Key result
Encephalomyocarditis virus (EMCV) replication is AUF1 independent, and unlike enterovirus infections, AUF1 is not cleaved during EMCV infection, suggesting it selectively targets Enteroviruses.
AUF1 does not act broadly as an inhibitor of all picornavirus infections but may selectively target members of the genus Enterovirus.
During infection by picornaviruses, the cellular environment is modified to favour virus replication. This includes the modification of specific host proteins, including the recently discovered viral proteinase cleavage of mRNA decay factor AU-rich binding factor 1 (AUF1). This cellular RNA-binding protein was shown previously to act as a restriction factor during poliovirus, rhinovirus and coxsackievirus infection. During infection by these viruses, AUF1 relocalizes to the cytoplasm and is cleaved by the viral 3C/3CD proteinase. In this study, we demonstrated that replication of encephalomyocarditis virus (EMCV), a picornavirus belonging to the genus Cardiovirus, is AUF1 independent. During EMCV infection, AUF1 relocalized to the cytoplasm; however, unlike what is seen during enterovirus infections, AUF1 was not cleaved to detectable levels, even at late times after infection. This suggests that AUF1 does not act broadly as an inhibitor of picornavirus infections but may instead act as a selective restriction factor targeting members of the genus Enterovirus.
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Cathcart et al. (2014) studied Picornavirus infection. Encephalomyocarditis virus (EMCV) infection vs. Enterovirus infections was evaluated on AUF1 cleavage and restriction factor activity. Encephalomyocarditis virus (EMCV) replication is AUF1 independent, and unlike enterovirus infections, AUF1 is not cleaved during EMCV infection, suggesting it selectively targets Enteroviruses.
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