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Protective effect of biological response modifiers on murine cytomegalovirus infection
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.
Insights
Biological response modifiers (BRMs) OK-432 and PS-K protect mice against lethal murine cytomegalovirus (MCMV) infection by enhancing natural killer (NK) cell activity. This immune modulation prevents MCMV-induced NK cell impairment, offering a protective effect.
Area of Science:
- Immunology
- Virology
Background:
- Murine cytomegalovirus (MCMV) infection poses a significant threat, often leading to lethal outcomes.
- Natural killer (NK) cell activity is crucial for controlling viral infections but can be suppressed during MCMV infection.
Purpose of the Study:
- To investigate the protective effects of biological response modifiers (BRMs), specifically OK-432 and PS-K, against MCMV infection.
- To elucidate the role of NK cells in the protective mechanism conferred by these BRMs.
Main Methods:
- Mice were pretreated with OK-432 or PS-K before MCMV infection.
- Survival rates, viral titers in liver and spleen, and ex vivo NK cell activity of spleen cells were assessed.
- The effect of antiasialo GM1 antibody on BRM-induced protection was evaluated.
- Interferon levels were monitored.
Main Results:
- BRM pretreatment significantly increased survival rates and reduced viral loads in MCMV-infected mice.
- Spleen cells from BRM-treated mice exhibited augmented NK cell activity and suppressed MCMV replication in vitro.
- NK cell activity remained high in BRM-treated mice during infection, unlike in untreated controls.
- BRM-induced protection was abolished by antiasialo GM1 antibody, indicating NK cell dependence.
- No induction or enhancement of interferon was observed.
Conclusions:
- OK-432 and PS-K confer protection against lethal MCMV infection in mice.
- The protective mechanism is primarily mediated by the activation of NK cells and the prevention of MCMV-induced NK cell suppression.
- Interferon does not appear to play a role in this BRM-induced protective effect.