Previous Article | Next Article ![]()
Journal of Virology, December 2008, p. 12535-12542, Vol. 82, No. 24
0022-538X/08/$08.00+0 doi:10.1128/JVI.00881-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Department of Microbiology and Immunology, Indiana University School of Medicine, Walther Oncology Center, Indianapolis, Indiana 46202, and the Walther Cancer Institute, Indianapolis, Indiana 46208
Received 25 April 2008/ Accepted 11 September 2008
Natural killer T (NKT) cells are unique T lymphocytes that recognize CD1d-bound lipid antigens and play an important role in both innate and acquired immune responses against infectious diseases and tumors. We have already shown that a vesicular stomatitis virus (VSV) infection results in the rapid inhibition of murine CD1d-mediated antigen presentation to NKT cells. In the present study, it was found that the VSV matrix (VSV-M) protein is an important element in this decrease in antigen presentation postinfection. The VSV-M protein altered the intracellular distribution of murine CD1d molecules, resulting in qualitative (but not quantitative) changes in cell surface CD1d expression. The M protein was distributed throughout the infected cell, and it was found to activate the mitogen-activated protein kinase (MAPK) p38 very early postinfection. Infection of CD1d+ cells with a temperature-sensitive VSV-M mutant at the nonpermissive temperature both substantially reversed the inhibition of antigen presentation by CD1d and delayed the activation of p38. Thus, the VSV-M protein plays an important role in permitting the virus to evade important components of the innate immune response by regulating specific MAPK pathways.
Published ahead of print on 24 September 2008.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»