The Absence of M1 Leads to Increased Establishment of Murine Gammaherpesvirus 68 Latency in IgD-Negative B Cells

• Type of Material: Article
• Authors: Laurie T. Krug, Emory University; Andrew G Evans, Emory University; Lisa M. Gargano, Emory University; Clinton R. Paden, Emory University; Samuel Speck, Emory University
• Language: English
• Date: 2013-03-01
• Publisher: American Society for Microbiology
• Publication Version: Final Published Version
• Copyright Statement: © 2013, American Society for Microbiology.
• Final Published Version (URL): http://dx.doi.org/10.1128/JVI.01953-12
• Title of Journal or Parent Work: Journal of Virology
• ISSN: 0022-538X
• Volume: 87
• Issue: 6
• Start Page: 3597
• End Page: 3604
• Grant/Funding Information: This research was supported by NIH grants R01 AI07830 and CA95318 to S.H.S. S.H.S. was also supported by NIH grants R01 CA52004, CA58524, CA87650, and AI58057.; L.T.K. was supported by NIH IRACDA K12-GM000680, NIH Ruth L. Kirschstein National Research service award F32 AI066818, and American Cancer Society Research Scholar grant RSG-11-160-01-MPC).
• Keywords: MAINTENANCE; DISEASE; Virology; PATHOGENESIS; INFECTIOUS-MONONUCLEOSIS; LYMPHOCYTES; VIROLOGY; Life Sciences & Biomedicine; LESSONS; IN-VIVO; SUPERANTIGEN; REACTIVATION; T-CELLS; Science & Technology
• Research Categories: Biology, Virology; Health Sciences, Immunology

Abstract

The secreted M1 protein of murine gammaherpesvirus 68 (MHV68) promotes effector Vβ4+ CD8+ T cell expansion to impact virus control and immune-mediated pathologies in C57BL/6 mice, but not BALB/c mice. We report a striking increase in the number of genome-positive, IgD- B cells during chronic infection of both mouse strains. This suggests a novel role for M1 in influencing long-term maintenance in a major latency reservoir irrespective of the degree of Vβ4+ CD8+ T cell expansion.