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- W1688842012 abstract "Herpes Simplex Virus-1 (HSV-1) infection has been shown to be very resistant to the effects of the cellular interferon response. However, in the absence of viral gene expression HSV-1 induces the expression of cellular interferon-stimulated genes, possibly through activation of the interferon-regulatory factor 3 (IRF-3) cascade. The induction of IRF-3 by HSV-1 infection has not been well characterized. Using an HSV-1 mutant deficient in the expression of viral genes, we show that HSV-1 can induce the cascade of IRF-3 activation by stimulating the phosphorylation of IRF-3 and the nuclear localization of the protein. We will show that activation of this pathway leads to the expression of interferon-stimulated genes and the production of a protective antiviral response. Further we will show that the expression of one viral gene, ICP0, is essential and sufficient to the inhibition of interferon-stimulated gene expression. An HSV-1 mutant deficient in expression of all immediate-early HSV-1 genes except ICP0 does not induce nuclear accumulation of IRF-3 and does not induce the expression of interferon-stimulated genes. This virus induces the mis-localization of the kinase (TBK-1) responsible for the phosphorylation of IRF-3. Cytoplasmically localized ICP0 expressed in wild-type infection stimulates the translocation of TBK-1 from the cytoplasm to the Golgi apparatus. This ICP0-mediated mis-localization, as well as a portion of that induced by the ICP0 expressing mutant, can be inhibited through the inhibition of the proteasome. Further, IRF-3 nuclear translocation and interferon-stimulated gene expression can be restored during infection with the ICP0-expressing mutant virus in the presence of proteasome inhibitors. This study explores the induction of the interferon regulatory factor-3 cellular antiviral response pathway, and presents a possible mechanism for the virus' resistance to the cellular antiviral response." @default.
- W1688842012 created "2016-06-24" @default.
- W1688842012 creator A5048398834 @default.
- W1688842012 date "2006-11-30" @default.
- W1688842012 modified "2023-09-27" @default.
- W1688842012 title "The Induction and Inhibition of an Antiviral Response by Herpes Simplex Virus 1" @default.
- W1688842012 cites W10482017 @default.
- W1688842012 cites W121402389 @default.
- W1688842012 cites W123433535 @default.
- W1688842012 cites W1485525860 @default.
- W1688842012 cites W1490731141 @default.
- W1688842012 cites W1494730114 @default.
- W1688842012 cites W1501348451 @default.
- W1688842012 cites W1503107508 @default.
- W1688842012 cites W1507428456 @default.
- W1688842012 cites W1516191360 @default.
- W1688842012 cites W1517021800 @default.
- W1688842012 cites W1555996845 @default.
- W1688842012 cites W1557451157 @default.
- W1688842012 cites W1558828789 @default.
- W1688842012 cites W1563565864 @default.
- W1688842012 cites W1567284421 @default.
- W1688842012 cites W1573116795 @default.
- W1688842012 cites W1583466448 @default.
- W1688842012 cites W1589334735 @default.
- W1688842012 cites W1592452078 @default.
- W1688842012 cites W1592653658 @default.
- W1688842012 cites W1606562486 @default.
- W1688842012 cites W1606830172 @default.
- W1688842012 cites W1608590926 @default.
- W1688842012 cites W1652751844 @default.
- W1688842012 cites W1656209509 @default.
- W1688842012 cites W1680293007 @default.
- W1688842012 cites W171936907 @default.
- W1688842012 cites W1723491130 @default.
- W1688842012 cites W1733825645 @default.
- W1688842012 cites W1738338042 @default.
- W1688842012 cites W1755293693 @default.
- W1688842012 cites W177007720 @default.
- W1688842012 cites W1813425624 @default.
- W1688842012 cites W1816590717 @default.
- W1688842012 cites W1824684517 @default.
- W1688842012 cites W1835686953 @default.
- W1688842012 cites W1838326446 @default.
- W1688842012 cites W1850750660 @default.
- W1688842012 cites W1876993892 @default.
- W1688842012 cites W1881510917 @default.
- W1688842012 cites W1886515277 @default.
- W1688842012 cites W1930598094 @default.
- W1688842012 cites W1931233319 @default.
- W1688842012 cites W1934070818 @default.
- W1688842012 cites W1954109446 @default.
- W1688842012 cites W1955412606 @default.
- W1688842012 cites W1962970685 @default.
- W1688842012 cites W1963631905 @default.
- W1688842012 cites W1964442232 @default.
- W1688842012 cites W1964659850 @default.
- W1688842012 cites W1966435564 @default.
- W1688842012 cites W1966673222 @default.
- W1688842012 cites W1967020705 @default.
- W1688842012 cites W1968270886 @default.
- W1688842012 cites W1968786201 @default.
- W1688842012 cites W1969078573 @default.
- W1688842012 cites W1971056267 @default.
- W1688842012 cites W1971781827 @default.
- W1688842012 cites W1972245437 @default.
- W1688842012 cites W1972285445 @default.
- W1688842012 cites W1972677202 @default.
- W1688842012 cites W1973682675 @default.
- W1688842012 cites W1974714570 @default.
- W1688842012 cites W1976822357 @default.
- W1688842012 cites W1977457899 @default.
- W1688842012 cites W1986791214 @default.
- W1688842012 cites W1988808478 @default.
- W1688842012 cites W1991717074 @default.
- W1688842012 cites W1992127131 @default.
- W1688842012 cites W1992910900 @default.
- W1688842012 cites W1993780482 @default.
- W1688842012 cites W1994730933 @default.
- W1688842012 cites W1994980446 @default.
- W1688842012 cites W1997501835 @default.
- W1688842012 cites W2000110844 @default.
- W1688842012 cites W2001339120 @default.
- W1688842012 cites W2001804120 @default.
- W1688842012 cites W2002301799 @default.
- W1688842012 cites W2003385732 @default.
- W1688842012 cites W2004465286 @default.
- W1688842012 cites W2004925049 @default.
- W1688842012 cites W2005042282 @default.
- W1688842012 cites W2006940895 @default.
- W1688842012 cites W2007634908 @default.
- W1688842012 cites W2012467811 @default.
- W1688842012 cites W2012482167 @default.
- W1688842012 cites W2013601771 @default.
- W1688842012 cites W2014619010 @default.
- W1688842012 cites W2014657724 @default.
- W1688842012 cites W2016266703 @default.
- W1688842012 cites W2017969950 @default.
- W1688842012 cites W2018106813 @default.
- W1688842012 cites W2019311806 @default.