This article is a preprint and has not been certified by peer review.
Posted March 18, 2021.
Xavier Montagutelli, Matthieu Prot, Laurine Levillayer, Eduard Baquero Salazar, Gregory Jouvion, Laurine Conquet, Flora Donati, Melanie Albert, Fabiana Gambaro, Sylvie Behillil, Vincent Enouf, Dominique Rousset, Jean Jaubert, Felix Rey, Sylvie van der Werf, Etienne Simon-Loriere
doi: https://doi.org/10.1101/2021.03.18.436013
Abstract
Receptor recognition is a major determinant of viral host range, as well as infectivity and pathogenesis. Emergences have been associated with serendipitous events of adaptation upon encounters with a novel host, and the high mutation rate of RNA viruses has been proposed to explain their frequent host shifts. SARS-CoV-2 extensive circulation in humans has been associated with the emergence of variants, including variants of concern (VOCs) with diverse mutations in the spike and increased transmissibility or immune escape. Here we show that unlike the initial virus, VOCs are able to infect common laboratory mice, replicating to high titers in the lungs. This host range expansion is explained in part by the acquisition of changes at key positions of the receptor binding domain that enable binding to the mouse angiotensin-converting enzyme 2 (ACE2) cellular receptor, although differences between viral lineages suggest that other factors are involved in the capacity of SARS-CoV-2 VOCs to infect mice. This abrogation of the species barrier raises the possibility of wild rodent secondary reservoirs and provides new experimental models to study disease pathophysiology and countermeasures.
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https://www.biorxiv.org/content/10.1101/2021.03.18.436013v1.full.pdf+html
Posted March 18, 2021.
Xavier Montagutelli, Matthieu Prot, Laurine Levillayer, Eduard Baquero Salazar, Gregory Jouvion, Laurine Conquet, Flora Donati, Melanie Albert, Fabiana Gambaro, Sylvie Behillil, Vincent Enouf, Dominique Rousset, Jean Jaubert, Felix Rey, Sylvie van der Werf, Etienne Simon-Loriere
doi: https://doi.org/10.1101/2021.03.18.436013
Abstract
Receptor recognition is a major determinant of viral host range, as well as infectivity and pathogenesis. Emergences have been associated with serendipitous events of adaptation upon encounters with a novel host, and the high mutation rate of RNA viruses has been proposed to explain their frequent host shifts. SARS-CoV-2 extensive circulation in humans has been associated with the emergence of variants, including variants of concern (VOCs) with diverse mutations in the spike and increased transmissibility or immune escape. Here we show that unlike the initial virus, VOCs are able to infect common laboratory mice, replicating to high titers in the lungs. This host range expansion is explained in part by the acquisition of changes at key positions of the receptor binding domain that enable binding to the mouse angiotensin-converting enzyme 2 (ACE2) cellular receptor, although differences between viral lineages suggest that other factors are involved in the capacity of SARS-CoV-2 VOCs to infect mice. This abrogation of the species barrier raises the possibility of wild rodent secondary reservoirs and provides new experimental models to study disease pathophysiology and countermeasures.
Preview PDF for full content
https://www.biorxiv.org/content/10.1101/2021.03.18.436013v1.full.pdf+html
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