Jarvis Gary A, Chang Theresa L
Center for Immunochemistry, Veterans Affairs Medical Center, San Francisco, CA 94121, USA.
Curr HIV Res. 2012 Apr;10(3):211-7. doi: 10.2174/157016212800618138.
Neisseria gonorrhoeae (GC), a major cause of pelvic inflammatory disease, can facilitate HIV transmission. In response to GC infection, genital epithelial cells can produce cytokines, chemokines and defensins to modulate HIV infection and infectivity. GC can also induce the production of cytokines and chemokines in monocytes and modulate T cell activation. In vivo, an increase in the number of endocervical CD4+ T cells has been found in GC-infected women. Additionally, GC appears to modulate HIV-specific immune responses in HIV-exposed sex workers. Interestingly, in vitro, GC exhibits HIV enhancing or inhibitory effects depending on the HIV target cells. This review summarizes molecular and immunological aspects of the modulation of HIV infection and transmission by GC. Future studies using a multi-cellular system or in animal models will offer insight into the mechanisms by which GC increases HIV transmission.
淋病奈瑟菌(GC)是盆腔炎性疾病的主要病因,可促进HIV传播。针对GC感染,生殖上皮细胞可产生细胞因子、趋化因子和防御素,以调节HIV感染和传染性。GC还可诱导单核细胞产生细胞因子和趋化因子,并调节T细胞活化。在体内,已发现GC感染女性的宫颈内CD4 + T细胞数量增加。此外,GC似乎可调节HIV暴露的性工作者体内的HIV特异性免疫反应。有趣的是,在体外,GC对HIV靶细胞表现出增强或抑制HIV的作用。本综述总结了GC对HIV感染和传播调节的分子和免疫学方面。未来使用多细胞系统或动物模型的研究将深入了解GC增加HIV传播的机制。