Murine gammaherpesvirus 68 (γHV68, MHV-68)-specific CD4 T cells control γHV68 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 γHV68 replication, demonstrating a helper-independent activity of CD4 T cells during γHV68 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 IFNγ has been previously shown to be important for control of acute, latent, and persistent γHV68 infection, we tested the hypothesis that CD4 T cells require IFNγ to limit γHV68 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 (γHV68.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 IFNγ for their anti-viral function in both acute and latent γHV68 infection. We additionally show that an in vitro derived T helper type 1 (TH1) CD4 T cell clone, which produces IFNγ, inhibits γHV68 replication after adoptive transfer into RAG mice. Together, data presented here demonstrate that both CD4 T cell-mediated helper-independent control of γHV68 replication and inhibition of the establishment of γHV68 latency require IFNγ.

Original languageEnglish
Pages (from-to)201-208
Number of pages8
Issue number2
StatePublished - Aug 1 2005


  • CD4 T cell
  • Gammaherpesvirus
  • Herpesvirus latency
  • IFNγ
  • TH1 T cell


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