Answering the 64,000 dollar question in the coonravirus AKA CoV-2 or Covid-19 global pandemic, European Union researchers at the University Medical Center [UMC] in Gronigen, Netherlands found the common denominator in why certain Covid-19 infections are severe-and-lethal and others are mild or aymptomatic. Whether old or young, with preexisting medical conditions or not, Gronigen researchers found the presence of Agiotensin-Coverting Enzyme [ACE2] receptors the common denominator in why certain Covd-19 cases turn severe-and-deadly, others mild or symptom free. Gronigen researchers, led by cardiology professor Adrian Voors, found the genetic propensity to have higher levels of ACE2 accounted for the severity of Covid-19 infections. Agiotensin-Converting Enzyme [ACE2] is found in the heart, lungs, kidneys blood vessels and other organs.
When infected with coronavirus, Voors found the high levels of ACE2 drive the Covid-19 infection into Severe Acute Respiratory Syndrome [SARS], the kinds of respiratory anomaly that require oxygen and even ventilators in some patients. Voors’ findings go a long way in explaining why men are disproportionately affected by Covd-19 than women. Women genetically have less ACE2, leaving them, compared to men, with lower blood pressure. Published in the European Heart Journal [EHJ], Voors’ study found that widely-prescribed ACE inhibitors or Angiotensin Receptor Blockers [ARBs] did not increase ACE2, a concern that some virologists had in dealing with Covid-19 patients.. ACE inhibitors are power vasodilators that open up blood vessels, allowing more blood flow to the heart and lungs lowering blood pressure. Voors found that ACE inhibitors do not increase ACE2 receptors.
Accounting for difference in severity and mortality rates from Covid-19, the Gronigen study gives compelling proof that the prevalence ACE2 receptors play a key role in physiologic responses to Covd-19. “Our findings do not support the discontinuation these drugs [ACE inhibitors] in Covid-19 patients,” Voors said. Voors examined with his research partner Iziah Sama the blood of 3,500 heart failure patients from 11 EU countries. Voors and Sama started their study before the SARS CoV-2 global pandemic but sheds light on which patients are particularly vulnerable to the disease. “When we found that one of the strongest biomarkers, ACE2 was much higher in men than women. I realized that this had the potential to explain why men were more likely to die from Covd-19 that women,” said Sama, Voor’s co-author. When ACE2 is present in the cell, coronavirus penetrates the cell membrane.
Voors and Sama found the ACE2 is found in high concentrations in the heart, lungs, kidneys, blood vessel linings and the testes, obviously not found in women. Both think that higher concentration of ACE2 in men accounts for higher hospitalizations, draconic treatments and deaths in men. Genetic differences exist not only between men and women with respect to ACE2 but with respect all age grouips. While men generally have higher blood pressure that women, it’s also true that some men have lower blood pressure than others, accounting for differences in ACE2 levels. “ACE2 receptors seem to be the common thread, the unifying factor—whether you’re young or old,” said Jeremy Payne, director of Stroke Center at Banner University Medicine Neuroscience Clinic. Payne believes that the greater the presence of ACE2, the easier coronavirus burrows into the cells.
Immunologist Philip Murphy at the National Institute of Health Infectious Disease Department said ACE2 makes it “easier or harder for the virus to get into the sells,” confirming findings of other researchers. A 2005 study examining the SARS virus, amounts of ACE2 “were poorly infected.” Cells with more ACE2 receptors were invaded more easily by the virus. Another study published in February, comparing SARS with CoV-2, showed ACE2 in body tissues “might be critical for the susceptibility symptoms and outcomes of SARS CoV-2 infections.” Measuring ACE2 receptors might be a warning sign in some patients to vulnerability to severe Covid-19 infections. Using a ACE2 Assay kit could be helpful in determining treatment for hospitalized Covid-19 patients. New drugs designed to reduce or inhibit ACE2 receptors could be developed in the research pipeline.
However ACE2 impacts Covid-19 infections, researchers at Oregon Health Sciences [OHS] showed that other genetic codes related to the body’s immune response also play a powerful role in the severity of Covid-19 infections. Once a foreign body [antigen] penetrates the cell, the Human Leukocyte Antigen [HLA] system comes into play. “Not all alarm systems are created equal,” the OHS group wrote this week. Difference in HLA account for how the human body fights off viruses like SARS CoV-2 once it enters the cell. OHS scientists isolated the B46.01 gene, the one responsible for recognizing viruses entering the body. “Based on our study, we think variation in HLA genes is part of explanation for the huge difference in infection severity in many Covid-19 patients,” OHS scientists concluded. Given the ACE2 and HLA findings, scientists should eventually find better treatments.
