Major capsid protein synthesis from the genomic RNA of Feline Calicivirus.

Caliciviruses have a positive strand RNA genome with a length of about 7.5 kb that contains 2, 3 or 4 functional ORFs. A subgenomic mRNA (sg-RNA) is transcribed in the infected cell, and both the major capsid protein VP1 and the minor capsid protein VP2 are translated from the sg-RNA. Translation of proteins from the genomic RNA (g-RNA) and from the sg-RNA is mediated by the RNA linked viral protein VPg. Most of the calicivirus genera have translation mechanisms leading to VP1 expression from the g-RNA. For sapoviruses, lagoviruses and neboviruses, VP1 is part of the polyprotein, and for noroviruses a termination/reinitiation mechanism was described. Vesiviruses have no known mechanism for the expression of VP1 from the g-RNA and it is the only genus of the Caliciviridae, that generates VP1 via a precursor protein (LC-VP1). Analyses of feline calicivirus (FCV) g-RNA translation showed a low level of VP1 expression with an initiation downstream of the original start codon of LC-VP1 leading to a smaller tLC-VP1 protein. Deletion and substitution analyses of the region surrounding the LC-VP1 start codon allowed the identification of sequences within the leader protein coding region of FCV that have an impact on VP1 translation frequency from the g-RNA. Introduction of such mutations into the virus showed an impact of strongly reduced tLC-VP1 levels translated from the g-RNA on viral replication. [ABSTRACT FROM AUTHOR]