Mays Jody K, Bacon Larry D, Pandiri Arun R, Fadly Aly M
U.S. Department of Agriculture, Agricultural Research Service, Avian Disease and Oncology Laboratory, 3606 East Mount Hope Road, East Lansing, MI 48823, USA.
Avian Dis. 2005 Jun;49(2):214-9. doi: 10.1637/7315-120104R.
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 (B2, B5, B12, B13, B15, B19, and B21) 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 B15 chickens had antibody and fewer B15 chickens shed virus than did the 16-wk-old B2, B5, or B13 chickens. Moreover, compared with B15 chickens, a higher percentage of B13 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 B13 than B21 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 B13 and B21 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.
来自7个15.B同基因系（除与主要组织相容性复合体[MHC]B单倍型相关的基因外，基因组成相似）和2个0.B半同基因系的白来航鸡在出壳时用J亚群禽白血病病毒（ALV-J）ADOL Hc-1株进行感染。在5、8、16和36周龄时，检测鸡的病毒血症、血清中和抗体及泄殖腔排毒情况。同时监测鸡肿瘤的发生情况。在15.B同基因系（B2、B5、B12、B13、B15、B19和B21）中，各B单倍型之间的病毒血症发生率无显著差异。实际上，所有15.B同基因系在出壳时感染均诱导了对ALV-J的耐受性，因为在整个36周的实验中，这些鸡100%出现病毒血症，仅少数鸡检测到短暂循环的血清中和抗体。然而，在16周龄时，与16周龄的B2、B5或B13鸡相比，更多的B15鸡产生了抗体，且更少的B15鸡排毒。此外，与B15鸡相比，从感染后8周直至感染后36周实验结束，持续排毒的B13鸡的比例更高。在0.B半同基因系中，B单倍型对病毒清除有短暂影响，因为至5周龄时，仍有病毒血症的B13鸡比B21鸡更多。0.B半同基因系的鸡很少（0%-18%）排毒。到36周龄时，所有0.B13和B21系的鸡均产生了血清中和抗体并清除了病毒。这些结果表明，出壳时感染ALV-J后，免疫反应受到B单倍型的短暂影响，并受到鸡品系的强烈影响。尽管本研究并非旨在研究内源性病毒对ALV-J感染的影响，但数据表明，与已知缺乏内源性病毒基因的0系相比，内源性病毒表达降低了15I5系对ALV-J的免疫力。
