Mouse adenovirus type 1 infection of natural killer cell-deficient mice.
Natural killer (NK) cells contribute to the initial nonspecific response to viral infection, and viruses exhibit a range of sensitivities to NK cells in vivo. We investigated the role of NK cells in infection of mice by mouse adenovirus type 1 (MAV-1) using antibody-mediated depletion and knockout mice. MAV-1 causes encephalomyelitis and replicates to highest levels in brains. NK cell-depleted mice infected with MAV-1 showed brain viral loads 8-20 days p.i. that were similar to wild-type control non-depleted mice. Mice genetically deficient for NK cells behaved similarly to wild-type control mice with respect to brain viral loads and survival. We conclude that NK cells are not required to control virus replication in the brains of MAV-1-infected mice.
D000256:Adenoviridae / Q000302:isolation & purification* / Q000472:pathogenicity* / Q000502:physiology; D000257:Adenoviridae Infections / Q000276:immunology* / Q000821:virology; D000818:Animals; D001921:Brain / Q000821:virology; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology*; D047589:Leukocyte Reduction Procedures; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D019562:Viral Load; D014779:Virus Replication