Ferrari Guido, Pollara Justin, Tomaras Georgia D, Haynes Barton F
Departments of Surgery.
Molecular Genetics and Microbiology and.
J Infect Dis. 2017 Mar 15;215(suppl_3):S152-S159. doi: 10.1093/infdis/jiw555.
Human immunodeficiency virus (HIV) type 1 uses the CD4 molecule as its principal receptor to infect T cells. HIV-1 integrates its viral genome into the host cell, leading to persistent infection wherein HIV-1 can remain transcriptionally silent in latently infected CD4+ T cells. On reactivation of replication-competent provirus, HIV-1 envelope glycoproteins (Env) are expressed and accumulate on the cell surface, allowing infected cells to be detected and targeted by endogenous immune responses or immune interventions. HIV-1 Env-specific antibodies have the potential to bind HIV-1 cell surface Env and promote elimination of infected CD4+ T cells by recruiting cytotoxic effector cells, such as natural killer cells, monocytes, and polymorphonuclear cells. Harnessing humoral and innate cellular responses has become one focus of research to develop innovative strategies to recruit and redirect cytotoxic effector cells to eliminate the HIV-1 latently infected CD4+ T-cell reservoir.
1型人类免疫缺陷病毒（HIV）利用CD4分子作为其主要受体来感染T细胞。HIV-1将其病毒基因组整合到宿主细胞中，导致持续性感染，其中HIV-1在潜伏感染的CD4+ T细胞中可保持转录沉默。在具有复制能力的前病毒重新激活时，HIV-1包膜糖蛋白（Env）表达并积聚在细胞表面，使受感染细胞能够被内源性免疫反应或免疫干预检测到并成为靶标。HIV-1 Env特异性抗体有可能结合HIV-1细胞表面的Env，并通过招募细胞毒性效应细胞（如自然杀伤细胞、单核细胞和多形核细胞）来促进清除受感染的CD4+ T细胞。利用体液和先天性细胞反应已成为开发创新策略的研究重点之一，这些策略旨在招募并重新引导细胞毒性效应细胞以消除HIV-1潜伏感染的CD4+ T细胞库。
