Abstract
Pretreatment with two biological response modifiers (BRM), OK-432 and PS-K, protected mice from lethal infection by murine cytomegalovirus (MCMV). This was evidenced by an increase in 50% lethal doses and a decrease in titers of infectious viruses replicated in the liver and spleen. Spleen cells from the BRM-treated mice augmented the natural killer (NK) cell activity and suppressed the replication of MCMV in vitro. During MCMV infection, the NK cell activity of the spleen cells was maintained at a high level in the BRM-treated mice, whereas it was severely impaired in untreated mice. The BRM-induced protection was nullified by concomitant administration of antiasialo GM1 antibody. Interferon was neither induced by BRM treatment nor enhanced in BRM-pretreated and MCMV-infected mice. Thus, the protective effect of OK-432 and PS-K seems to be based on activation of NK cells and prevention of MCMV-induced inhibition of the NK cell activity.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Reference41 articles.
1. Effect of murine cytomegalovirus infection on mitogen responses in genetically resistant and susceptible mice;Allan J. E.;Infect. Immun.,1982
2. Genetic influences on the augmentation of natural killer (NK) cells during murine cytomegalovirus infection: correlation with patterns of resistance;Bancroft G. J.;J. Immunol.,1981
3. Natural killer cell depletion enhances virus synthesis and virus-induced hepatitis in vivo;Bukowski J. F.;J. Immunol.,1983
4. Interferon as a defence mechanism in mouse cytomegalovirus infection;Chong K. T.;J. Gen. Virol.,1983
5. of the spleen replication cells in the liver T T + Survival
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