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Nearly every cell in the human body has the capacity to respond to a viral infection with the production of interferons—critical components of cell intrinsic immunity that drive resolution of disease, and, unfortunately, much of the resultant immunopathology. Unsurprisingly, viruses circumvent, co-opt, or otherwise subvert the induction of an antiviral state. Regardless, no defense (or offense) is perfect, and viral populations almost invariably induce interferon in a small fraction of infected cells. Some of this rarity of response is driven by rare viral failure to suppress interferon, in part due to the extreme variation evinced by many viral populations. However, the rarity of response is also partially explained by intrinsic host mechanisms suppressing spurious activation—seeking to avoid the resultant cost from an overly sensitive triggering of inflammatory processes.
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论文共 33 篇作者统计合作学者相似作者
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Jordan N. Ranum, Mitchell P. Ledwith,Fadi G. Alnaji,Meghan Diefenbacher,Richard Orton,Elizabeth Sloan, Melissa Guereca, Elizabeth M. Feltman,Katherine Smollett,Ana da Silva Filipe,Michaela Conley,Alistair B. Russell,
PLOS PATHOGENSno. 1 (2024): e1011898-e1011898
biorxiv(2022)
crossref(2022)
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