Journal
JOURNAL OF VIROLOGY
Volume 87, Issue 21, Pages 11924-11929Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02128-13
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Funding
- National Institutes of Health [AI093179, 1K01DA024654]
- Peter and Shelagh Godsoe Family Foundation through the AIDS Research Institute at UCSF
- UCSF-Gladstone Institute of Virology & Immunology Center for AIDS Research [P30-AI027763]
- Academic Senate under the UCSF RAP awards program
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Expression of cell-intrinsic antiviral factors suppresses HIV-1 replication. We hypothesized that cellular activation modulates host restriction and susceptibility to HIV-1 infection. We measured the gene expression of 34 antiviral factors in healthy peripheral blood mononuclear cells (PBMC). Cellular activation induced expression of interferon-stimulated gene 15 (ISG15), tripartite motif 5 alpha (TRIM5 alpha), bone marrow stromal cell antigen 2 (BST-2)/tetherin, and certain apolipoprotein B mRNA editing enzyme 3 (APOBEC3) family members. Expression of RTF1, RNA polymerase II-associated factor 1 (PAF1), TRIM11, TRIM26, and BST-2/tetherin correlated with decreased HIV-1 infectivity. This report demonstrates synchronous effects of activation-induced antiviral genes on HIV-1 infectivity, providing candidates for pharmacological manipulation.
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