Genetic determinants of susceptibility to coxsackievirus B1-induced chronic inflammatory myopathy: Effects of host background and major histocompatibility complex genes

摘要: Infection of outbred CD-1 mice with the Tucson strain coxsackievirus B1 (CVB1T) leads to development chronic hind limb weakness and associated inflammatory muscle disease. Host factors that influence susceptibility have not been studied in this mouse model myopathy (IM). Therefore, pathogenesis was examined by using different inbred strains mice. Initially, seven either H-2d or H-2b major histocompatibility complex (MHC) haplotype were evaluated. All showed similar levels acute mortality caused viral infection, but inflammation did develop two B6 background, regardless their MHC haplotype. In susceptible mice, more likely than Based on these results, H-2 congenic B10 background (C57BL/10 B10.D2) resistant (C57BL/6 B6.C-H2d) greater detail. During kinetics degree replication among strains. By 4 weeks after intense pathology observed those Resistant show signs calcification, they exhibit some myopathic features, including centralized nuclei variations myofiber size shape. These changes less common significant when compared uninfected controls. Viral RNA persistence elevated titers antiviral IgG prevalent restricted studies demonstrate host genes confer resistance IM also disease severity. They reveal CVB1T infection is under genetic control which mediates post-viral IM.