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◆ Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases2026-08-21

A mouse monoclonal antibody against H7N9 influenza virus cross-react with human platelets.

Jingying Sun, Yangmeng Feng, Qing Feng, Yan Li, Haixiang Zhang, Cuixiang Xu

一句话结论 · In one sentence

These findings suggest that the specific antibodies induced by the H7N9 virus may mediate platelet damage through cross-reactivity with platelet autoantigens. This mechanism warrants further investigation to provide experimental evidence for the pathogenesis of secondary ITP associated with H7N9 infection.

原始摘要(英文原文)· Original abstract
OBJECTIVE: To investigate the association and potential mechanisms between H7N9 influenza virus infection or vaccination and immune thrombocytopenia (ITP), providing foundational data for the prevention and treatment of related ITP. METHODS: Using laboratory-prepared anti-H7N9 influenza virus monoclonal antibodies (mAbs) (H7N9-98 and H7N9-120) as research subjects, the interactions between these antibodies and human platelets were analyzed through Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF) techniques. RESULTS: The mAb H7N9-98 exhibited specific binding to human platelets, showing positive results in both IHC and IF assays. Western blotting results demonstrated that this antibody could specifically recognize approximately 60 kDa human platelet proteins. The isotype control mAb H7N9-120 did not exhibit the aforementioned binding reactions, with all test results being negative. CONCLUSION: These findings suggest that the specific antibodies induced by the H7N9 virus may mediate platelet damage through cross-reactivity with platelet autoantigens. This mechanism warrants further investigation to provide experimental evidence for the pathogenesis of secondary ITP associated with H7N9 infection.
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A mouse monoclonal antibody against H7N9 influenza virus cross-react with human platelets. — 科研速览 Science Skim