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Author Notes:

Address correspondence to, Laurie T. Krug, laurie.krug@stonybrook.edu

We thank Robert Karaffa for expertise and assistance with flow cytometry and members of the Speck laboratory for helpful discussions and critical reading of the manuscript.

Subjects:

Research Funding:

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:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Virology
  • VIROLOGY
  • T-CELLS
  • INFECTIOUS-MONONUCLEOSIS
  • IN-VIVO
  • REACTIVATION
  • MAINTENANCE
  • SUPERANTIGEN
  • PATHOGENESIS
  • LYMPHOCYTES
  • LESSONS
  • DISEASE

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

Tools:

Journal Title:

Journal of Virology

Volume:

Volume 87, Number 6

Publisher:

, Pages 3597-3604

Type of Work:

Article | Final Publisher PDF

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.

Copyright information:

© 2013, American Society for Microbiology.

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