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The Journal of Immunology, Vol 131, Issue 1 30-36, Copyright © 1983 by American Association of Immunologists

ARTICLES

Effect of vesicular stomatitis virus (VSV) infection on the development and regulation of T cell-mediated immune responses

MS Sy, M Tsurufuji, R Finberg and B Benacerraf

Infection of mice with vesicular stomatitis virus (VSV) at the time of immunization failed to enhance T cell-mediated immune response to azobenzenearsonate-(ABA) conjugated spleen cells as measured by delayed- type hypersensitivity and by in vitro proliferation and in vitro generation of ABA-specific cytotoxic T cells. However, mice infected with VSV are incapable of responding to signals from suppressor T cells or their soluble factors. Further analysis revealed that VSV infection does not interfere with the induction of Ts-1 or Ts-2 cells. Because infection of Ts-1 or Ts-2 donors had no effect on the subsequent response seen in the recipients of antigen and suppressor T cells, the most likely candidate for the target of VSV infection is therefore the Ts-3 cell or another T cell interacting with Ts-3. This is supported by our observation that it is possible to bypass the VSV effect by providing the recipients of VSV with normal Lyt-2+-bearing T cells.


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S. Zhou, E. A. Kurt-Jones, K. A. Fitzgerald, J. P. Wang, A. M. Cerny, M. Chan, and R. W. Finberg
Role of MyD88 in Route-Dependent Susceptibility to Vesicular Stomatitis Virus Infection
J. Immunol., April 15, 2007; 178(8): 5173 - 5181.
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