HIV endocytosis after dendritic cell to T cell viral transfer leads to productive virus infection

• Published in: Antiviral research Vol. 83; no. 1; pp. 94 - 98
• Main Authors: Clotet-Codina, Imma, Bosch, Berta, Senserrich, Jordi, Fernández-Figueras, María Teresa, Peña, Ruth, Ballana, Ester, Bofill, Margarita, Clotet, Bonaventura, Esté, José A.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier B.V 01.07.2009; Elsevier
• Subjects: Action of physical and chemical agents; Antibiotics. Antiinfectious agents. Antiparasitic agents; Antiviral agents; Biological and medical sciences; CD4-Positive T-Lymphocytes - virology; Cells, Cultured; Coculture Techniques; Dendritic cell; Dendritic Cells - virology; Endocytosis; Entry inhibitor; Fundamental and applied biological sciences. Psychology; HIV entry; HIV-1 - growth & development; Human immunodeficiency virus 1; Humans; Medical sciences; Microbiology; Pharmacology. Drug treatments; Virology; Virus transfer; Dendritic cell; Entry inhibitor; Virus transfer; HIV entry; Immunopathology; HIV-1 virus; Retroviridae; Immune deficiency; Lentivirus; Infection; Virus; Endocytosis; Viral disease; T-Lymphocyte; Infected cell; Human immunodeficiency virus
• ISSN: 0166-3542; 1872-9096
• DOI: 10.1016/j.antiviral.2009.03.009

Contacts between HIV-producing T cells and primary CD4+ T cells may induce the uptake of HIV by target cells that are endocytosed into trypsin-resistant compartments. We have now compared the mechanism of virus transmission from T cell-to-T cell versus infected dendritic cells (DCs)-to-T cell. In cocultures of HIV-1-infected DCs with primary CD4+ T cells, virus transmission to the target cells was resistant to trypsin treatment and could only be prevented by the anti-SUgp120 antibody IgGb12 but not by TAK-779, C34 or AZT. Importantly, upon stimulation of purified HIV-1-loaded CD4+ T cells with PHA/IL-2, cells became productively infected as measured by intracellular CAp24 staining and antigen determination in the cell supernatant. These results suggest that the viral endocytic transfer may represent a escape mechanism in the presence of drugs targeting HIV-1 entry or the host immune system.