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Updated: May 1, 2026
MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Differential restriction patterns of mRNA decay factor AUF1 during picornavirus infections
Andrea L Cathcart1, Bert L Semler1
1Department of Microbiology and Molecular Genetics, School of Medicine, University of California, Irvine, CA 92697, USA.
Abstract:
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.
Insights
Encephalomyocarditis virus (EMCV) replication is independent of the host protein AU-rich binding factor 1 (AUF1). Unlike enteroviruses, EMCV does not cleave AUF1, suggesting AUF1 selectively targets enteroviruses, not all picornaviruses.
Area of Science:
- Virology
- Molecular Biology
- Host-Pathogen Interactions
Background:
- Picornaviruses manipulate host cells for replication, including modifying host proteins like AU-rich binding factor 1 (AUF1).
- AUF1 acts as a restriction factor against certain picornaviruses (poliovirus, rhinovirus, coxsackievirus) by relocalizing and being cleaved by viral proteinases.
- This cleavage is a key mechanism by which these viruses overcome AUF1-mediated restriction.
Purpose of the Study:
- To investigate the role of AUF1 during encephalomyocarditis virus (EMCV) infection, a Cardiovirus genus member.
- To determine if EMCV infection leads to AUF1 cleavage, similar to enteroviruses.
- To ascertain if AUF1 functions as a broad inhibitor of picornavirus replication.
Main Methods:
- Infection of cells with EMCV.
- Monitoring the cellular localization of AUF1.
- Assessing AUF1 cleavage by viral proteinases during EMCV infection using Western blotting or similar techniques.
- Comparing AUF1 behavior during EMCV infection with its behavior during enterovirus infections.
Main Results:
- EMCV infection caused AUF1 to relocalize to the cytoplasm.
- Unlike enterovirus infections, AUF1 was not significantly cleaved during EMCV infection, even at late stages.
- EMCV replication proceeded effectively without detectable AUF1 cleavage.
Conclusions:
- Encephalomyocarditis virus (EMCV) replication is independent of AUF1-mediated restriction.
- AUF1 does not act as a broad-spectrum inhibitor for all picornaviruses.
- AUF1 appears to be a selective restriction factor, primarily targeting members of the Enterovirus genus within the Picornaviridae family.
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