HIV and SIV infection: the role of cellular restriction and immune responses in viral replication and pathogenesis.
HIV and SIV infection: the role of cellular restriction and immune responses in viral replication and pathogenesis.
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DOI：
10.1111/j.1600-0463.2009.02450.x
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发表时间：
2009-05
期刊：
影响因子：
--
通讯作者：
Burdo TH
中科院分区：
文献类型：
--
作者：
Williams KC;Burdo TH
人类免疫缺陷病毒（HIV）和猿猴免疫缺陷病毒（SIV）具有悠久的生物学历史。这两种病毒都是从非洲进化而来的，它们的变种可以在几个物种的“化石记录”中找到，而这些物种不是地方性的。SIV在非洲的几种猴子中仍然是地方性的，在那里它不会引起免疫缺陷。HIV和SIV在人类和亚洲非人灵长类动物中积极复制，尽管有细胞和遗传病毒限制因素和基因，有时也有强大的先天性和适应性免疫反应。虽然慢病毒被认为是“慢病毒”，但在人类和易感的亚洲猴中很明显，病毒产生是快速和高活性的，导致感染后早期CD 4+记忆效应T细胞的大量损失，以及病毒进化、细胞毒性淋巴细胞和中和抗体应答失败之间的持续竞争。同时，HIV和SIV可以感染血液中的单核细胞/巨噬细胞群体，更重要的是在包括中枢神经系统在内的组织中，病毒可以保持隔离并且不能被抗逆转录病毒治疗清除，并且隐藏多年。本文将讨论物种和细胞感染的障碍，先天性和获得性免疫的作用与感染和发病机制的艾滋病毒和SIV在选择物种。
The human immune deficiency (HIV) and simian immune deficiency (SIV) viruses have long biological history. Both viruses evolved from Africa and reminants of them can be found in the “fossil record” of several species in which they are not endemic. SIV remains endemic in several species of monkeys in Africa where it does not cause immune deficiency. HIV and SIV actively replicate within humans and Asian non-human primates, despite cellular and genetic viral restriction factors and genes, and at times robust innate and adaptive immune responses. While Lentivirus are considered “slow viruses” it is clear in humans and susceptible Asian monkeys that virus production is rapid and highly active resulting in a massive loss of CD4+ memory effector T cells early after infection and a continued race between viral evolution, cytotoxic lymphocytes, and failed neutralizing antibody responses. Concurrently, HIV and SIV can infect monocyte/macrophage populations in blood and more importantly in tissues, including the central nervous system, where the virus can remain sequestered and not cleared by antiretroviral therapy, and hide for years. This review will discuss species and cellular barriers to infection, and the role of innate and acquired immunity with infection and pathogenesis of HIV and SIV in select species.
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