Comparative influenza protein interactomes identify the role of plakophilin 2 in virus restriction

Lingyan Wang, Bishi Fu, Wenjun Li, Girish Patil, Lin Liu, Martin E. Dorf and Shitao Li ()
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Lingyan Wang: Oklahoma State University
Bishi Fu: Harvard Medical School
Wenjun Li: School of Stomatology, Peking University
Girish Patil: Oklahoma State University
Lin Liu: Oklahoma State University
Martin E. Dorf: Harvard Medical School
Shitao Li: Oklahoma State University

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms13876

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