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- W2313472175 abstract "Coronaviruses (CoV) are vertebrate pathogens that cause common colds, bronchiolitis and acute respiratory distress syndrome. In fact, their relevance increased when the causative agent of the severe acute respiratory syndrome (SARS) was identified as a CoV. CoV E protein is a small transmembrane protein of between 76-109 amino acids in length that modulates coronavirus morphogenesis, tropism and virulence [1]. We sought to elucidate the role of E protein IC activity in virus pathogenesis by combining our knowledge of residues essential for E protein ion conductivity with the manipulation of SARS-CoV genome. To test the contribution of E protein IC activity in virus pathogenesis, two recombinant mouse-adapted SARS CoVs, each containing one single amino acid mutation that suppressed ion conductivity, were engineered. After serial infections, mutant viruses, in general, incorporated compensatory mutations within E gene that rendered active ion channels. Furthermore, IC activity conferred better fitness in competition assays, suggesting that ion conductivity represents an advantage for the virus. Interestingly, mice infected with viruses displaying E protein IC activity, either with the wild-type E protein sequence or with the revertants that restored ion transport, rapidly lost weight and died. In contrast, mice infected with mutants lacking IC activity, which did not incorporate mutations within E gene during the experiment, recovered from disease and most survived. We have shown that SARS-CoV E protein IC activity is a virulence determinant. [1] DeDiego, M.L., et al 2008. Virology 376, 379-389. [2] Verdiá-Báguena C., et al. 2012. Virology. 432: 485-494." @default.
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- W2313472175 date "2015-01-01" @default.
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- W2313472175 title "Relevance of SARS-CoV E Protein Ion Channel Activity in Virus Pathogenesis" @default.
- W2313472175 doi "https://doi.org/10.1016/j.bpj.2014.11.3178" @default.
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