CD4 T cell control of acute and latent murine gammaherpesvirus infection requires IFNgamma

Murine gammaherpesvirus 68 (gammaHV68, MHV-68)-specific CD4 T cells control gammaHV68 infection by reducing the frequency of latently infected cells and by inhibiting viral replication. We have previously demonstrated that CD4 T cells do not require CD8 T or B cells to control gammaHV68 replication,...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2005-08, Vol.338 (2), p.201-208
Main Authors: Sparks-Thissen, Rebecca L, Braaten, Douglas C, Hildner, Kai, Murphy, Theresa L, Murphy, Kenneth M, Virgin, 4th, Herbert W
Format: Article
Language:English
Subjects:
Acute Disease
Animals
CD4-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - immunology
Chronic Disease
Disease Models, Animal
Gammaherpesvirinae - immunology
Herpesviridae Infections - immunology
Interferon-gamma - therapeutic use
Mice
T-Lymphocytes, Helper-Inducer - immunology
Virus Latency - immunology
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Summary:Murine gammaherpesvirus 68 (gammaHV68, MHV-68)-specific CD4 T cells control gammaHV68 infection by reducing the frequency of latently infected cells and by inhibiting viral replication. We have previously demonstrated that CD4 T cells do not require CD8 T or B cells to control gammaHV68 replication, demonstrating a helper-independent activity of CD4 T cells during gammaHV68 infection. The effector mechanism(s) required for this helper-independent function of CD4 T cells and for the inhibition of the establishment of latency by CD4 T cells are not known. Since IFNgamma has been previously shown to be important for control of acute, latent, and persistent gammaHV68 infection, we tested the hypothesis that CD4 T cells require IFNgamma to limit gammaHV68 latency and replication. We utilized a previously described system in which T cell receptor (TCR) transgenic T cells (DO.11.10) and a recombinant virus (gammaHV68.OVA) allow for evaluation of high numbers of virus-specific CD4 T cells during both acute and latent infection. We show here that virus-specific CD4 T cells require IFNgamma for their anti-viral function in both acute and latent gammaHV68 infection. We additionally show that an in vitro derived T helper type 1 (TH1) CD4 T cell clone, which produces IFNgamma, inhibits gammaHV68 replication after adoptive transfer into RAG mice. Together, data presented here demonstrate that both CD4 T cell-mediated helper-independent control of gammaHV68 replication and inhibition of the establishment of gammaHV68 latency require IFNgamma.
ISSN:0042-6822