Abstract
Upon viral infection, the major defensive strategy employed by the host immune system is the activation of the interferon (IFN)-mediated antiviral pathway, which is overseen by IFN regulatory factors (IRFs). In order to complete their life cycles, viruses must find a way to modulate the host IFN-mediated immune response. Kaposi's sarcoma-associated herpesvirus (KSHV), a human tumor-inducing herpesvirus, has developed a unique mechanism for antagonizing cellular IFN-mediated antiviral activity by incorporating viral homolog of the cellular IRFs, called vIRFs, into its genome. Here, we summarize the novel evasion mechanisms by which KSHV, through its vIRFs, circumvents IFN-mediated innate immune responses and deregulates the cell growth control mechanism.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Apoptosis
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Cell Proliferation
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Cell Transformation, Neoplastic
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Herpesvirus 8, Human / pathogenicity
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Herpesvirus 8, Human / physiology*
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Humans
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Immunity, Innate
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Interferon Regulatory Factors / genetics
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Interferon Regulatory Factors / immunology*
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Interferons / genetics
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Interferons / immunology*
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Interferons / metabolism
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Protein Stability
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Sarcoma, Kaposi* / genetics
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Sarcoma, Kaposi* / immunology
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Sarcoma, Kaposi* / virology
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Transcriptional Activation
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / immunology
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Tumor Suppressor Protein p53 / metabolism*
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Viral Proteins / genetics
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Viral Proteins / immunology*
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Virulence
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Virus Replication
Substances
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Interferon Regulatory Factors
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Tumor Suppressor Protein p53
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Viral Proteins
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viral interferon regulatory factors
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Interferons