Early clearance of a thymidine kinase-deficient strain of herpes simplex virus type 2 from the female genital tract required T-cell-produced gamma interferon (IFN-γ). Transfer of activated CD8+ T cells to irradiated C57BL/6 mice resulted in rapid virus clearance, but clearance was greatly delayed in recipients deficient in the IFN-γ receptor (IFN-γR). Early virus clearance was demonstrated in radiation chimeras in which IFN-γR expression was limited to parenchymal cells, but resolution was significantly delayed in chimeras deficient in IFN-γR expression and chimeras expressing IFN-γR only on hematopoietic cells. Together, these results suggest that early IFN-γ-mediated protection was manifested mainly by stimulation of genital parenchymal cells.
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