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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

05/28/2013

Pubmed ID

23706314

Pubmed Central ID

PMC3703304

DOI

10.1016/j.virol.2013.04.036

Scopus ID

2-s2.0-84879783929   10 Citations

Abstract

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 VL

Author

Vera Tarakanova PhD Associate Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Immediate-Early Proteins
Interferon Regulatory Factor-3
Interferon Type I
Macrophages
Mice
Receptor, Interferon alpha-beta
Rhadinovirus
Signal Transduction
Trans-Activators
Virus Replication
jenkins-FCD Prod-482 91ad8a360b6da540234915ea01ff80e38bfdb40a