Understanding mechanisms of HIV-1 entry into cells
Paul R Gorry
+ Author Affiliations
- Author Affiliations
Centre for Biomedical Research, Burnet Institute, GPO Box 2284, Melbourne, Vic. 3001, Australia
Department of Infectious Diseases, Monash University Central Clinical School, Melbourne, Vic., Australia
Department of Microbiology and Immunology, University of Melbourne, Parkville, Vic., Australia
Tel: +61 3 9282 2129
Fax: +61 3 9282 2100
Email: gorry@burnet.edu.au
Microbiology Australia 35(2) 99-100 https://doi.org/10.1071/MA14031
Published: 5 May 2014
Abstract
Human immunodeficiency virus type 1 (HIV-1) attaches to cells by the stepwise interaction of its envelope glycoproteins (Env), which exist as trimers that stud the exterior of the virus particle, with cellular CD4 and a coreceptor, principally either of the chemokine receptors CCR5 or CXCR4. Virus entry into cells then proceeds via exposure of a viral fusion peptide, and fusion between the viral and cellular membranes. Adaptability in Env conformation is a hallmark of HIV-1, which permits the virus to escape the humoral immune response. HIV-1 may also harness this power of adaptability to alter its target cell tropism and develop resistance to CCR5 antagonist HIV-1 entry inhibitors. Our work has shown that this may occur through a more efficient interaction between the Env glycoproteins and cellular receptors, as well as by an altered (but not necessarily more efficient) mechanism of interaction. Understanding the complexity of these interactions is pivotal for elucidating the molecular determinants of HIV-1 pathogenesis.
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