Critical role for CD4+ T cells in controlling retrovirus replication and spread in persistently infected mice
Critical role for CD4+ T cells in controlling retrovirus replication and spread in persistently infected mice
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DOI：
10.1128/jvi.72.8.6559-6564.1998
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发表时间：
1998-08-01
影响因子：
5.4
通讯作者：
Dittmer, U
中科院分区：
文献类型：
--
作者：
Hasenkrug, KJ;Brooks, DM;Dittmer, U
持续性病毒感染的再激活在免疫功能低下的癌症、移植和艾滋病患者中构成了一个重大的医学问题，但人们对持续性病毒感染是如何被免疫控制的知之甚少。在这里，我们描述了一种小鼠模型，用于研究免疫反应在控制持续性逆转录病毒感染中的作用。我们证明，从急性Friend病毒感染中恢复后，少数B细胞逃避免疫破坏并携带持续的病毒。持续感染小鼠体内T细胞亚群的耗竭揭示了CD4（+）T细胞在控制病毒复制、向红细胞系扩散和诱导红白血病中的关键作用。CD4（+）T细胞效应不依赖于CD8（+）T细胞，在某些情况下也不依赖于病毒中和抗体应答。因此，CD4（+）T细胞可能具有直接的抗病毒作用。这些结果可能与人类免疫缺陷病毒（HIV）感染有关，其中CD4（+）T细胞的丢失与HIV复制增加、持续病毒的重新激活以及病毒相关癌症的高发病率有关。
Reactivations of persistent viral infections pose a significant medical problem in immunocompromised cancer, transplant, and AIDS patients, yet little is known about how persistent viral infections are immunologically controlled. Here we describe a mouse model for investigating the role of the immune response in controlling a persistent retroviral infection. We demonstrate that, following recovery from acute Friend virus infection, a small number of B cells evade immunological destruction and harbor persistent virus. In vivo depletions of T-cell subsets in persistently infected mice revealed a critical role for CD4(+) T cells in controlling virus replication,spread to the erythroid lineage, and induction of erythroleukemia, The CD4(+) T-cell effect was independent of CD8(+) T cells and in some cases was also independent of virus-neutralizing antibody responses. Thus, the CD4(+) T cells may have had a direct antiviral effect. These results may have relevance for human immunodeficiency virus (HIV) infections where loss of CD4(+) T cells is associated,vith an increase in HIV replication, reactivation of persistent viruses, and a high incidence of virus-associated cancers.