期刊
VIROLOGY
卷 338, 期 2, 页码 201-208出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2005.05.011
关键词
CD4 T cell; gammaherpesvirus; IFN gamma; herpesvirus latency; TH1 T cell
类别
资金
- NCI NIH HHS [NIH T32 CA09547, R01 CA96511] Funding Source: Medline
- NHLBI NIH HHS [R01 HL 60090] Funding Source: Medline
- NIAID NIH HHS [NIH T32 AI07172-22] Funding Source: Medline
Murine Laninialierpesvirus 68 (gamma HV68, MHV-68)-specific CD4 T cells control -yHV68 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 gamma HV68 replication, demonstrating a helper-independent activity of CD4 T cells during gamma HV68 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 IFN gamma has been previously shown to be important for control of acute, latent, and persistent -yHV68 infection, we tested the hypothesis that CD4 T cells require IFN gamma to limit gamma HV68 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 (gamma HV68.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 IFN gamma for their anti-viral function in both acute and latent gamma HV68 infection. We additionally show that an in vitro derived T helper type 1 (TH 1) CD4 T cell clone, which produces IFN gamma, inhibits gamma HV68 replication after adoptive transfer into RAG mice. Together, data presented here demonstrate that both CD4 T cel-mediated helper-independent control of gamma HV68 replication and inhibition of the establishment of gamma HV68 latency require IFN gamma. (c) 2005 Elsevier Inc. All rights reserved.
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