Intranasal or intraperitoneal infection with the highly hepatotropic MHV-3 leads to intense liver damage characterized by hepatitis; necrosis; an intense infiltration of macrophages and neutrophils; increased expression of IL-6, TNF, CXCL1, CCL2, and IP-10; high serum levels of alanine aminotransferase (ALT); and death, while infection with MHV-A59 induces a comparable mild and subclinical hepatitis [5,9]. Here, CXCL1 is linked to hepatitis A virus infection.