HTLV-1 Tax activates HIV-1 transcription in latency models
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Universidade Federal de Minas Gerais
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Artigo de periódico
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Membros da banca
Resumo
HIV-1 latency is a major obstacle to HIV-1 eradication. Coinfection with HTLV-1 has been associated with faster progression to AIDS. HTLV-1 encodes the transactivator Tax which can activate both HTLV-1 and HIV-1 transcription. Here, we demonstrate that Tax activates HIV transcription in latent CD4+ T cells. Tax promotes the activation of P-TEFb, releasing CDK9 and Cyclin T1 from inactive forms, promoting transcription elongation and reactivation of latent HIV-1. Tax mutants lacking interaction with the HIV-1-LTR promoter were not able to activate P-TEFb, with no subsequent activation of latent HIV. In HIV-infected primary resting CD4+ T cells, Tax-1 reactivated HIV-1 transcription up to five fold, confirming these findings in an ex vivo latency model. Finally, our results confirms that HTLV-1/Tax hijacks cellular partners, promoting HIV-1 transcription, and this interaction should be further investigated in HIV-1 latency studies in patients with HIV/ HTLV-1 co-infection.
Abstract
Assunto
HIV (Virus), HTLV-I (Virus)
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HIV-1, Latency, HTLV-1, Tax, Tax, Resting cells
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https://www.sciencedirect.com/science/article/pii/S0042682217300235?via%3Dihub