Comparative influenza protein interactomes identify the role of plakophilin 2 in virus restriction
Open/View files
Date
2017
Author(s)
Wang, Lingyan
Li, Wenjun
Patil, Girish
Liu, Lin
Li, Shitao
Publisher
Nature Publishing Group
The Harvard community has made this article openly available. Please share how this access benefits you.
Citation
Wang, Lingyan, Bishi Fu, Wenjun Li, Girish Patil, Lin Liu, Martin E. Dorf, and Shitao Li. 2017. “Comparative influenza protein interactomes identify the role of plakophilin 2 in virus restriction.” Nature Communications 8 (1): 13876. doi:10.1038/ncomms13876. http://dx.doi.org/10.1038/ncomms13876.
Abstract
Cellular protein interaction networks are integral to host defence and immune signalling pathways, which are often hijacked by viruses via protein interactions. However, the comparative virus–host protein interaction networks and how these networks control host immunity and viral infection remain to be elucidated. Here, we mapped protein interactomes between human host and several influenza A viruses (IAV). Comparative analyses of the interactomes identified common and unique interaction patterns regulating innate immunity and viral infection. Functional screening of the ‘core‘ interactome consisting of common interactions identified five novel host factors regulating viral infection. Plakophilin 2 (PKP2), an influenza PB1-interacting protein, restricts IAV replication and competes with PB2 for PB1 binding. The binding competition leads to perturbation of the IAV polymerase complex, thereby limiting polymerase activity and subsequent viral replication. Taken together, comparative analyses of the influenza–host protein interactomes identified PKP2 as a natural inhibitor of IAV polymerase complex.
Other Available Sources
Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material (LAA), as set forth at Terms of Service
Collection