T cell-extrinsic IL-1 signaling controls long-term gammaherpesvirus infection by suppressing viral reactivation. Virology 2022 Nov;576:134-140
Date
10/17/2022Pubmed ID
36244319Pubmed Central ID
PMC10069094DOI
10.1016/j.virol.2022.09.006Scopus ID
2-s2.0-85139738671 (requires institutional sign-in at Scopus site)Abstract
Gammaherpesviruses establish life-long infection in over 95% of adults and are associated with several cancers, including B cell lymphomas. Using the murine gammaherpesvirus 68 (MHV68) animal model, we previously showed a pro-viral role of Interleukin-1 (IL-1) signaling that supported viral reactivation during the establishment of chronic infection. Unexpectedly, in this study we found that the proviral effects of IL-1 signaling originally observed during the establishment of chronic gammaherpesvirus infection convert to antiviral effects during the long-term stage of infection. Specifically, IL-1 signaling promoted expansion of antiviral CD8+ T cells and control of viral reactivation in the peritoneal cavity of a long-term infected host. Using a novel mouse model of T cell-specific IL-1 signaling deficiency, we found that the antiviral effects of IL-1 signaling were T cell extrinsic. Our study highlights a dynamic nature of host factors that shape the parameters of chronic gammaherpesvirus infection.
Author List
Sylvester PA, Corbett JA, Tarakanova VLAuthors
John A. Corbett PhD Chair, Professor in the Biochemistry department at Medical College of WisconsinVera Tarakanova PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsAntiviral Agents
B-Lymphocytes
CD8-Positive T-Lymphocytes
Gammaherpesvirinae
Herpesviridae Infections
Interleukin-1
Mice
Mice, Inbred C57BL
Virus Latency
