Murine Cytomegalovirus Virion-Associated Protein M45 Mediates Rapid NF-kappa B Activation after Infection
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Publication Details
Output type: Journal article
Author list: Krause E, de Graaf M, Fliss PM, Dolken L, Brune W
Publisher: American Society for Microbiology
Publication year: 2014
Journal: Journal of Virology (0022-538X)
Volume number: 88
Issue number: 17
Start page: 9963
End page: 9975
Number of pages: 13
ISSN: 0022-538X
eISSN: 1098-5514
Languages: English-Great Britain (EN-GB)
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Open access status: bronze
Full text URL: https://jvi.asm.org/content/jvi/88/17/9963.full.pdf
Abstract
Transcription factor NF-kappa B is an important regulator of innate and adaptive immunity. Its activation can be beneficial or detrimental for viral pathogens. Therefore, many viruses interfere with NF-kappa B signaling by stimulating or inhibiting the activation of this transcription factor. Cytomegaloviruses, opportunistic pathogens that cause lifelong infections in their hosts, activate NF-kappa B rapidly and transiently upon infection but block NF-kappa B signaling soon thereafter. Here we report the surprising finding that the murine cytomegalovirus protein M45, a component of viral particles, plays a dual role in NF-kappa B signaling. It not only blocks NF-kappa B signaling later in infection but also triggers the rapid activation of NF-kappa B immediately following virus entry into host cells. Both activation and inhibition involve M45 interaction with the cellular signaling mediators RIP1 and NEMO. Similar dual functions in NF-kappa B signaling are likely to be found in other viral proteins.
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