Human Immunodeficiency Virus Type 1 gp41 Binds toCandida albicansvia Complement C3‐like Regions
Author(s) -
Reinhard Würzner,
Andreas Gruber,
Heribert Stoiber,
Martin Spruth,
YingHua Chen,
Elisabeth Lukasser-Vogl,
Michael G. Schwendinger,
Manfred P. Dierich
Publication year - 1997
Publication title -
the journal of infectious diseases
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/514069
Subject(s) - candida albicans , corpus albicans , virology , biology , microbiology and biotechnology , virus , gp41 , immunodeficiency , antibody , immunology , immune system , epitope
Oral candidiasis in human immunodeficiency virus type 1 (HIV-1)-infected persons is believed to be caused by the acquired T lymphocyte immunodeficiency. The direct interaction of C. albicans and HIV-1 in vitro was investigated. Twice as many yeasts adhered to cells transfected with the HIV-1 env gene as they did to controls. HIV-1 rsgp160 and rsgp41 but not rsgp120 were found to bind to Candida albicans via two C3-like regions within gp41. Normal human serum, but not C3-depleted serum, was able to inhibit rsgp41 binding to C. albicans. Vice versa, rsgp160 and rsgp41 were able to block rosetting of C. albicans with iC3b-coated sheep erythrocytes. Binding to C. albicans, and its inhibition by rsgp41 or rsgp160, was confirmed for the whole virus. Therefore, oral candidiasis in HIV-1-infected subjects may be augmented or may even be initiated by direct interaction between C. albicans and HIV-1 or HIV-1-infected cells.
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