Key result
Enterovirus infection induces the massive recruitment of all isoforms of small cellular Arf GTPases to replication organelles, with Arf1 being the first recruited and most critical for viral replication.
Why the study?
Specific anti-enterovirus therapeutics are lacking, and the roles of small Arf GTPases in the intracellular membrane remodeling required for viral replication were unclear.
Enterovirus infection induces massive remodeling of cellular membrane pathways, recruiting all isoforms of small cellular Arf GTPases to replication organelles, which may offer new targets for antiviral therapies.
Arf recruitment supports host-targeted antiviral strategies; leaves open isoform-specific inhibition as therapy.
Enteroviruses include many known and emerging pathogens, such as poliovirus, enteroviruses 71 and D68, and others. However, licensed vaccines are available only against poliovirus and enterovirus 71, and specific anti-enterovirus therapeutics are lacking. Enterovirus infection induces the massive remodeling of intracellular membranes and the development of specialized domains harboring viral replication complexes, replication organelles. Here, we investigated the roles of small Arf GTPases during enterovirus infection. Arfs control distinct steps in intracellular membrane traffic, and one of the Arf-activating proteins, GBF1, is a cellular factor required for enterovirus replication. We found that all Arfs expressed in human cells, including Arf6, normally associated with the plasma membrane, are recruited to the replication organelles and that Arf1 appears to be the most important Arf for enterovirus replication. These results document the rewiring of the cellular membrane pathways in infected cells and may provide new ways of controlling enterovirus infections.
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Moghimi et al. (2020) studied Enterovirus infection. Enterovirus infection (Poliovirus, Coxsackievirus B3) vs. Mock-infected cells was evaluated on Recruitment of Arf GTPases to replication organelles and sensitivity to GBF1 inhibition. Enterovirus infection induces the massive recruitment of all isoforms of small cellular Arf GTPases to replication organelles, with Arf1 being the first recruited and most critical for viral replication.
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