Identification of novel genes associated with duck OASL in response to influenza A virus

Wang, Xiaoxue; Lu, Chao; Rong, Enguang; Hu, Jiaxiang; Xing, Yanling; Liu, Zhengyu; Gao, Chu-ze; Liu, Jinhua; Huang, Yinhua

doi:10.1016/s2095-3119(19)62685-7

Cited by 2 publications

(1 citation statement)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chicken IRF7 (chIRF7) is involved in antiviral responses and plays analogous roles to that of mammalian IRF3. Recent studies have found that chIRF7 can be induced to translocate across the nucleus downstream of both chMAVS and chicken stimulator of interferon genes (chSTING), and chIRF7 dimerizes following chTBK1 activation, allowing it to increase IFN-β signaling (Wang et al, 2019). Initial experiments investigating function found that overexpression of chIRF7 increased IFN-β expression (Kim and Zhou, 2015).…”

Section: Irf7mentioning

confidence: 99%

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens

Campbell

Magor

2020

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Mallard ducks are a natural host and reservoir of avian Influenza A viruses. While most influenza strains can replicate in mallards, the virus typically does not cause substantial disease in this host. Mallards are often resistant to disease caused by highly pathogenic avian influenza viruses, while the same strains can cause severe infection in humans, chickens, and even other species of ducks, resulting in systemic spread of the virus and even death. The differences in influenza detection and antiviral effectors responsible for limiting damage in the mallards are largely unknown. Domestic mallards have an early and robust innate response to infection that seems to limit replication and clear highly pathogenic strains. The regulation and timing of the response to influenza also seems to circumvent damage done by a prolonged or dysregulated immune response. Rapid initiation of innate immune responses depends on viral recognition by pattern recognition receptors (PRRs) expressed in tissues where the virus replicates. RIG-like receptors (RLRs), Toll-like receptors (TLRs), and Nod-like receptors (NLRs) are all important influenza sensors in mammals during infection. Ducks utilize many of the same PRRs to detect influenza, namely RIG-I, TLR7, and TLR3 and their downstream adaptors. Ducks also express many of the same signal transduction proteins including TBK1, TRIF, and TRAF3. Some antiviral effectors expressed downstream of these signaling pathways inhibit influenza replication in ducks. In this review, we summarize the recent advances in our understanding of influenza recognition and response through duck PRRs and their adaptors. We compare basal tissue expression and regulation of these signaling components in birds, to better understand what contributes to influenza resistance in the duck.

show abstract

Section: Irf7mentioning

confidence: 99%