Skip to main content

COVID-19 drug prospects boosted


COVID-19 drug prospects boosted 

A shadow over the promising inhaled interferon beta COVID-19 therapy has been cleared with the discovery that although it appears to increase levels of ACE2 protein -- coronavirus' key entry point into nose and lung cells -- it predominantly increases levels of a short version of that protein, which the virus cannot bind to.

The virus that causes COVID-19, known as SARS-CoV-2, enters nose and lung cells by binding its spike protein to the cell surface protein angiotensin-converting enzyme 2 (ACE2).

A new, short-form of ACE2 has been identified by Professor Jane Lucas, Professor Donna Davies, Dr. Gabrielle Wheway, and Dr. Vito Mennella at the University of Southampton and University Hospital Southampton NHS Foundation Trust.

The study, published in Nature Genetics, shows that as well as the long-form of ACE2 used by SARS-CoV-2, a shorter form of ACE2 lacks the SARS-CoV-2 binding site.

Naturally occurring antiviral proteins called interferons have shown promise in treating COVID-19. However, previous studies have shown that interferons increase levels of ACE2 -- casting doubts over the potential for such treatments, with the possibility that increased ACE2 could see these drugs actually worsen COVID-19 impacts.

But this latest research shows that it is predominantly the short ACE2, which lacks the viral binding site, that is increased in response to interferons. Since levels of the longer form of ACE2 remain unchanged, interferons do not appear to boost entry points for the virus, supporting their use in treating COVID-19 patients.

This helps explain the hugely promising results for a trial of an inhaled interferon-beta treatment for COVID-19 patients, developed in Southampton by a team led by Professor Tom Wilkinson of the University of Southampton.

This research gives a new insight into this short form of ACE2 and shows how it has a very different role to the longer form of ACE2 that acts as an entry point for SARS-CoV-2.

Short ACE2 lacks the binding site for SARS-CoV-2, so it cannot be used as an entry point for the virus. Instead, its regulation by interferons suggests it may be involved in the body's antiviral response.

As the researchers showed that short ACE2 does not increase in response to SARS-CoV-2 infection, it is unlikely to be involved in the body's immune response to COVID-19. Still, it did increase in response to another common respiratory virus.

These results will enable researchers to distinguish between these two forms of ACE2, which could prove invaluable for developing more sophisticated treatments for COVID-19 patients.

Professor Jane Lucas, Professor of Paediatric Respiratory Medicine at the University of Southampton and Honorary Consultant Paediatric Respiratory Medicine at University Hospitals Southampton and one of the lead authors for the study, said:

"We were excited to discover a new form of ACE2 and became even more interested when we realized that it may be protective against SARS-CoV-2 in the airways rather than an entry site for infection. We believe this may have important implications for managing COVID-19 infection, and we are starting further studies to investigate this further."



Popular posts from this blog


Cracking coconut oil’s "health halo" Thanks to marketing strategies that tout coconut oil as healthy, many people consider this solid, white fat a portion of healthy food. But a new analysis confirms what nutrition experts have said for years: Coconut oil raises harmful LDL cholesterol (a well-known contributor to heart disease) much more than other vegetable oils. The study, published online March 10, 2020, by the journal  Circulation , pooled findings from 16 trials involving a total of 730 people. Most of the trials lasted one to two months and compared coconut oil consumption with that of other fats, including other vegetable oils such as soybean, safflower, canola, and olive oils. Compared with these vegetable oils, coconut oil raised LDL cholesterol by 10 points, on average. An editorial accompanying the study states "In culinary practice, coconut oil should not be used as regular cooking oil, although it can be used sparingly for flavor or texture.

Autophagy:The Body's Anti-aging process

Autophagy: The body's Anti-aging process Autophagy is how the body removes and recycles dangerous, and damaged organelles and particles, as well as pathogens, from inside cells, thus aiding your immune system and greatly reducing your risk of developing cancer, heart disease, chronic inflammation, osteoarthritis, and neurological disorders such as depression and dementia. Autophagy makes us physiologically more efficient by getting rid of defective parts, promoting healthy metabolism, stopping cancerous growths, and preventing metabolic disorders such as diabetes and obesity --- which means that by boosting your body's autophagy, you dampen inflammation, slow down the aging process, reduce your risk of developing certain diseases, and optimize your biological function. The autophagy process is activated by intermittent fasting and calorie restriction. Intermittent fasting and calorie restriction turn up the autophagy dial, increasing protein turnover and cellular repai


How to lower your cholesterol without drugs You can begin to reduce your “bad” LDL cholesterol by making a few simple changes in your diet. If your cholesterol is creeping upward, your doctor has probably told you that diet and exercise — the traditional cornerstones of heart health — could help to bring it down. And if you’d prefer to make just one change at a time, you might want to begin with your diet. A major 2012 analysis of several controlled trials involving hundreds of men and women found that dietary changes reduced LDL and total cholesterol while exercise alone had no effect on either. (However, adding aerobic exercise did enhance the lipid-lowering effects of a heart-healthy diet.) The people in the studies followed a variety of diets, from the Mediterranean to low-fat to low-calorie. However, the most effective diets substituted foods with cholesterol-lowering power for those that boost cholesterol. According to Kathy McManus, director of the Department of Nutrition at Bri