Mouse gammaherpesvirus-68 infection acts as a rheostat to set the level of type I interferon signaling in primary macrophages. Virology 2013 Aug 15;443(1):123-33
Date
05/28/2013Pubmed ID
23706314Pubmed Central ID
PMC3703304DOI
10.1016/j.virol.2013.04.036Scopus ID
2-s2.0-84879783929 (requires institutional sign-in at Scopus site) 25 CitationsAbstract
Type I interferon (IFN) is a critical antiviral response of the host. We found that Interferon Regulatory Factor 3 (IRF-3) was responsible for induction of type I IFN following mouse gammaherpesvirus-68 (MHV68) infection of primary macrophages. Intriguingly, type I IFN signaling was maintained throughout the entire MHV68 replication cycle, in spite of several known viral IFN antagonists. However, MHV68-infected primary macrophages displayed attenuated responses to exogenous type I IFN, suggesting that MHV68 controls the level of type I IFN signaling that is allowed to occur during replication. Type I IFN receptor and IRF-3 were necessary to attenuate transcription of MHV68 RTA, an immediate early gene critical for replication. Furthermore, higher constitutive activity of RTA promoters was observed in the absence of type I IFN signaling. Our study suggests that MHV68 has preserved the ability to sense type I IFN status of the host in order to limit lytic replication.
Author List
Wood BM, Mboko WP, Mounce BC, Tarakanova VLAuthor
Vera Tarakanova PhD Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsImmediate-Early Proteins
Interferon Regulatory Factor-3
Interferon Type I
Macrophages
Mice
Receptor, Interferon alpha-beta
Rhadinovirus
Signal Transduction
Trans-Activators
Virus Replication
