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1型人类免疫缺陷病毒感染发病机制中的黏膜事件

Mucosal events in the pathogenesis of human immunodeficiency virus type 1 infection.

作者信息

Smith P D, Li L, Meng G

机构信息

Department of Medicine (Gastroenterology and Hepatology), University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA.

出版信息

J Infect Dis. 1999 May;179 Suppl 3:S436-40. doi: 10.1086/314812.

DOI:10.1086/314812
PMID:10099114
Abstract

The interaction between human immunodeficiency virus type 1 (HIV-1) and primary mucosal cells isolated from normal human small intestine was investigated. Purified primary intestinal epithelial cells could transport cell-free HIV-1 to mononuclear cells, although the epithelial cells did not support viral replication. An unexpected finding was that primary intestinal macrophages were markedly less permissive to HIV-1 than were blood monocytes. The reduced permissiveness appeared to be due to the near absence of surface CCR5 on resident intestinal macrophages. Surface CCR5 could be up-regulated on the monocytes but not the intestinal macrophages by HIV-1 and gp120. Impaired permissiveness of intestinal macrophages to HIV-1 may play an important role in the low prevalence of HIV-1 mRNA-expressing macrophages in the lamina propria during HIV-1 infection in vivo. Characterization of the biologic properties of HIV-1 transport and infection in primary mucosal cells will be key to elucidating the pivotal role of mucosal surfaces in HIV-1 disease.

摘要

研究了1型人类免疫缺陷病毒(HIV-1)与从正常人小肠分离的原代黏膜细胞之间的相互作用。纯化的原代肠上皮细胞可将无细胞的HIV-1转运至单核细胞,尽管上皮细胞不支持病毒复制。一个意外的发现是,原代肠巨噬细胞对HIV-1的易感性明显低于血液单核细胞。易感性降低似乎是由于驻留肠巨噬细胞表面几乎不存在CCR5。HIV-1和gp120可使单核细胞表面的CCR5上调,但不能使肠巨噬细胞表面的CCR5上调。肠巨噬细胞对HIV-1的易感性受损可能在体内HIV-1感染期间固有层中表达HIV-1 mRNA的巨噬细胞低流行率中起重要作用。表征HIV-1在原代黏膜细胞中的转运和感染的生物学特性将是阐明黏膜表面在HIV-1疾病中的关键作用的关键。

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