INSERM, U1016, Institut Cochin, Paris, France.
CNRS, UMR 8104, Paris, France.
Front Immunol. 2018 Mar 23;9:531. doi: 10.3389/fimmu.2018.00531. eCollection 2018.
Human immunodeficiency virus type 1 (HIV-1) infects and kills T cells, profoundly damaging the host-specific immune response. The virus also integrates into memory T cells and long-lived macrophages, establishing chronic infections. HIV-1 infection impairs the functions of macrophages both and , which contributes to the development of opportunistic diseases. Non-typhoidal serovar Typhimurium has been identified as the most common cause of bacterial bloodstream infections in HIV-infected adults. In this review, we report how the functions of macrophages are impaired post HIV infection; introduce what makes invasive Typhimurium specific for its pathogenesis; and finally, we discuss why these bacteria may be particularly adapted to the HIV-infected host.
人类免疫缺陷病毒 1 型(HIV-1)感染并杀死 T 细胞,严重破坏宿主特异性免疫反应。该病毒还整合到记忆 T 细胞和长寿巨噬细胞中,从而建立慢性感染。HIV-1 感染损害了 和 巨噬细胞的功能,这有助于机会性疾病的发展。非伤寒血清型鼠伤寒沙门氏菌已被确定为 HIV 感染成年人细菌性血流感染的最常见原因。在这篇综述中,我们报告了 HIV 感染后巨噬细胞功能如何受损;介绍了使侵袭性鼠伤寒沙门氏菌具有其发病机制特异性的因素;最后,我们讨论了为什么这些细菌可能特别适应 HIV 感染宿主。