株AL V- J的感染细胞中同时有 REV感染。由此表明 ,发生肿瘤的肉鸡中 ,AL V- J和 REV的共感染已相当普遍。将这 3株 REV- SD0 0 0 3、SD0 0 0 4和 SD0 10 2的 3′- L TR用 PCR扩增、克隆和序列比较 ,发现分离的 SD0 0 0 3、SD0 0 0 4和SD0 10 2与国内的另外 2株 REV- SD990 1和 HA990 1的同源性为 96 .7%和 96 .1% ;而与另 1株 REV参考株鸭脾坏死性病毒 (SNV)的同源性高达 99%。 相似文献
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Feather pulp from experimentally infected chickens was used as a source of DNA for polymerase chain reaction (PCR) amplification of avian leukosis virus subgroup J (ALV-J) proviral DNA. A primer set that produces a large amplicon (approximately 2,125) was used to detect ALV-J proviral DNA. This primer set was used in lieu of previously published primers because it allows for sequencing of the entire envelope gene and because it was able to detect diagnostically a number of North American ALV-J isolates that could not be detected with previously published primers and PCR conditions. ALV-J proviral DNA was detected in feather pulp at 7 days of age in more than 90% of birds infected as embryos and 7 days postinoculation in over 50% of chickens infected at 3 days of age. The results obtained with PCR on feather pulp were compared with those of virus isolation. In the embryo-inoculated birds, the percentages of agreement between PCR and virus isolation were 92.5% at 7 days of age and 100% at 28, 42, 49, and 56 days of age. However, the overall sensitivity of virus isolation in embryo-infected birds was higher, particularly at 7 and 56 days of age. In chickens inoculated at 3 days of age, the percentages of agreement of detection between PCR and virus isolation ranged from 75% at 10 days of age to 100% at 42 days of age. Agreement of negative results of ALV-J detection by PCR and virus isolation in chickens infected posthatch ranged between 66.6% and 100% between the ages of 10 and 42 days. Virus isolation requires chicken embryo fibroblasts of specific genetic lines, and the process takes onaverage 7-9 days. Aseptic collection of blood and tissues for virus isolation and molecular detection of ALV-J requires sterile necropsy instruments as well as syringes and needles for each individual chicken, whereas sterile microcentrifuge tubes and gloves are the only equipment necessary for aseptic feather pulp collection for ALV-J detection by PCR. PCR-based detection of ALV-J in feather pulp is especially suitable when ALV-J infection must be diagnosed rapidly and unequivocally without killing the chicken(s) and in situations where crucial reagents or suitable virus propagation substrates are not readily available for isolation and propagation of ALV-J in cell culture. 相似文献
17.
Infection of broiler chickens with subgroup J avian leukosis virus (ALV) results in the induction of myeloid tumors. However, although egg-type chickens are susceptible to infection with ALV-J, the tumor incidence is very low, and on rare occasions the tumors observed are of the myeloid lineage. We recently described the isolation of an ALV (AF115-4) from commercial egg-type chickens suffering from myeloid leukosis. AF115-4 was initially identified as an ALV-J isolate based on PCR analysis of the long terminal repeat (LTR). However, further characterization of the viral envelope indicated that the virus is recombinant with subgroups B envelope and J LTR. Here we further characterize this recombinant virus at both the molecular and biological levels. We show that the AF115-4 isolate expresses a recombinant envelope glycoprotein encoded by a subgroup B gp85 region and a subgroup E gp37 region. The host range ofAF115-4 was analyzed using cells resistant to infection by subgroups A/B, J, or E; this shows that no ALV-J was present in the isolates obtained from the affected chickens. Additional antigenic characterization of AF115-4 using chicken sera specific for subgroups B or J indicated that no ALV-J was present in the samples examined. Inoculation of AF 115-4 into ALV-susceptible 1515 X 71 chickens resulted in the induction of lymphoid leukosis but not the expected myeloid leukosis affecting the commercial chickens. These results suggest that differences in the genetic makeup of the chickens from which AF115-4 was isolated and the line 1515 X 71 used in the present experiments may be responsible for the observed differences in pathogenicity. In addition, the results suggest that ALV-J continues to evolve by recombination, generating new viruses with different pathological properties. 相似文献
18.
Qi Wang Yulong GaoXiaolin Ji Xiaole QiLiting Qin Honglei GaoYongqiang Wang Xiaomei Wang 《Veterinary microbiology》2013
Avian leukosis virus subgroup J (ALV-J) has become pandemic and induced serious clinical outbreaks in chickens in China. In particular, ALV-J induced various clinical tumors in infected chickens, which caused enormous economic losses to poultry. In this study, an infectious clone from an epidemic ALV-J Chinese isolate designated HLJ09SH01 was constructed and rescued. The rescued virus (named rHLJ09SH01) was inoculated into specific-pathogen-free (SPF) layer chickens, and infected chickens were observed for 238 days to explore the oncogenicity of rHLJ09SH01. As a result, 57.9% of rHLJ09SH01-infected chickens produced tumors. Accumulating evidence shows that microRNAs (miRNAs) have a close relationship with tumorigenesis. To gain more insight into the tumorigenesis of ALV-J, a miRNA microarray was performed as part of an investigation of changes in host miRNA expression in a liver tumor from ALV-J infected chickens. The results showed that four miRNAs were significantly differentially expressed; these data were verified using real-time PCR. Bioinformatics analysis showed the differentially expressed miRNAs to be involved in some tumorigenesis-related signaling pathways, such as the MAPK signaling pathway and the Wnt signaling pathway, which may represent a possible signaling pathway that was involved in the ALV-J-induced tumorigenesis. 相似文献
19.
White leghorn chickens from seven 15.B congenic lines (genetically similar except for genes linked to the major histocompatibility complex [MHC] B haplotype) and two Line 0.B semicongenic lines were infected at hatch with strain ADOL Hc-1 of subgroup J avian leukosis virus (ALV-J). At 5, 8, 16, and 36 wk of age, chickens were tested for viremia, serum-neutralizing antibody, and cloacal shedding. Chickens were also monitored for development of neoplasia. In the 15.B congenic lines (B*2, B*5, B*12, B*13, B*15, B*19, and B*21) there were no significant differences in the incidence of viremia between B haplotypes. In fact, infection at hatch in all of the 15.B congenic lines induced tolerance to ALV-J because 100% of these chickens were viremic and transient circulating serum-neutralizing antibody was detected in only a few chickens throughout the 36 wk experiment. However, at 16 wk of age more B*15 chickens had antibody and fewer B*15 chickens shed virus than did the 16-wk-old B*2, B*5, or B*13 chickens. Moreover, compared with B*15 chickens, a higher percentage of B*13 chickens consistently shed virus from 8 wk postinfection to termination at 36 wk postinfection. The B haplotype had a transient effect on viral clearance in Line 0.B semicongenics, as more B*13 than B*21 chickens remained viremic through 5 wk of age. Very few (0%-18%) of the Line 0.B semicongenic chickens shed virus. By 36 wk of age, all Line 0 B*13 and B*21 chickens produced serum-neutralizing antibodies and cleared the virus. These results show that following ALV-J infection at hatch the immune response is influenced transiently by the B haplotype and strongly by the line of chicken. Although this study was not designed to study the effect of endogenous virus on ALV-J infection, the data suggest that endogenous virus expression reduced immunity to ALV-J in Line 15I5, compared with Line 0, a line known to lack endogenous virus genes. 相似文献