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Human immunodeficiency virus type 1 Tat binds to Candida albicans , inducing hyphae but augmenting phagocytosis in vitro
Author(s) -
Gruber Andreas,
Lell Claudia P.,
Speth Cornelia,
Stoiber Heribert,
LassFlörl Cornelia,
Sonneborn Anja,
Ernst Joachim F.,
Dierich Manfred P.,
Würzner Reinhard
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01328.x
Subject(s) - candida albicans , phagocytosis , microbiology and biotechnology , biology , corpus albicans , virulence , antibody opsonization , in vitro , peptide , hypha , opsonin , biochemistry , gene
Summary Tat, the human immunodeficiency virus type 1 (HIV‐1) transactivating protein, binds through its RGD‐motif to human integrin receptors . Candida albicans , the commonest cause of mucosal candidiasis in subjects infected with HIV‐1, also possesses RGD‐binding capacity. The present study reveals that Tat binds to C. albicans but not to C. tropicalis . Tat binding was markedly reduced by laminin and to a lesser extent by a complement C3 peptide containing the RGD motif, but not by a control peptide. The outgrowth of C. albicans was accelerated following binding of Tat, but phagocytosis of opsonized C. albicans was also increased after Tat binding. Thus, Tat binding promotes fungal virulence by inducing hyphae but may also reduce it by augmenting phagocytosis. The net effect of Tat in vivo is difficult to judge but in view of the many disease‐promoting effects of Tat we propose that accelerating the formation of hyphae dominates over the augmentation of phagocytosis.