PubMed:9845362 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9845362","sourcedb":"PubMed","sourceid":"9845362","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9845362","text":"Host control of HIV-1 parasitism in T cells by the nuclear factor of activated T cells.\nPost HIV-1 entry, productive HIV-1 infection of primary T cells requires overcoming several cellular blocks to provirus establishment and replication. Activation of unknown host intracellular events overcomes such inhibitory steps and is concomitant with HIV-1 replication. We show that the transcription factor NFATc was sufficient as a cellular factor to induce a highly permissive state for HIV-1 replication in primary CD4+ T cells. NFATc overcame a blockade at reverse transcription and permitted active HIV-1 replication. Pharmacologic blockade of endogenous NFAT activity by FK506 or CsA inhibited synthesis of reverse transcription and also potently blocked HIV-1 replication. T cells therefore can become competent for HIV-1 replication by control of regulated host factors such as the NFATc transcription factor. The host mechanisms regulated by such permissivity factors are potential targets for anti-HIV-1 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