Study finds that ACE-2 is not biochemically required for SARS-CoV2 membrane fusion biorxivpreprint UVA uppsalauni SARSCoV2 COVID19 coronavirus covid ACE2 biochemistry
By Susha Cheriyedath, M.Sc.Oct 27 2022Reviewed by Danielle Ellis, B.Sc. A study posted to the bioRxiv* preprint server tested the hypothesis that the angiotensin-converting enzyme 2 receptor of severe acute respiratory syndrome coronavirus 2 is not only an attachment factor in viral infection but also plays a role in activating the viral spike protein to facilitate membrane fusion.
The study In the present study, the researchers used deoxyribonucleic acid -lipid tethers as they can insert into membranes irreversibly and allow programmable self-assembly. The team separately incubated target membranes and viral particles with complementary DNA strands conjugated to DPPE lipids. They immobilized target membranes in a microfluidic flow cell, allowing the viral particles to bind.
The observed difference in fusion rates could be due to a variety of factors, including spike protein density variations on the VLPs vs. the HIV core, E and M proteins in the VLPs, the D614G/N501Y mutations, and the active spike percentage on the VLP surface. On the addition of soluble ACE-2 simultaneous to protease, a significant increase in the speed of lipid mixing kinetics was observed in experiments using both Wuhan and Omicron spikes. This shows that although the spike protein conformations needed for membrane fusion are accessible without ACE-2, the ACE-2 receptor promotes spike conformations that favor membrane fusion.
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