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单纯疱疹病毒诱导的人宫颈器官培养物上皮损伤和对人类免疫缺陷病毒 1 型感染的易感性。

Herpes simplex virus-induced epithelial damage and susceptibility to human immunodeficiency virus type 1 infection in human cervical organ culture.

机构信息

Department of Microbiology, University of Minnesota, Minneapolis, Minnesota, United States of America.

出版信息

PLoS One. 2011;6(7):e22638. doi: 10.1371/journal.pone.0022638. Epub 2011 Jul 27.

DOI:10.1371/journal.pone.0022638
PMID:21818356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3144918/
Abstract

Normal human premenopausal cervical tissue has been used to derive primary cell populations and to establish ex vivo organ culture systems to study infections with herpes simplex virus (HSV-1 or HSV-2) and human immunodeficiency virus type 1 (HIV-1). Infection with either HSV-1 or HSV-2 rapidly induced multinuclear giant cell formation and widespread damage in mucosal epithelial cells. Subsequent exposure of the damaged mucosal surfaces to HIV-1 revealed frequent co-localization of HSV and HIV-1 antigens. The short-term organ culture system provides direct experimental support for the epidemiological findings that pre-existing sexually transmitted infections, including primary and recurrent herpes virus infections at mucosal surfaces, represent major risk factors for acquisition of primary HIV-1 infection. Epithelial damage in combination with pre-existing inflammation, as described here for overtly normal human premenopausal cervix, creates a highly susceptible environment for the initiation and establishment of primary HIV-1 infection in the sub-mucosa of the cervical transformation zone.

摘要

正常的绝经前人类宫颈组织已被用于获得原代细胞群体,并建立离体器官培养系统,以研究单纯疱疹病毒(HSV-1 或 HSV-2)和人类免疫缺陷病毒 1 型(HIV-1)的感染。感染 HSV-1 或 HSV-2 会迅速诱导多核巨细胞形成,并广泛损伤黏膜上皮细胞。随后,将受损的黏膜表面暴露于 HIV-1 下,发现 HSV 和 HIV-1 抗原经常共定位。短期器官培养系统为流行病学发现提供了直接的实验支持,即包括原发性和复发性疱疹病毒感染在内的先前存在的性传播感染是获得原发性 HIV-1 感染的主要危险因素。上皮损伤结合这里所述的先前存在的炎症,在明显正常的绝经前人类宫颈中创造了一个高度易感的环境,用于在宫颈转化区的黏膜下层启动和建立原发性 HIV-1 感染。

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Herpes Simplex Virus Type 2 Infection-Induced Expression of CXCR3 Ligands Promotes CD4 T Cell Migration and Is Regulated by the Viral Immediate-Early Protein ICP4.单纯疱疹病毒 2 型感染诱导的 CXCR3 配体表达促进 CD4 T 细胞迁移,并受病毒即刻早期蛋白 ICP4 调控。
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