Abstract
It has been reported that HIV-1 Vpu mediates the degradation of interferon regulatory factor 3 (IRF-3) to avoid innate immune sensing. Here, we show that Vpu does not deplete IRF-3 from transfected cell lines or HIV-1-infected primary cells. Furthermore, the Vpu-dependent suppression of beta interferon expression described in previous studies could be ascribed to inhibition of NF-κB activation. Thus, Vpu suppresses innate immune activation through inhibition of NF-κB rather than degradation of IRF-3.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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HIV-1 / genetics
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HIV-1 / metabolism
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HIV-1 / pathogenicity*
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HeLa Cells
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Human Immunodeficiency Virus Proteins / genetics
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Human Immunodeficiency Virus Proteins / metabolism*
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Humans
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Immunity, Innate / drug effects
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Interferon Regulatory Factor-3 / genetics
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Interferon Regulatory Factor-3 / metabolism*
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NF-kappa B / antagonists & inhibitors*
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T-Lymphocytes / metabolism
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T-Lymphocytes / virology
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Transfection
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Viral Regulatory and Accessory Proteins / genetics
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Viral Regulatory and Accessory Proteins / metabolism*
Substances
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Human Immunodeficiency Virus Proteins
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IRF3 protein, human
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Interferon Regulatory Factor-3
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NF-kappa B
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Viral Regulatory and Accessory Proteins
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vpu protein, Human immunodeficiency virus 1