| Summary: | <p>Abstract</p> <p>Background</p> <p>Interferon-γ acts to multiply the potency with which innate interferons (α/β) suppress herpes simplex virus type 1 (HSV-1) replication. Recent evidence suggests that this interaction is functionally relevant in host defense against HSV-1. However, it is not clear which WBCs of the innate immune system, if any, limit HSV-1 spread in an IFN-γ dependent manner. The current study was initiated to determine if natural killer (NK) cells provide innate resistance to HSV-1 infection, and if so to determine if this resistance is IFN-γ-dependent.</p> <p>Results</p> <p>Lymphocyte-deficient <it>scid </it>or <it>rag2</it><sup>-/- </sup>mice were used to test four predictions of the central hypothesis, and thus determine if innate resistance to HSV-1 is dependent on <b>1. </b>NK cell cytotoxicity, <b>2. </b>NK cells, <b>3. </b>WBCs, or <b>4. </b>the IFN-activated transcription factor, Stat 1. Loss of NK cell cytotoxic function or depletion of NK cells had no effect on the progression of HSV-1 infection in <it>scid </it>mice. In contrast, viral spread and pathogenesis developed much more rapidly in <it>scid </it>mice depleted of WBCs. Likewise, loss of Stat 1 function profoundly impaired the innate resistance of <it>rag2</it><sup>-/- </sup>mice to HSV-1.</p> <p>Conclusion</p> <p>Lymphocyte-deficient mice possess a very tangible innate resistance to HSV-1 infection, but this resistance is not dependent upon NK cells.</p>
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