HIV-1逃避免疫反应和抗逆转录病毒药物的机制。

Mechanisms of HIV-1 escape from immune responses and antiretroviral drugs.

作者信息

Bailey Justin, Blankson Joel N, Wind-Rotolo Megan, Siliciano Robert F

机构信息

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21204, USA.

出版信息

Curr Opin Immunol. 2004 Aug;16(4):470-6. doi: 10.1016/j.coi.2004.05.005.

DOI:10.1016/j.coi.2004.05.005

PMID:15245741

Abstract

Despite the fact that HIV-1 induces vigorous antiviral immune responses, viral replication is never completely controlled in infected individuals. Recent studies have provided insight into the mechanisms by which focused immune pressure directed at particular B or T cell epitopes leads to the rapid appearance of escape mutations. Even if anti-HIV-1 immune responses could be enhanced to the point where they inhibit viral replication to the same extent as certain combinations of antiretroviral drugs, eradication would be unlikely because of the persistence of the virus in an extremely stable latent reservoir in resting memory CD4(+) T cells.

摘要

尽管人类免疫缺陷病毒1型（HIV-1）能引发强烈的抗病毒免疫反应，但在受感染个体中，病毒复制从未得到完全控制。最近的研究深入探讨了针对特定B或T细胞表位的集中免疫压力导致逃逸突变迅速出现的机制。即便抗HIV-1免疫反应能够增强到与某些抗逆转录病毒药物组合相同程度地抑制病毒复制，由于病毒在静息记忆CD4(+) T细胞中处于极其稳定的潜伏库中持续存在，根除病毒仍不太可能。