Acute hepatic failure in IFN-γ-deficient BALB/c mice after murine coronavirus infection

Abstract

We previously showed that an intraperitoneal infection with mouse hepatitis virus (MHV) persists in interferon-gamma (IFN-gamma)-deficient C57BL/6 (B6-GKO) mice and results in subacute fatal peritonitis, which bears a resemblance to feline infectious peritonitis. To examine the role of other host factors in MHV infection in mice, IFN-gamma-deficient mice with a BALB/c background (BALB-GKO) were infected intraperitoneally with MHV and compared with B6-GKO mice. In contrast to B6-GKO mice, BALB-GKO mice died within 1 week due to acute hepatic failure. The viral titer of the liver in BALB-GKO mice was significantly higher than that in B6-GKO mice. All hepatocytes in BALB-GKO mice were necrotic at 5 days post-infection, which was clearly distinct from large but limited lesion in the liver from infected B6-GKO mice. The serum alanine aminotransferase activity of infected BALB-GKO mice were higher than that of B6-GKO mice and was paralleled with the severity of the pathological changes and viral titers in infected mice. Administration of exogenous IFN-gamma to BALB-GKO partially inhibited the acute death. These results indicate that BALB-GKO and B6-GKO mice clearly show different diseases following MHV infection, although wild type counterparts of both mice apparently showed the same clinical course after MHV infection.

Indirect ELISA and Indirect Immunofluorescent Antibody Assay for Detecting the Antibody against Murine Norovirus S7 in Mice

“…Several studies have indicated that resistance against viral infections is dependent on mouse strain [1,8,9,11,17]. Namely, numerous host factors, both major histocompatibility complex (MHC)-dependent and MHCindependent, account for viral resistance.…”

Production of protective gamma interferon by natural killer cells during early mouse hepatitis virus infection

“…Gamma interferon (IFN-c) is required for the protection against lethal infection with MHV-JHM and -A59 (Kyuwa et al, 1998(Kyuwa et al, , 2002Schijns et al, 1996Schijns et al, , 1998Smith et al, 1991). Both viral replication and hepatocellular injury are increased after infection of IFN-c receptor-deficient mice with MHV-A59 (Schijns et al, 1996).…”

Recombinant Mouse Hepatitis Virus Strain A59 from Cloned, Full-Length cDNA Replicates to High Titers In Vitro and Is Fully Pathogenic In Vivo

“…The A59 strain of MHV (MHV-A59) was isolated in 1961 from a colony of BALB/c mice that was being used to serially propagate leukemia (22). There are a number of different animal disease models based upon MHV infection, including models of virus-associated demyelination and viral hepatitis (12,18). These models provide important insights into the pathogenesis of virus infections.…”