A novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) recently emerged and is rapidly spreading in humans, causing COVID-19. A key to tackling this pandemic is to understand the receptor recognition mechanism of the virus, which regulates its infectivity, pathogenesis and host range. SARS-CoV-2 and SARS-CoV recognize the same receptor—angiotensin-converting enzyme 2 (ACE2)—in humans.
Now, Dana Bohan and colleagues recognized another set of receptors called Phosphatidylserine (PS) which enhances the SARS-CoV-2 entry. They found that the PS receptors, AXL, TIM-1 & TIM-4, synergize with low levels of ACE2 to enhance SARS-CoV-2 infection.
They also examined the mechanism by which PS receptors interact with SARS-CoV-2 and found that, PS receptors interact with SARS-CoV-2 virions through a well-established mechanism of virion-associated PS binding to TIM-1 and AXL.
“If we shall be able to inhibit AXL, TIM-1 or both, it will block SARS-CoV-2 entry”
In addition, it has been demonstrated that, SARS-CoV-2 utilizes AXL to enhance virion binding and entry in some lung cell lines, and that this mechanism can be effectively disrupted by small molecule inhibitors like Bemcentinib and genetic albation of AXL.
“Appreciation of this route of entry provides an additional pathway that could be therapeutically targeted to inhibit virus entry and subsequent infection”— concluded authors of the study
Featured image credit: Unsplash
Reference: Dana Bohan, Hanora Van Ert, Natalie Ruggio, Kai J. Rogers, Mohammad Badreddine, José A. Aguilar Briseño, Roberth Anthony Rojas Chavez, Boning Gao, Tomasz Stokowy, Eleni Christakou, David Micklem, Gro Gausdal, Hillel Haim, John Minna, James B. Lorens, Wendy Maury, “Phosphatidylserine Receptors Enhance SARS-CoV-2 Infection: AXL as a Therapeutic Target for COVID-19”, bioRxiv 2021.06.15.448419; doi: https://doi.org/10.1101/2021.06.15.448419
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