Protective mechanisms against murine coronavirus infection in individual mice and its transmission between mice.

Murine coronavirus, commonly known as mouse hepatitis virus (MHV), is a representative pathogenic virus in mice. MHV infection in mice is used as a model for viral infections and is utilized to analyze the mechanisms of protection and transmission. By establishing MHV-specific T cell clones and conducting adoptive transfer experiments in infected mice, it was demonstrated that T cells play a crucial role in the protection against MHV infection and that cytotoxic T lymphocytes induce apoptosis in infected cells and suppress viral production. Furthermore, studies using IFN-γ-deficient C57BL/6 mice demonstrated exacerbation of acute hepatitis, establishment of persistent viral infection, and subsequent death due to subacute granulomatous serositis resembling feline infectious peritonitis in cats, possibly in association with persistent infection and the emergence of immune-escape variants. In contrast, all MHV-infected IFN-γ-deficient BALB/c mice died within a short period due to acute fulminant hepatitis, indicating that genetic background differences significantly influence disease progression. Furthermore, in vitro studies demonstrated that BALB/c mouse hepatocytes are more susceptible to MHV than C57BL/6 mouse hepatocytes. Additionally, the mode of transmission of MHV was experimentally analyzed, and clearly correlated with viral growth in the intestine. Other studies have explored a wide range of topics in relation to MHV infection, including autoimmune responses, genetic susceptibility, and the maintenance of pluripotency in MHV-infected embryonic stem cells. MHV has also been utilized as a surrogate virus for COVID-19 research.