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British Medical Bulletin 58:43-59 (2001)
© 2001 The British Council

HIV-1 receptors and cell tropism

Paul R Clapham* and Áine McKnight{dagger}

* Center for AIDS Research, Program in Molecular Medicine, Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
{dagger} The Wohl Virion Center, Department of Immunology and Molecular Pathology, The Windeyer Institute for Medical Sciences, University College, London, UK

HIV virus particles interact with several receptors on cell surfaces. Two receptors, CD4 and a co-receptor act sequentially to trigger fusion of viral and cellular membranes and confer virus entry into cells. For HIV-1, the chemokine receptor CCR5 is the predominant co-receptor exploited for transmission and replication in vivo. Variants that switch to use CXCR4 and perhaps other co-receptors evolve in some infected individuals and have altered tropism and pathogenic properties. Other cell surface receptors including mannose binding protein on macrophages and DC-SIGN on dendritic cells also interact with gp120 on virus particles but do not actively promote fusion and virus entry. These receptors may tether virus particles to cells enabling interactions with suboptimal concentrations of CD4 and/or co-receptors. Alternatively such receptors may transport cell surface trapped virions into lymph nodes before transmitting them to susceptible cells. Therapeutic strategies that prevent HIV from interacting with receptors are currently being developed. This review describes how the interaction and use of different cellular receptors influences HIV tropism and pathogenesis in vivo.


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