Trichomonas vaginalis-induced epithelial monolayer disruption and human immunodeficiency virus type 1 (HIV-1) replication:: Implications for the sexual transmission of HIV-1
Trichomonas vaginalis-induced epithelial monolayer disruption and human immunodeficiency virus type 1 (HIV-1) replication:: Implications for the sexual transmission of HIV-1
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DOI：
10.1128/iai.73.7.4155-4160.2005
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发表时间：
2005-07-01
影响因子：
3.1
通讯作者：
Dezzutti, CS
中科院分区：
文献类型：
--
作者：
Guenthner, PC;Secor, WE;Dezzutti, CS
本研究的目的是评估阴道毛滴虫参与人类免疫缺陷病毒1型（HIV-1）传播的潜在机制。原代宫颈和前列腺上皮细胞或细胞系与T。通过监测经皮电阻来测量迷走神经。T.对HIV-1通过极化上皮细胞单层的阴道分离株进行了基底侧上清液中HIV-1 p24（gag）的评价。与T.迷走神经分离物诱导单层完整性的破坏，并导致病毒通过单层的基底外侧。此外，有分离株的变异性，其中两个分离株诱导更大的单层损伤和增加HIV-1的传代比其他两个分离株。T.用急性HIV-1感染的外周血单个核细胞培养的迷走神经分离物增强了HIV-1的复制。这种增强与细胞增殖和活化以及肿瘤坏死因子α的产生有关。与单层细胞破坏相反，T.迷走神经刺激对HIV-1复制的抑制作用不依赖于分离株。因此，已经确定了两种机制，可能有助于滴虫病与HIV-1性传播的流行病学关联。(i)T.迷走神经破坏泌尿生殖道上皮单层可促进HIV-1进入下层。(ii)T.在感染性HIV-1的情况下进行迷走神经刺激可能导致病毒复制增加。总的来说，这些数据表明，在T。在妇女和男子中，特别是在艾滋病毒-1高流行率的国家，
The objective of this study was to evaluate potential mechanisms of Trichomonas vaginalis involvement in human immunodeficiency virus type 1 (HIV-1) transmission. Polarized monolayer integrity of primary cervical and prostate epithelial cells or cell lines cultured with T. vaginalis was measured by monitoring transepithelium resistance. The effect of T. vaginalis isolates on HIV-1 passage through polarized epithelial cell monolayers was evaluated for HIV-1 p24(gag) in the basolateral supernatants. Coincubation with T. vaginalis isolates induced disruption of monolayer integrity and resulted in passage of virus to the basolateral side of the monolayer. Furthermore, there was isolate variability in which two isolates induced greater monolayer damage and increased HIV-1 passage than did the other two isolates. Coincubation of T. vaginalis isolates with acutely HIV-1-infected peripheral blood mononuclear cells enhanced HIV-1 replication. This enhancement was associated with cellular proliferation and activation, as well as with tumor necrosis factor alpha production. In contrast to the monolayer disruption, the effect of T. vaginalis on HIV-1 replication was not isolate dependent. Thus, two mechanisms have been identified that could contribute to the epidemiologic association of trichomoniasis with the sexual transmission of HIV-1. (i) T. vaginalis disruption of urogenital epithelial monolayers could facilitate passage of HIV-1 to underlying layers. (ii) Activation of local immune cells by T. vaginalis in the presence of infectious HIV-1 might lead to increased viral replication. Collectively, these data suggest the need for more vigilant efforts in the diagnosis and treatment of T. vaginalis in women and men, especially in countries with a high prevalence of HIV-1.