期刊
VIROLOGY JOURNAL
卷 8, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1743-422X-8-166
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资金
- MIUR [20072J9RWM_004, 2007M52HTT_004]
- University of Padova
- Istituto Superiore di Sanita (Rome) [30G.24, 30G.55, 40G.44]
Epidemiological and clinical data indicate that genital ulcer disease (GUD) pathogens are associated with an increased risk of human immunodeficiency virus type 1 (HIV-1) acquisition and/or transmission. Among them, genital herpes simplex virus type 2 (HSV-2) seems to play a relevant role. Indeed, the ability of HSV-2 to induce massive infiltration at the genital level of cells which are potential targets for HIV-1 infection may represent one of the mechanisms involved in this process. Here we show that infection of human primary macrophages (MDMs) by HSV-2 results in an increase of CCR5 expression levels on cell surface and allows higher efficiency of MDMs to support entry of R5 HIV-1 strains. This finding could strengthen, at the molecular level, the evidence linking HSV-2 infection to an increased susceptibility to HIV-1 acquisition.
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