SUMMARY

Natural killer (NK) cell-depleted or control mice were treated prophylactically with polyinosinic:polycytidylic acid (polyI:polyC) or purified beta interferon (IFN) and then infected with either vaccinia virus or murine cytomegalovirus. NK cell depletion alone enhanced virus titres in the spleen and peritoneal cavity. However, poly I: polyC and IFN inhibited virus replication equally well in control and NK cell-depleted mice. This suggests that prophylactic IFN treatment mediates antiviral effects indepen-dently of NK cells. Virus-induced interferon (IFN) stimulates the activation (Gidlund et al., 1978; Welsh, 1978) and proliferation (Biron et al., 1984) of natural killer (NK) cells which have been suggested to play a role in resistance to virus infection. Mice deficient in NK cell activity as a result of youth (Boos & Wheelock, 1971), immunosuppressive drugs (Osborn et al., 1968), genetic background (Bancroft et al., 1981), the beige mutation (Shellam et al., 1981), or treatment with antiserum to the ganglioside, asialo GM1 (Bukowski et al., 1983) are highly susceptible to murine cytomegalovirus (MCMV) infection. Adoptive transfer studies revealed that the protective cell population isasialo GM1 ÷, NK 2.1 ÷, Ly 5 +, Thy-l-, Lyt-2-, Ia-, and is thus identifiable as N