Why the study?
Understanding the prerequisites of efficient calicivirus replication is crucial to develop strategies for prevention and treatment of related diseases.
This study provides the first evidence that a member of the genus Vesivirus has a translation initiation mechanism by which a precursor protein of the VP1 major capsid protein is expressed from the genomic RNA, pointing to a functional role in early replication.
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Broadens calicivirus VP1 translation mechanisms to vesiviruses; extends prior models but leaves open therapeutic targeting.
Caliciviruses are a cause of important diseases in humans and animals. It is crucial to understand the prerequisites of efficient replication of these viruses in order to develop strategies for prevention and treatment of these diseases. It was shown before that all caliciviruses except vesiviruses have established mechanisms to achieve major capsid protein (VP1) translation from the genomic RNA. Here, we show for the first time that a member of the genus Vesivirus also has a translation initiation mechanism by which a precursor protein of the VP1 protein is expressed from the genomic RNA. This finding clearly points at a functional role of the calicivirus VP1 capsid protein in early replication, and we provide experimental data supporting this hypothesis.
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Urban et al. (2020) studied this question.
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