Key result
EV71 infection significantly altered approximately 17% of over 4100 monitored host cell proteins at 8 or 20 hours post-infection (p<0.01), identifying CHCH2 as a regulator of innate immunity.
p-value: p=<0.01
A triple-SILAC proteomics study of EV71 infection identified significant host proteome changes and revealed CHCH2 as a negative regulator of innate immune responses.
May inform antiviral target discovery; leaves open validation in prospective models before clinical translation.
Enterovirus 71 (EV71), a member of Picornaviridae, causes severe neurological and systemic illness in children. To better understand the virus-host cell interactions, we performed a triple-SILAC-based quantitative proteomics study monitoring host cell proteome changes after EV71 infection. Based on the quantitative data for more than 4100 proteins, ∼17% of the proteins were found as significantly changed (p<0.01) at either 8 or 20 hours post infection. Five biological processes and seven protein classes showed significant differences. Functional screening of nine regulated proteins discovered the regulatory role of CHCH2, a mitochondrial protein known as a transcriptional activator for cytochrome c oxidase, in EV71 replication. Further studies showed that CHCH2 served as a negative regulator of innate immune responses. All MS data have been deposited in the ProteomeXchange with identifier PXD002483 (http://proteomecentral.proteomexchange.org/dataset/PXD002483).
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Li et al. (2015) studied Enterovirus 71 (EV71) infection. EV71 infection was evaluated on Host cell proteome changes (p=<0.01). EV71 infection significantly altered approximately 17% of over 4100 monitored host cell proteins at 8 or 20 hours post-infection (p<0.01), identifying CHCH2 as a regulator of innate immunity.
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