Rational treatment strategies for SARS-CoV-2 derived from human pluripotent stem cells models SARSCoV2 StemCells Coronavirus Disease COVID biorxivpreprint UniMelb MCRI_for_kids MonashUni Sydney_Uni WEHI_research RCHMelbourne TheDohertyInst
Study: Parallel use of pluripotent human stem cell lung and heart models provide new insights for treatment of SARS-CoV-2. Image Credit: Kateryna Kon / Shutterstock
The SARS-CoV-2 S protein initiates infection by binding to the angiotensin-converting enzyme 2 receptor on the host cell surface. Host cell proteases such as furin cleave the S protein into two subunits — S1 and S2. The subsequent fusion of the viral and host cell membranes requires the cleavage of S1 from S2 by serine proteases or cathepsins.
The team used clustered regularly interspaced short palindromic repeats -associated protein 9 mediated knockout of the ACE2 receptor to understand its importance in SARS-CoV-2 infection. Additionally, small molecule inhibitors were used to tease out the different mechanisms of viral entry. They also used phosphoproteomics and transcriptome profiling to understand differences in cellular responses during SARS-CoV-2 infections.
Aborted SARS-CoV-2 infection in knockout ACE2 lung and heart cells demonstrated that ACE2 receptors were essential for viral infection. However, using a combination of anti-ACE2 antibodies blocked SARS-CoV-2 infection in lung and heart tissue, but low doses of anti-ACE2 antibodies prevented viral infection only in cardiac cells.
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