Genome rearrangements of rotaviruses
Rotaviruses (and other members of the Reoviridae family) undergo rearrangements of their genomes. This review describes evidence of rearranged genomes in rotaviruses. Their structure and functions are reviewed. Possible mechanisms of their emergence are d
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VIrology
Arch Virol (1996) [Suppl] 12: 37-51
© Springer-Verlag 1996
Genome rearrangements of rota viruses lJ. I>esselberger
Clinical Microbiology and Public Health Laboratory, Addenbrooke's Hospital, Cambridge, UK
Summary. Rotaviruses (and other members of the Reoviridae family) undergo
rearrangements of their genomes. This review describes evidence of rearranged genomes in rotaviruses. Their structure and functions are reviewed. Possible mechanisms of their emergence are discussed, and the significance of genome rearrangements for viral evolution is considered. Introduction
Rotaviruses are one out of 9 genera of the Reoviridae family infecting a wide
variety of vertebrate species including man [36a]. They are the main cause of infantile gastroenteritis in man and also of acute diarrhoea in the young of many mammalian species. Rotaviruses possess a characteristic double-shelled icosahedral capsid surrounding a core ribonucleoprotein. Both capsids are perforated by numerous channels; the outer capsid carries 5 dozen short spikes [16, 36a]. The genome of rotaviruses consists of 11 segments of double-stranded (ds) RNA molecules ranging in size between 667 and 3302 base pairs (bps) and yielding a total molecular size of appr. 18550 bps. Gene-protein assignments have been completed for several strains [16, 36a]. Rotaviruses replicate totally in the cytoplasm of infected cells. The viral core contains the viral RNA-dependent RNA polymerase complex which ensures the formation of capped (non-polyadenylated) mRNA. The transcripts are used for both protein translation and as templates for minus strand RNA synthesis in nascent subviral particles. Those acquire their outer capsid proteins by budding from aggregates termed "viroplasm" through the membrane of the endoplasmic reticulum. Particle release is by cell lysis. Details of replication including involvement of different viral proteins at the different steps are described in [16]. The multi-segmented nature of the viral genome allows reassortment on a large scale in doubly infected cells. Rotavirus classification is based on serology and gene composition of three major structural proteins:
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U. Desselberger
- VP6, the inner capsid protein coded for by RNA 6, determines group and subgroup specificity. At least seven groups (A-G) and, within group A, at least 4 different subgroups (I, II, I + II, non-I, non-II) have been identified; - VP7, the major outer capsid protein coded for by RNA 7,8 or 9 (depending on the virus strain), is a glycoprotein and determines VP7-specific serotype (G type). So far 14 different G types have been identified; - VP4, the outer capsid protein forming dime ric spikes and coded for by RNA 4, is a protease-sensitive protein and determines VP4-specific serotype (P type). So far over 20 different P types have been differentiated genotypically, but not all of them have been clearly identified as different serotypes. Designation of strains is illustrated by the following examples (for details see [16]: - A/hu/Wa G IPIA [8J, the human rotav
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