Haase Ashley T
Department of Microbiology, Medical School, University of Minnesota, MMC 196, 420 Delaware Street South East, Minneapolis, Minnesota 55455, USA.
Nat Rev Immunol. 2005 Oct;5(10):783-92. doi: 10.1038/nri1706.
HIV-1 and simian immunodeficiency virus (SIV), as well as their hosts, face perils at mucosal front lines in early infection. At these sites, 'resting' CD4+ memory T cells fuel infection (because they are hosts for virus), depleting CD4+ memory T cells throughout the lymphoid tissues, particularly in the gut, and eliciting an immunosuppressive regulatory T-cell response that impairs host defence. But HIV-1 and SIV also risk elimination at the earliest stage of infection, at the mucosal point of entry, if founder populations of infected cells do not expand sufficiently to establish a self-propagating infection. Microbicides and vaccines could increase these viral vulnerabilities at mucosal front lines.
人类免疫缺陷病毒1型（HIV-1）和猴免疫缺陷病毒（SIV）以及它们的宿主在感染初期的黏膜前沿面临着危险。在这些部位，“静止”的CD4+记忆T细胞助长感染（因为它们是病毒的宿主），耗尽整个淋巴组织中的CD4+记忆T细胞，尤其是在肠道中，并引发损害宿主防御的免疫抑制性调节性T细胞反应。但是，如果受感染细胞的起始群体没有充分扩增以建立自我传播的感染，HIV-1和SIV在感染的最早阶段，即在黏膜进入点，也有被清除的风险。杀微生物剂和疫苗可能会增加这些病毒在黏膜前沿的脆弱性。
