The SARS-CoV-2 variant, Omicron, shows rapid replication in human primary nasal epithelial cultures and efficiently uses the endosomal route of entry
Peacock et al.,
The SARS-CoV-2 variant, Omicron, shows rapid replication in human primary nasal epithelial cultures and..,
bioRxiv, doi:10.1101/2021.12.31.474653 (Preprint) (In Vitro)
In Vitro study showing that omicron can efficiently enter cells via the endosomal route, independent of TMPRSS2.
Bromhexine may be less effective for omicron due to the entry process moving towards TMPRSS2-independent fusion.
Peacock et al., 3 Jan 2022, preprint, 10 authors.
In Vitro studies are an important part of preclinical research, however results may be very different in vivo.
Abstract: bioRxiv preprint doi: https://doi.org/10.1101/2021.12.31.474653; this version posted January 3, 2022. The copyright holder for this preprint
(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is
made available under aCC-BY-NC 4.0 International license.
The SARS-CoV-2 variant, Omicron, shows
rapid replication in human primary nasal
epithelial cultures and efficiently uses the
endosomal route of entry.
Thomas P. Peacock1#, Jonathan C. Brown1#, Jie Zhou1#, Nazia Thakur2, Joseph Newman2, Ruthiran
Kugathasan1, Ksenia Sukhova1, Myrsini Kaforou1, Dalan Bailey2, and Wendy S. Barclay1*
#
These authors contributed equally to this work
Department of Infectious Disease, Imperial College London, UK, W2 1PG
1
The Pirbright Institute, Woking, Surrey, UK, GU24 0NF
2
*Corresponding author: w.barclay@imperial.ac.uk
Abstract
At the end of 2021 a new SARS-CoV-2 variant, Omicron, emerged and quickly spread across
the world. It has been demonstrated that Omicron’s high number of Spike mutations lead to partial
immune evasion from even polyclonal antibody responses, allowing frequent re-infection and vaccine
breakthroughs. However, it seems unlikely these antigenic differences alone explain its rapid growth;
here we show Omicron replicates rapidly in human primary airway cultures, more so even than the
previously dominant variant of concern, Delta. Omicron Spike continues to use human ACE2 as its
primary receptor, to which it binds more strongly than other variants. Omicron Spike mediates
enhanced entry into cells expressing several different animal ACE2s, including various domestic avian
species, horseshoe bats and mice suggesting it has an increased propensity for reverse zoonosis and
is more likely than previous variants to establish an animal reservoir of SARS-CoV-2. Unlike other SARSCoV-2 variants, however, Omicron Spike has a diminished ability to induce syncytia formation.
Furthermore, Omicron is capable of efficiently entering cells in a TMPRSS2-independent manner, via
the endosomal route. We posit this enables Omicron to infect a greater number of cells in the
respiratory epithelium, allowing it to be more infectious at lower exposure doses, and resulting in
enhanced intrinsic transmissibility.
bioRxiv preprint doi: https://doi.org/10.1101/2021.12.31.474653; this version posted January 3, 2022. The copyright holder for this preprint
(which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is
made available under aCC-BY-NC 4.0 International license.
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