HIV-1 gp120 induces NFAT nuclear translocation in resting CD4+ T-cells
- Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC 1876, Building 10, Room 11N210, Bethesda, MD 20892-1876 (United States)
- Laboratory of Immunopathogenesis and Bioinformatics, National Institute of Allergy and Infectious Disease, National Institutes of Health, Frederick, MD 21702 (United States)
- Laboratory of Molecular and Cellular Biology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Frederick, MD 21702 (United States)
The replication of human immunodeficiency virus (HIV) in CD4+ T-cells is strongly dependent upon the state of activation of infected cells. Infection of sub-optimally activated cells is believed to play a critical role in both the transmission of virus and the persistence of CD4+ T-cell reservoirs. There is accumulating evidence that HIV can modulate signal-transduction pathways in a manner that may facilitate replication in such cells. We previously demonstrated that HIV gp120 induces virus replication in resting CD4+ T cells isolated from HIV-infected individuals. Here, we show that in resting CD4+ T-cells, gp120 activates NFATs and induces their translocation into the nucleus. The HIV LTR encodes NFAT recognition sites, and NFATs may play a critical role in promoting viral replication in sub-optimally activated cells. These observations provide insight into a potential mechanism by which HIV is able to establish infection in resting cells, which may have implications for both transmission of HIV and the persistence of viral reservoirs.
- OSTI ID:
- 20779454
- Journal Information:
- Virology, Journal Name: Virology Journal Issue: 1 Vol. 345; ISSN VIRLAX; ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
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