Background: Enterovirus 71 (EV71) infection occasionally causes severe neurological diseases manifesting as aseptic meningitis, encephalitis or poliomyelitis-like paralysis. Its pathogenesis is still unclear. Some researches indicated that EV71 induced IgG cross-reacted with human brain tissues[1]. However, its significance remains controversial for vaccine designing. In our EV71 infected mouse model, we find that a large amount of endogenous IgG exists in the skeletal muscle tissues.
Result: 7-week-old BALB/c mice were infected with an EV71 strain. These mice presented progressive paralysis within 7 days post infection. Histological and ultrastructural findings revealed severe degeneration and necrosis of skeletal muscle tissues. Immunohistochemistry and immunofluorescence staining showed that EV71 antigen and endogenous IgG were mainly detected in skeletal muscle tissues, indicating that both the EV71 and endogenous IgG contributed to the muscle injury.
Conclusion: Muscle injury is the main feature of our EV71 infected mouse model. Besides the virus itself, endogenous IgG, which is observed in the mouse skeletal muscle tissues , is one of the pathogenic factors. We speculate that the endogenous IgG may be induced by EV71 and cross-react with the mouse skeletal muscle, contributing to the muscle injury. Further study is required to verify this speculation.
(Corresponding author: Hong Shen)
Funding:
1. Specialized Research Fund for the Doctoral Program of Higher Education, 20124433110009
2. Guangdong Natural Science Foundation, S2012010009540