These findings indicate that selective forces have favoured the accumulation of hepadnaviral sequences at specific loci in the saurian germline. We also show that eHBVs have been intra-genomically amplified in some saurian lineages, and that eHBVs located at approximately equivalent genomic loci have been acquired in entirely distinct germline integration events. Furthermore, we provide a completely new perspective on hepadnavirus evolution by showing that the metahepadnaviruses (genus Metahepadnavirus ) originated >300 million years ago in the Paleozoic Era, and has historically infected a broad range of vertebrates. Through in-depth characterisation of eHBV elements we establish the existence of four distinct subgroups within the genus Avihepadnavirus and trace their evolution through the Cenozoic Era. We show that germline incorporation of hepadnaviruses is exclusive to a single vertebrate group (Sauria) and that the eHBVs contained in saurian genomes represent a far greater diversity of hepadnaviruses than previously recognised. Here, we use a novel, data-oriented approach to recover and analyse the complete repertoire of eHBV elements in published animal genomes. Vertebrate genomes contain DNA sequences derived from ancient hepadnaviruses, and these ‘endogenous hepatitis B viruses’ (eHBVs) reveal aspects of the long-term coevolutionary relationship between hepadnaviruses and their vertebrate hosts. Hepadnaviruses (family Hepadnaviviridae ) are reverse-transcribing animal viruses that infect vertebrates. Our investigation provides a range of new insights into the long-term evolutionary history of reverse-transcribing DNA viruses and shows that germline incorporation of hepadnaviruses has played a role in shaping the evolution of saurian genomes.
Furthermore, we provide a completely new perspective on hepadnavirus evolution by showing that the metahepadnaviruses (genus Metahepadnavirus) originated >300 million years ago in the Paleozoic Era and have historically infected a broad range of vertebrates. DNA sequences derived from ancient hepadnaviruses have been identified in the germline genome of numerous vertebrate species, and these ‘endogenous hepatitis B viruses’ (eHBVs) reveal aspects of the long-term coevolutionary relationship between hepadnaviruses and their vertebrate hosts. Hepadnaviruses (family Hepadnaviviridae) are reverse-transcribing animal viruses that infect vertebrates.
Thus, our findings not only help to explain the poor interferon response in COVID-19 patients but also describe the emergence of natural SARS-CoV-2 quasispecies with an extended ORF3b gene that may potentially affect COVID-19 pathogenesis. This variant was isolated from two patients with severe disease and further increased the ability of ORF3b to suppress interferon induction. Furthermore, analyses of approximately 17,000 SARS-CoV-2 sequences identify a natural variant in which a longer ORF3b reading frame was reconstituted. Phylogenetic analyses and functional assays reveal that SARS-CoV-2-related viruses from bats and pangolins also encode truncated ORF3b gene products with strong anti-interferon activity. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of type I interferon more efficiently than its SARS-CoV ortholog. One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene.
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