期刊
NATURE MICROBIOLOGY
卷 4, 期 6, 页码 914-924出版社
NATURE RESEARCH
DOI: 10.1038/s41564-019-0421-x
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资金
- National Institutes of Health [R01 AI138797, R01AI107301]
- American Cancer Society [RSG-15-04801-MPC]
- Burroughs Wellcome Fund Award for Investigators in Pathogenesis
- New Jersey Health Foundation
- US Department of Defense [W81XWH18'10237]
- Princeton University
- National Institute of General Medicine Sciences of the National Institutes of Health [T32GM007388]
- National Science Foundation
Interferon (IFN)-mediated antiviral responses are central to host defence against viral infection. Despite the existence of at least 20 IFNs, there are only three known cell surface receptors. IFN signalling and viral evasion mechanisms form an immensely complex network that differs across species. In this Review, we begin by highlighting some of the advances that have been made towards understanding the complexity of differential IFN signalling inputs and outputs that contribute to antiviral defences. Next, we explore some of the ways viruses can interfere with, or circumvent, these defences. Lastly, we address the largely under-reviewed impact of IFN signalling on host tropism, and we offer perspectives on the future of research into IFN signalling complexity and viral evasion across species.
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