NIH: Finding the Body Cell Targets for COVID-19


Health Editor’s Note: For a cure or vaccine to be developed to address SARS-CoV-2, the novel coronavirus that causes COVID-19 it must be determined exactly how the virus enters the body cells it uses to replicate. The body has a renin-angiotensin-aldosterone system (RAAS) which is made of peptides that are usually used to maintain blood pressure. To further explain the RAAS: The RAAS system maintains plasma sodium concentration by using feedback from blood pressure, baroreceptors, and sodium and potassium levels. For starters the kidneys secrete renin, which changes angiotensinogen into angiotensin I. Then the kidneys and lungs secrete ACE, which converts angiotensin I into angiotensin II. Finally, angiotensin II stimulates vasoconstriction (constriction of the blood vessels), cardiovascular response, and aldosterone and ADH production which will increase blood pressure and body fluid volume through sodium, potassium, and water resorption.

The ACE2 receptor, a homolog (homologus gene) of the angiotensin I-converting enzyme (ACE) receptor, is a type I transmembrane aminopeptidase which shows up in heart and lung tissue, but which is also found in the lining of the vessels and kidney. ACE2 receptor appears to counter-regulate RAAS activation by degrading angiotensin II. The RAAS system is accused of being associated with diabetes mellitus, high blood pressure, and heart failure which could/should/may be the reason why COVID-19 patients with these conditions are more apt to have more severe cases of COVID-19 and be more apt to succumb to COVID-19. 

Severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1) and SARS-CoV-2 and the current coronavirus disease, COVID-19, all interact with RAAS through the antiotensin-converting enzyme 2 (ACE2.)  ACE2 is a receptor for the SARS viruses and is the potential route of the virus’ entry into the body cells. 

Coronaviruses that count on ACE2 to enter body cells, use the body’s immune system to produce more inflammation factor (interferons which alert adjacent cells to increase the anti-viral attack) which causes more ACE2 production which only gives the virus an increased ability to attack to lung cells. Discovering how ACE2 receptors play a factor in allowing viral infection into the body would allow for prevention of this path by which the virus causes infection in humans and lead to potential cures and vaccines….Carol

The Prime Cellular Targets for the Novel Coronavirus

Dr. Francis Collins/NIH Directors Blog

There’s still a lot to learn about SARS-CoV-2, the novel coronavirus that causes COVID-19. But it has been remarkable and gratifying to watch researchers from around the world pull together and share their time, expertise, and hard-earned data in the urgent quest to control this devastating virus.

That collaborative spirit was on full display in a recent study that characterized the specific human cells that SARS-CoV-2 likely singles out for infection [1]. This information can now be used to study precisely how each cell type interacts with the virus. It might ultimately help to explain why some people are more susceptible to SARS-CoV-2 than others, and how exactly to target the virus with drugs, immunotherapies, and vaccines to prevent or treat infections.

This work was driven by the mostly shuttered labs of Alex K. Shalek, Massachusetts Institute of Technology, Ragon Institute of MGH, MIT, and Harvard, and Broad Institute of MIT and Harvard, Cambridge; and Jose Ordovas-Montanes at Boston Children’s Hospital. In the end, it brought together (if only remotely) dozens of their colleagues in the Human Cell Atlas Lung Biological Network and others across the U.S., Europe, and South Africa.

The project began when Shalek, Ordovas-Montanes, and others read that before infecting human cells, SARS-CoV-2 docks on a protein receptor called angiotensin-converting enzyme 2 (ACE2). This enzyme plays a role in helping the body maintain blood pressure and fluid balance.    Read More:



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