Key result
The host restriction factor A3G inhibits the replication of Enterovirus D68, but not CA6, by competitively binding to the 5' untranslated region with PCBP1.
Why the study?
Enteroviruses such as CA6 and EVD68 occur sporadically or spread worldwide, necessitating more information to develop broad-spectrum anti-EV inhibitors.
A3G inhibits EVD68 replication by competitively binding its 5' UTR with PCBP1, revealing a mechanism of host restriction against enteroviruses.
No immediate clinical application for enteroviral infections; extends mechanistic insight into selective A3G restriction but requires validation.
As the two major pathogens causing hand, foot, and mouth disease (HFMD), enterovirus 71 (EV71) and coxsackievirus A16 (CA16) attract a lot of attention for the study of their pathogenesis, their involvement with cellular proteins, and so on. However, other EVs such as CA6 and EVD68 constantly occur sporadically or have spread worldwide in recent years. Therefore, more information related to these EVs is needed in order to develop a broad-spectrum anti-EV inhibitor. In this study, we first reveal that the protein poly(C)-binding protein 1 (PCBP1), involved in PV- and EV71 virus replication, is also required for the replication of EVD68, but not for the replication of CA6. Next, we found that the host-restriction factor A3G specifically inhibits the replication of EVD68, but not the replication of CA6, by competitively binding to the 5' UTR of EVD68 along with PCBP1. Our findings broaden knowledge related to EV replication and the interplay between EVs and host factors.
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Li et al. (2021) studied Enterovirus D68 infection (in vitro). APOBEC3G (A3G) overexpression vs. Control vector was evaluated on Viral replication (VP1 expression, viral mRNA levels, and viral titers). The host restriction factor A3G inhibits the replication of Enterovirus D68, but not CA6, by competitively binding to the 5' untranslated region with PCBP1.
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