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Murine gamma-herpesvirus 68 hijacks MAVS and IKKβ to initiate lytic replication
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نویسنده
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dong x. ,feng h. ,sun q. ,li h. ,wu t.t. ,sun r. ,tibbetts s.a. ,chen z.j. ,feng p.
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منبع
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plos pathogens - 2010 - دوره : 6 - شماره : 7 - صفحه:1 -16
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چکیده
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Upon viral infection,the mitochondrial antiviral signaling (mavs)-ikkβ pathway is activated to restrict viral replication. manipulation of immune signaling events by pathogens has been an outstanding theme of host-pathogen interaction. here we report that the loss of mavs or ikkβ impaired the lytic replication of gamma-herpesvirus 68 (γhv68),a model herpesvirus for human kaposi's sarcoma-associated herpesvirus and epstein-barr virus. γhv68 infection activated ikkβ in a mavs-dependent manner; however,ikkβ phosphorylated and promoted the transcriptional activation of the γhv68 replication and transcription activator (rta). mutational analyses identified ikkβ phosphorylation sites,through which rtamediated transcription was increased by ikkβ,within the transactivation domain of rta. moreover,the lytic replication of recombinant γhv68 carrying mutations within the ikkβ phosphorylation sites was greatly impaired. these findings support the conclusion that γhv68 hijacks the antiviral mavs-ikkβ pathway to promote viral transcription and lytic infection,representing an example whereby viral replication is coupled to host immune activation. © 2010 dong et al.
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آدرس
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department of microbiology,ut southwestern medical center,dallas,tx, United States, department of microbiology,ut southwestern medical center,dallas,tx, United States, the state key laboratory of biomembrane and membrane biotechnology,institute of zoology,chinese academy of sciences,chao yang district,beijing, China, department of microbiology and immunology,louisiana state university health science center,shreveport,la, United States, department of molecular and medical pharmacology,university of california los angeles,los angeles,ca, United States, department of molecular and medical pharmacology,university of california los angeles,los angeles,ca, United States, department of microbiology and immunology,louisiana state university health science center,shreveport,la, United States, department of molecular biology,ut southwestern medical center,dallas,tx, United States, department of microbiology,ut southwestern medical center,dallas,tx, United States
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Authors
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