Unité Génomique Virale et Vaccination, CNRS URA3015, Institut Pasteur, 28 rue du Dr Roux, 75015 Paris, France.
Viruses. 2011 May;3(5):586-612. doi: 10.3390/v3050586. Epub 2011 May 12.
Human immunodeficiency virus (HIV) infection is principally a mucosal disease and the gastrointestinal (GI) tract is the major site of HIV replication. Loss of CD4+ T cells and systemic immune hyperactivation are the hallmarks of HIV infection. The end of acute infection is associated with the emergence of specific CD4+ and CD8+ T cell responses and the establishment of a chronic phase of infection. Abnormal levels of immune activation and inflammation persist despite a low steady state level of viremia. Although the causes of persistent immune hyperactivation remain incompletely characterized, physiological alterations of gastrointestinal tract probably play a major role. Failure to restore Th17 cells in gut-associated lymphoid tissues (GALT) might impair the recovery of the gut mucosal barrier. This review discusses recent advances on understanding the contribution of CD4+ T cell depletion to HIV pathogenesis.
人类免疫缺陷病毒(HIV)感染主要是一种黏膜疾病,胃肠道(GI)是 HIV 复制的主要部位。CD4+T 细胞的丧失和全身免疫过度激活是 HIV 感染的标志。急性感染的结束与特定的 CD4+和 CD8+T 细胞反应的出现以及感染的慢性阶段的建立有关。尽管病毒血症处于低稳定状态,但免疫激活和炎症的异常水平仍然持续存在。尽管持续性免疫过度激活的原因仍不完全清楚,但胃肠道的生理改变可能起主要作用。未能在肠道相关淋巴组织(GALT)中恢复 Th17 细胞可能会损害肠道黏膜屏障的恢复。这篇综述讨论了理解 CD4+T 细胞耗竭对 HIV 发病机制的贡献的最新进展。