Abstract
Caliciviruses use reinitiation of translation governed by a ‘termination upstream ribosomal binding site’ (TURBS) for expression of their minor capsid protein VP2. Mutation analysis allowed to identify sequences surrounding the translational start/stop site of the feline calicivirus (FCV) that fine tune reinitiation frequency. A selection of these changes was introduced into the infectious FCV cDNA clone to check the influence of altered VP2 levels on virus replication. In addition, full length constructs were established that displayed a conformation, in which VP2 expression occurred under control of a duplicated subgenomic promoter. Viable viruses recovered from such constructs revealed a rather broad range of VP2 expression levels but comparable growth kinetics showing that caliciviruses can tolerate gross changes of the VP2 expression level.
Highlights
The members of the family Caliciviridae represent nonenveloped viruses that are causative for gastrointestinal diseases in humans and different diseases in animals [1]
In the murine Norovirus (MNV) a fourth ORF has been found coding for VF1, a protein involved in counteracting the innate immune response of the host cell
Expression of the minor capsid protein VP2 occurs via a translation termination/reinitiation mechanism governed by the termination upstream ribosomal binding site’ (TURBS) located upstream of the start/stop site within the region coding for the major capsid protein VP1
Summary
The members of the family Caliciviridae represent nonenveloped viruses that are causative for gastrointestinal diseases in humans and different diseases in animals [1]. The genomic RNA is nonsegmented with a length of about 7.5 kb and contains 2 or 3 functional ORFs for members of the genera Lagovirus, Sapovirus and Nebovirus or Vesivirus and Norovirus, respectively [1]. A subgenomic mRNA (sg mRNA) coterminal with the 39 terminal 2.2 kb of the genome is transcribed in the infected cell This sg mRNA carries both VPg and a 39 Poly(A) tail and is packaged into virus particles [8,9]. Both the major capsid protein VP1 of ca. The viral particle contains only a few molecules of VP2, so that this protein can hardly be of structural importance for the capsid. There is so far no convincing hypothesis for the fact that this protein is essential for generation of infectious virus particles [16]
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