EtienneSimon-Loriere

The host range of the virus was rapidly evaluated after its emergence with humans, hamster, minks or cats etc… being susceptible, but not mice, as the rodent ACE2 receptor was too different. 2/9

SARS-CoV-2 has accumulated quite a few changes during its extensive circulation, esp. the VOCs discovered in UK, South Africa or Brazil, in particular with N501Y subst. which enhance binding to hACE2 or E484K contributing to partial immune escape (see @jbloom_lab cool work) 3/9

It turns out that these changes (at least) now allow these 3 variants to infect cells expressing murine ACE2. In vivo, only the B.1.351 (SA) and P.1 (Br) were able to replicate to high titer, suggesting that N501Y change is not sufficient in the B.1.1.7 (UK) context. 4/9

This process might not involve only the spike changes, and is a fascinating example of natural host range expansion likely acquired as a by-product of selection in its current host (humans) 5/9

This is great news for in vivo studies as the mice models are incredibly rich and diverse, but it also raises One-health questions (if the virus can be transmitted, rodents as a potential reservoir risk?) that will need to be assessed by the proper experts. 6/9

Great collaborative work with the GMVR lab, @virusfusion007 and our amazing mice expert X. Montagutelli and his colleagues (not on twitter) 7/9

Interestingly, there are speculations on the process of emergence of the VOCs, with 1(improvable) hypothesis of the involvement of immunocompromised individuals where the virus could have accumulated many mutations over a loong course of infection @GuptaR_lab @robertson_lab 8/9