"Our new preprint where we show that SARS-CoV-2 VOCs are able to infect mice" | The B1.351 and P.1 variants extend SARS-CoV-2 host range to mice - bioRxiv | Sars-cov-2 in animals | Wild rodent secondary reservoirs of sars-cov-2
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RT @YourDailyCurse: @mikenov twitter.com/ArisKatzouraki… by elalege (YourDailyCurse)
@mikenov twitter.com/ArisKatzouraki…
Very interesting thread on the work from @SimonLoriereLab & coworkers on the possibility of extension of the host range of P1 & B1351 to rodents. twitter.com/SimonLoriereLa…
14 likes, 3 retweets
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Our new preprint where we show that SARS-CoV-2 VOCs are able to infect mice is out. Collaborative work @institutpasteur *not peer reviewed yet*, short 🧵
biorxiv.org/cgi/content/sh… 1/9
742 likes, 314 retweets
sars-cov-2 in rats and mice - Google Search google.com/search?q=sars-… news-medical.net/news/20210308/…
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SARS-CoV-2 infection, neuropathogenesis and transmission ...
The B1.351 and P.1 variants extend SARS-CoV-2 ... - bioRxiv
The B1.351 and P.1 variants extend SARS-CoV-2 ... - bioRxiv
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The B1.351 and P.1 variants extend SARS-CoV-2 host range to mice
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 1. 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 2. 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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