Eriksson K, McInnes E, Ryan S, Tonks P, McConnell I, Blacklaws B
Department of Clinical Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, CB3 OES, United Kingdom.
Virology. 1999 Jun 5;258(2):355-64. doi: 10.1006/viro.1999.9711.
The role of CD4(+) lymphocytes in the establishment of lentivirus infection in macrophages has been studied in an in vivo system of lentivirus infection where CD4(+) lymphocytes are not the targets for infection. Using the non-T-cell-tropic lentivirus, maedi-visna virus (MVV), in CD4-depleted sheep, we have found that CD4(+) T cells were required for MVV infection in macrophages but not dendritic cells. CD4-depleted sheep had significantly lower levels of MVV-infected cells in lymph nodes and efferent lymph after MVV challenge in the drainage area of the lymph node. Due to the absence of virus in combination with the lack of CD4(+) T helper cells, virus-specific immune responses were reduced. There was delayed induction of cytotoxic T cell precursors, a marked reduction in virus-specific in vitro proliferative responses, and a delay in the appearance of MVV-specific antibodies. By contrast, CD4 depletion had no effect on the establishment of MVV infection in afferent lymph dendritic cells migrating from the skin infection site to the lymph node.
在慢病毒感染的体内系统中，研究了CD4(+)淋巴细胞在巨噬细胞中建立慢病毒感染的作用，在该系统中CD4(+)淋巴细胞不是感染靶标。利用非T细胞嗜性慢病毒梅迪-维斯纳病毒（MVV），在CD4细胞耗竭的绵羊中，我们发现巨噬细胞中MVV感染需要CD4(+) T细胞，但树突状细胞则不需要。在淋巴结引流区域用MVV攻击后，CD4细胞耗竭的绵羊在淋巴结和输出淋巴中MVV感染细胞水平显著降低。由于缺乏病毒并伴有CD4(+) T辅助细胞的缺失，病毒特异性免疫反应减弱。细胞毒性T细胞前体的诱导延迟，病毒特异性体外增殖反应显著降低，MVV特异性抗体出现延迟。相比之下，CD4细胞耗竭对从皮肤感染部位迁移至淋巴结的输入淋巴树突状细胞中MVV感染的建立没有影响。
