I'm not a virologist and don't pretend to be. But I can read a fugging manual with the best of them, and understand what I've read. That said, slowly reread the nature paper from 2015 yourself.
Therefore, to examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs, we built a chimeric virus encoding a novel, zoonotic CoV spike protein—from the RsSHC014-CoV sequence that was isolated from Chinese horseshoe bats1—in the context of the SARS-CoV mouse-adapted backbone. The hybrid virus allowed us to evaluate the ability of the novel spike protein to cause disease independently of other necessary adaptive mutations in its natural backbone. Using this approach, we characterized CoV infection mediated by the SHC014 spike protein in primary human airway cells and in vivo, and tested the efficacy of available immune therapeutics against SHC014-CoV. Together, the strategy translates metagenomics data to help predict and prepare for future emergent viruses.
Shi Zhengli - you know you done f'd up....,
Mebbe what I'm watching from other "gain of function" virologists is a poster-child instance of the Weinstein's Distributed Information Suppression Complex?
The Proximal Origin of SARS-C0V2
virological | Since the first reports of a novel pneumonia (COVID-19) in
Wuhan city, Hubei province, China there has been considerable discussion
and uncertainty over the origin of the causative virus, SARS-CoV-2.
Infections with SARS-CoV-2 are now widespread in China, with cases in
every province. As of 14 February 2020, 64,473 such cases have been
confirmed, with 1,384 deaths attributed to the virus. These official
case numbers are likely an underestimate because of limited reporting of
mild and asymptomatic cases, and the virus is clearly capable of
efficient human-to-human transmission. Based on the possibility of
spread to countries with weaker healthcare systems, the World Health
Organization has declared the COVID-19 outbreak a Public Health
Emergency of International Concern (PHEIC). There are currently neither
vaccines nor specific treatments for this disease.
SARS-CoV-2 is the seventh member of the Coronaviridae
known to infect humans. Three of these viruses, SARS CoV-1, MERS, and
SARS-CoV-2, can cause severe disease; four, HKU1, NL63, OC43 and 229E,
are associated with mild respiratory symptoms. Herein, we review what
can be deduced about the origin and early evolution of SARS-CoV-2 from
the comparative analysis of available genome sequence data. In
particular, we offer a perspective on the notable features in the
SARS-CoV-2 genome and discuss scenarios by which these features could
have arisen. Importantly, this analysis provides evidence that
SARS-CoV-2 is not a laboratory construct nor a purposefully manipulated
virus.
Say What?
The genomic comparison of both alpha- and betacoronaviruses (family Coronaviridae
) described below identifies two notable features of the SARS-CoV-2
genome: (i) based on structural modelling and early biochemical
experiments, SARS-CoV-2 appears to be optimized for binding to the human
ACE2 receptor; (ii) the highly variable spike (S) protein of SARS-CoV-2
has a polybasic (furin) cleavage site at the S1 and S2 boundary via the
insertion of twelve nucleotides. Additionally, this event led to the
acquisition of three predicted O-linked glycans around the polybasic
cleavage site.
