An early event in the herpes simplex virus type-2 replication cycle is sufficient to induce Chlamydia trachomatis persistence
An early event in the herpes simplex virus type-2 replication cycle is sufficient to induce Chlamydia trachomatis persistence
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DOI：
10.1111/j.1462-5822.2006.00823.x
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发表时间：
2007-03-01
影响因子：
3.4
通讯作者：
Schoborg, Robert V.
中科院分区：
文献类型：
--
作者：
Deka, Srilekha;Vanover, Jennifer;Schoborg, Robert V.
流行病学研究表明，单纯疱疹病毒2型(HSV-2)和沙眼衣原体的混合感染在体内发生。来自沙眼衣原体/HSV-2混合感染的组织培养模型的数据表明，病毒混合感染刺激持续衣原体的形成。透射电子显微镜分析表明，在HeLa和HEC-1B细胞中，混合感染导致发育中的衣原体呈现肿胀的、形状不规则的网状小体(RBS)，这是持续观察到的特征。此外，HSV-2混合感染抑制了两种宿主细胞中感染性衣原体基本体(EBS)的产生。单纯疱疹病毒1型(HSV-1)与单纯疱疹病毒(HSV-1)混合感染可引起相似的形态改变，并抑制感染性EB的产生。这些数据表明，病毒诱导的衣原体持久性既不是宿主细胞特异性的，也不是病毒株特异性的。对HSV-2粗提物的纯化表明，病毒颗粒是发生混合感染诱导的衣原体持久性所必需的。最后，在环己胺存在的情况下，与紫外线灭活的、复制不能的病毒或复制能力强的HSV-2病毒混合感染，在不改变衣原体基因组DNA积累的情况下，降低了衣原体的感染性。这些数据表明，高效的病毒复制不是诱导衣原体持续存在所必需的，并表明HSV的附着和进入可以提供必要的刺激来改变沙眼衣原体的发育。
Epidemiological studies have demonstrated that co-infections of herpes simplex virus type 2 (HSV-2) and Chlamydia trachomatis occur in vivo. Data from a tissue culture model of C. trachomatis/HSV-2 co-infection indicate that viral co-infection stimulates the formation of persistent chlamydiae. Transmission electron microscopic (TEM) analyses demonstrated that in both HeLa and HEC-1B cells, co-infection caused developing chlamydiae to exhibit swollen, aberrantly shaped reticulate bodies (RBs), characteristically observed in persistence. Additionally, HSV-2 co-infection suppressed production of infectious chlamydial elementary bodies (EBs) in both host cell types. Co-infection with HSV type 1 (HSV-1) produced similar morphologic alterations and abrogated infectious EB production. These data indicate that virus-induced chlamydial persistence was neither host cell- nor virus strain-specific. Purification of crude HSV-2 stocks demonstrated that viral particles were required for coinfection-induced chlamydial persistence to occur. Finally, co-infection with either UV-inactivated, replication-incompetent virus or replication-competent HSV-2 in the presence of cyclohexamide reduced chlamydial infectivity without altering chlamydial genomic DNA accumulation. These data demonstrate that productive viral replication is not required for the induction of chlamydial persistence and suggest that HSV attachment and entry can provide the necessary stimulus to alter C. trachomatis development.