HIV-1 envelope–receptor interactions required for macrophage infection and implications for current HIV-1 cure strategies
Year: 2013
Type: review
Abstract: Myeloid cells residing in the CNS and lymphoid tissues are targets for productive HIV-1 replication, and their infection contributes to the pathological manifestations of HIV-1 infection. The Envs can adopt altered configurations to overcome entry restrictions in macrophages via a more efficient and/or altered mechanism of engagement with cellular receptors. This review highlights evidence supporting an important role for macrophages in HIV-1 pathogenesis and persistence, which need to be considered for strategies aimed at achieving a functional or sterilizing cure. We also highlight that the molecular mechanisms underlying HIV-1 tropism for macrophages are complex, involving enhanced and/or altered interactions with CD4, CCR5, and/or CXCR4, and that the nature of these interactions may depend on the anatomical location of the virus.
Source: Journal of Leukocyte Biology
DOI: 10.1189/jlb.0713368
Language: English
Topic: HIV Research and Treatment
Subfield: Virology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
Funders: University of Pennsylvania, Burnet Institute, National Institutes of Health, Center for AIDS Research, Duke University, Australian Research Council, National Health and Medical Research Council, National Medical Research Council, Health and Medical Research Fund, National Institute of Mental Health, National Institute of Allergy and Infectious Diseases
Awards: The role of chemokines in the establishment of HIV latency, DARE: Delaney AIDS Research Enterprise to find a cure., HIV Pathogenesis, Vaccination and Cure, G5812077480, Entry Coreceptor Use & Target Cell Tropism in Nonpathogenic SIV Infection, G674907753, Downmodulating Monocyte/Macrophage Activation for HAND, G8260647612, G8883985553, Tulane National Primate Research Center, Penn Center for AIDS Research
OpenAlex ID: W2147586896