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An intercellular adhesion molecule‐3 (ICAM‐3) ‐grabbing nonintegrin (DC‐SIGN) efficiently blocks HIV viral budding
Author(s) -
Wang Qiuwei,
Pang Shen
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.07-9443com
Subject(s) - dc sign , budding , microbiology and biotechnology , intercellular adhesion molecule 1 , intracellular , biology , internalization , cell adhesion molecule , icam 1 , dendritic cell , virology , cell , immunology , antigen , biochemistry
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. Cotrans‐fection 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. Wang, Q., Pang, S. An intercellular adhesion molecule‐3 (ICAM‐3) ‐grabbing nonintegrin (DC‐SIGN) efficiently blocks HIV viral budding. FASEB J. 22, 1055–1064 (2008)