Good news!
See also why the Covid-19 is a relative harmless disease!
"A computational tool allows researchers to precisely predict locations on the surfaces of human and COVID-19 viral proteins that bind with each other, a breakthrough that will greatly benefit our understanding of the virus and the development of drugs that block binding sites. ...
The study ... describes the tool and uses it to predict how the SARS-COV-2 diverged structurally from SARS-COV-1 (which caused a SARS outbreak in 2002-04); how genetic variation of proteins in human populations may contribute to virus-human binding and higher risk of infection; and which existing drugs show promise for binding to targets on surfaces of human proteins. ..."
The study ... describes the tool and uses it to predict how the SARS-COV-2 diverged structurally from SARS-COV-1 (which caused a SARS outbreak in 2002-04); how genetic variation of proteins in human populations may contribute to virus-human binding and higher risk of infection; and which existing drugs show promise for binding to targets on surfaces of human proteins. ..."
From the abstract:
"... To facilitate broader exploration of how pathogen–host interactions might impact transmission and virulence in the ongoing COVID-19 pandemic, we performed state-of-the-art interface prediction followed by molecular docking to construct a three-dimensional structural interactome between SARS-CoV-2 and human. We additionally carried out downstream meta-analyses to investigate enrichment of sequence divergence between SARS-CoV-1 and SARS-CoV-2 or human population variants along viral–human protein-interaction interfaces, predict changes in binding affinity by these mutations/variants and further prioritize drug repurposing candidates predicted to competitively bind human targets. ..."
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