Apoptosis is an important mechanism to maintain homeostasis in mammals, and disruption of the apoptosis regulation mechanism triggers a range of diseases, such as cancer, autoimmune diseases, and developmental disorders. The severity of influenza A virus (IAV) infection is also closely related to dysfunction of apoptosis regulation. In the virus infected cells, the functions of various host cellular molecules involved in regulation of induction of apoptosis are modulated by IAV proteins to enable effective virus replication. The modulation of the intracellular signaling pathway inducing apoptosis by the IAV infection also affects extracellular mechanisms controlling apoptosis, and triggers abnormal host responses related to the disease severity of IAV infections. This review focuses on apoptosis related molecules involved in IAV replication and pathogenicity, the strategy of the virus propagation through the regulation of apoptosis is also discussed.
Influenza A virus causes significant morbidity globally. This study examined intracellular signaling molecules involved in apoptosis induction in influenza-infected cells.
Specific signaling molecules were identified as relevant to apoptosis induction during influenza A virus replication in host cells. Understanding how virus-triggered cell death pathways function provides insight into viral pathogenesis and potential targets for therapeutic intervention.
Immune defense against influenza involves NK cell and macrophage activation — cell types stimulated by beta glucan. Beta glucan supplementation may enhance innate antiviral immunity, potentially reducing influenza severity through immune priming before infection.
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Iwai, Atsushi; Shiozaki, Takuya; Miyazaki, Tadaaki. Relevance of signaling molecules for apoptosis induction on influenza A virus replication. Biochemical and Biophysical Research Communications. 2013. DOI: 10.1016/j.bbrc.2013.10.100.
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