At our monthly Zoom call we had an excellent presentation on Covid 19 from Dr. Gerald Barry of the UCD Vet School. Below is a piece Gerald kindly contributed for this month’s newsletter. 

Since late 2019 the newly emerged SARS-CoV-2 (Severe Acute Respiratory Syndrome – coronavirus -2) has swept across many parts of the world from its origins in China. The emergence of these virulent coronaviruses in 2002 (SARS), 2012 (MERS), and 2019 (SARS-CoV-2) have marked a dramatic shift in our understanding of the pathogenic potential of coronaviruses. SARS-CoV-2 binds the human ACE2 receptor and the protein TMPRSS2 on the surface of cells to infect them. Once in, it makes 1000’s of copies of itself, killing the infected cell in the process.

Covid 19 Presentation | VistaMilkThe interactions between ACE2, TMPRSS2, and the virus Spike protein are crucial and SNPs within Spike, TMPRSS2, and ACE2 can increase or decrease the binding efficiency and may give clues as to why some people get sicker than others. It is predicted in silico that SARS-CoV-2 Spike binds to ACE2 more efficiently than SARS or MERS, potentially allowing it to spread more effectively while it also contains a furin-like cleavage site which is unique and may promote binding to ACE2. While genetic variation in humans is relatively restricted, the virus can change and mutate and may adapt to ACE2 and TMPRSS2 over time, to become more effective at infecting human cells as well as other species with similar proteins. There is a huge amount of research on-going into the virus with over 1000 publications in less than just over 3 months, and we are learning more about it every day. 


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