Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10756959 | Biochemical and Biophysical Research Communications | 2013 | 7 Pages |
Abstract
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.
Keywords
IAVtumor necrosis factor receptor type 1-associated DEATH domain proteinTNF-α receptor 1DAP3IFN regulatory factor 3IPS-1c-jun amino-terminal kinaseXIAPTRADDDR5DR4RIG-IIRF3NS1FADDAPAf-1NF-κBPI3KJnkBcl-2v-akt murine thymoma viral oncogene homolog 1AktinterferonIFNBaxtumor necrosis factor αFas-associated death domainApoptosisapoptotic protease activating factor 1TNF-αnuclear factor-κBphosphatidylinositol-3 kinaseTRAILB-cell lymphoma 2TNF-related apoptosis inducing ligandneuraminidaseSignal transductionNucleoproteinBcl-2 homologyInfluenza A virusBcl-2-associated X proteinX-linked Inhibitor of Apoptosis ProteinNon-structural protein 1matrix proteinretinoic acid-inducible gene-ICaspasesDeath receptor 4death receptor 5
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Authors
Atsushi Iwai, Takuya Shiozaki, Tadaaki Miyazaki,