Abstract
Noroviruses are highly diverse viruses that are the major viral cause of acute gastroenteritis in humans. Although these viruses can infect multiple mammalian species, their potential for zoonosis is not well understood, especially within Genogroup IV (GIV), which contains viruses that infect humans, canines, and felines. The study of GIV viruses has been, in part, hindered by the limited number of complete genomes. Here, we developed a full-genome amplicon-based platform that facilitated the sequencing of canine noroviruses circulating in the United States. Eight novel nearly full-length canine norovirus genomes and two nearly complete VP1 sequences, including four GIV.2, three GVI.1, and three GVI.2 viruses, were successfully obtained. Only animal strains exhibited GVI/GIV chimeric viruses, demonstrating restrictions in norovirus recombination. Using genomic, phylogenetic, and structural analyses, we show that differences within the major capsid protein and the non-structural proteins of GIV and GVI noroviruses could potentially limit cross-species transmission between humans, canines, and felines.
Highlights
Noroviruses are a highly diverse group of viruses from the Caliciviridae family
Samples positive for noroviruses were tested for full-genome sequencing by using primers that anneal to the conserved end and the 30 poly-A tail of the genomes (Figure 1A)
Numerous attempts have been made to develop animal models to study human noroviruses, with varying success [33,34,35,36,37,38,39], but this strong segregation at the host level could be involved in limiting the robustness of most of these models
Summary
Noroviruses are a highly diverse group of viruses from the Caliciviridae family. They have a positive-sense RNA genome of approximately 7.5 kilobases that is organized into at least three open reading frames (ORFs). ORF2 encodes the major capsid protein, VP1, which forms the virus capsid. ORF3 encodes the minor capsid protein, VP2, which is thought to play a role in capsid stabilization and viral entry [5,6,7]. Both VP1 and VP2 are expressed from a subgenomic RNA
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