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. 1980 Jul;29(1):42–49. doi: 10.1128/iai.29.1.42-49.1980

Resistance to highly virulent mouse hepatitis virus acquired by mice after low-virulence infection: enhanced antiviral activity of macrophages.

F Taguchi, A Yamada, K Fujiwara
PMCID: PMC551072  PMID: 6156913

Abstract

As early as 1 to 2 days after intranasal inoculation with a mouse hepatitis virus of low virulence, MHV-S, susceptible DDD mice became fully resistant to a normally lethal challenge with a highly virulent MHV-2. The resistance of MHV-S-pretreated mice was correlated with significantly decreased MHV-2 multiplication in the liver, spleen, and brain. Infection with MHV-S did not induce a high level of interferon in DDD mice, and no neutralizing antibody against MHV-2 was detected in the sera of mice until day 6 of MHV-S infection. The multiplication of MHV-2 was suppressed in peritoneal cells (PC) in vivo and peritoneal adherent cells (PAC) in vitro of MHV-S-pretreated mice was compared with those of normal mice. This suppression of virus multiplication was demonstrated in PAC collected during days 1 to 3 of infection but not in PAC collected from day 5 on. PC from MHV-S-pretreated mice were also suppressive to MHV-2 growth in DK cells as compared with PC from normal mice. By treatment of MHV-S-pretreated mice with silica, suppression of virus growth in the liver was partially diminished. These findings suggest that increased suppression of MHV-2 growth in PAC (mostly macrophages) of MHV-S-pretreated mice is responsible for resistance.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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