Why the study?
How Enterovirus 71 efficiently assesses its life cycle with elaborate interactions with multiple host factors remains to be elucidated.
Activity-based proteomics identified ATG4B as a key host factor that processes EV71 viral polyprotein, aiding in viral replication.
May offer host-directed EV71 antiviral strategy via ATG4B; leaves open human translation from animal data.
Enterovirus 71 (EV71), one of the major pathogens of human HFMD, has caused outbreaks worldwide. How EV71 efficiently assesses its life cycle with elaborate interactions with multiple host factors remains to be elucidated. In this work, we deconvoluted that the host ATG4B protein processes the viral polyprotein with its cysteine protease activity and helps EV71 replicate through a chemical biology strategy. Our results not only further the understanding of the EV71 life cycle but also provide a sample for the usage of activity-based proteomics to reveal host-pathogen interactions.
No takes yet. Share an insight, caveat, or question.
Sun et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: