Non-enveloped, spherical, capsid of about 35 nm with T=3 icosahedral symmetry. Surface projections are small and surface appears rough, spikes protruding from the 30 vertices.
The capsid precursor protein (180 copies per particle) undergoes C-terminal cleavages by host caspases during virus maturation. Infectious particles are generated by further cleavages of VP70 by extracellular proteases resulting in three structural proteins .
Monopartite, linear ssRNA(+) genome of 6.8-7kb in size. The 5’-terminus is linked to a VPg protein and the 3’-terminus has a poly(A) tract.
The virion RNA is infectious and serves as both the genome and viral messenger RNA. The genome contains three overlapping open reading frames (ORF1a, ORF1b, and ORF2). The nonstructural proteins are translated from the genomic RNA as two large polyproteins, nsP1a and nsP1a/1b, through a translational ribosomal frameshifting mechanism. ORF1a and ORF1b encode the viral protease and polymerase respectively (and probably other proteins involved in genome replication). ORF2 is expressed from a subgenomic RNA and encodes the VP90 capsid precursor protein.
- Attachement to host receptors probably mediates endocytosis of the virus into the host cell.
- Uncoating, and release of the viral genomic RNA into the cytoplasm.
- Viral RNA is translated into two processed polyproteins to produce replication proteins.
- Replication occurs in viral factories made of membrane vesicles derived from the ER. A dsRNA genome is synthesized from the genomic ssRNA(+).
- The dsRNA genome is transcribed/replicated thereby providing viral mRNAs/new ssRNA(+) genomes.
- Subgenomic RNA translation gives rise to the capsid protein precursor.
- Assembly of new virus particles.
- Non-lytic virus release and maturation of the capsid by proteolytic cleavages.