Interferon as a defence mechanism in mouse cytomegalovirus infection.
Mouse cytomegalovirus (MCMV) grew to higher titres in spleen, liver, kidney and salivary gland of mice, and caused more sickness and death in susceptible (CD1) mice following treatment with anti-interferon globulin (AIG). In the resistant (C3H) strain of mice, organ titres were higher following AIG treatment but there was no sickness or mortality. Spleen necrosis was more severe in AIG-treated mice, indicating that this necrosis was not caused by interferon-mediated activation of natural killer (NK) cells. CD1 mice developed a high level of NK activity during MCMV infection and this was greatly reduced by AIG treatment. AIG was equally effective in increasing virus titres in NK-deficient beige (bg/bg) C57 B1.6 mice which showed a low level of NK activity even after MCMV infection, suggesting that interferon protects against MCMV by its direct antiviral effect on cells rather than by activating NK cells.
D000818:Animals; D003586:Cytomegalovirus Infections / Q000276:immunology*; D007106:Immune Sera; D007370:Interferon Type I / Q000276:immunology; D007372:Interferons / Q000494:pharmacology*; D007668:Kidney / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D008099:Liver / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D008815:Mice, Inbred Strains; D012469:Salivary Glands / Q000276:immunology; D013154:Spleen / Q000276:immunology
D007106:Immune Sera; D007370:Interferon Type I; D007372:Interferons