4.7 Article

An intercellular adhesion molecule-3 (ICAM-3)- grabbing nonintegrin (DC-SIGN) efficiently blocks HIV viral budding

期刊

FASEB JOURNAL
卷 22, 期 4, 页码 1055-1064

出版社

FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.07-9443com

关键词

gp120; viral production

资金

  1. NIAID NIH HHS [AI047722] Funding Source: Medline

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Efficient inhibition of the HIV infection, life cycle at the stages of viral infection, reverse transcription, and post-translational processing has been extensively studied. However, efficient inhibition of HIV assembly and budding has not been reported. Here, we report that dendritic cell-specific intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) and its related protein, DC-SIGNR, effectively block HIV budding from infected cells. Cotransfection of DC-SIGN or DC-SIGNR with HIV demonstrated 95-99.5% inhibition of viral production from host cells. DC-SIGN or DC-SIGNR can also effectively inhibit 90-95% of HIV generation from infected cells. DC-SIGN efficiently reduces the amount of gp120 present on the cell plasma membrane, and completely strips off gp120 from the virions produced by the host cells, suggesting that blockage of HIV budding is due to internalization of gp120 by DC-SIGN.

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