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- Researchers studying the immune responses of coronavirus patients may finally be able to explain why some people are at risk of developing life-threatening COVID-19 complications.
- The COVID Human Genetic Effort detailed a couple of groundbreaking findings on interferon problems that could be life-threatening during the course of COVID-19.
- Scientists have found that some people have autoantibodies to interferon, while others may suffer from previously undiagnosed genetic conditions that affect the functionality of the interferon.
Whether it’s the new coronavirus or a different infectious disease that can lead to life-threatening complications, vaccines are only part of the solution. The biggest news of the week was Pfizer and BioNTech’s incredible announcement that their drug has been found to be over 90% effective against the pathogen so far. The final results of the phase 3 study may vary and that efficacy figure may end up being lower, but it’s obviously a great place to start.
Preventing infections and severe cases of COVID-19 will not be enough as long as thousands of people continue to die of complications around the world. It will take time for the vaccines to meet demand and in the meantime more people will be infected. The world still needs effective therapies that can further reduce the risk of death until a large percentage of the world is immunized and the risk of transmission is significantly reduced. A couple of studies may have just produced the groundbreaking coronavirus discovery that could allow doctors to do just that, preventing more deaths from COVID-19 in the coming months as we await vaccines and other effective treatments.
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Doctors explained in mid-May that the coronavirus does something incredibly sneaky when it infects cells: it blocks local interferon production and delays the immune response, allowing the virus to replicate and infect more cells out of control. That’s why so many teams have started interferon-based trials, thinking that treating COVID-19 with interferon could prevent serious illness. A study by the World Health Organization failed to show that interferon can prevent deaths. But several developments could allow doctors to fine-tune interferon therapy and test it further.
It all started in late September, when a couple of studies described a key interferon-related phenomenon that can increase the risk of death in COVID-19 patients, including younger men. Genetic problems affecting interferon that go undetected until a diagnosis of COVID-19 could worsen the prognosis. These studies indicated that looking for hidden interferon imbalances would allow doctors to determine which COVID-19 patients are at risk of developing serious complications.
This brings us to a couple of larger studies that NBC News just highlighted, which provide further details on interferon problems that could lead to complications.
An international team of researchers published a study in Science this says that 10% of the 987 patients admitted to hospital with severe COVID-19 had antibodies that disabled interferon. These are known as autoantibodies and can appear in autoimmune diseases or medical conditions where the body attacks itself. Of the patients who had autoantibodies, 94% were men.
The study comes from the COVID Human Genetic Effort, which includes 200 research centers in 40 countries. It has a much broader scope than the September studies.
Autoantibodies to interferon were absent in a group of 663 asymptomatic COVID-19 patients. The researchers stated that only 4 of the 1,227 healthy people in the control group had the same autoantibodies. If the data is accurate, doctors treating COVID-19 patients may soon begin testing interferon autoantibodies to detect potential serious cases as soon as possible.
People who have autoantibodies to interferon have always had them. It is not a byproduct of coronavirus infection. It is not clear why other infectious diseases such as the flu have not brought these interferon problems to light in the past.
“This is one of the most important things we’ve learned about the immune system since the start of the pandemic,” said Scripps Research Vice President Dr. Eric Topol NBC. Topol was not involved in the studies.
This isn’t the only interferon problem that the COVID Human Genetic Effort group has identified. He is also the author of a second study which states that 3.5% of critically ill patients had mutations in the genes that control interferon. The body has 500 to 600 of such genes, with Dr. Qian Zhang saying they could identify more mutations. Zhang was the lead author of the second study. The finding may also explain why men of all ages may be more affected by interferon problems than women.
“Interferons are like a fire alarm and irrigation system all in one,” explained virologist Angela Rasmussen NBC. Rasmussen was not involved in any of the studies. If the virus can suppress interferon activity, people who may suffer from a genetic condition of interferon may have a higher risk of developing a serious illness.
“Your body should have alarms that go off everywhere,” when the coronavirus arrives, Zhang explained. “If you don’t go off the alarm, you could have viruses everywhere in large numbers.”
Screening for interferon autoantibodies could become the norm for managing COVID-19, but scientists will need more data. NBC notes that there are more than 100 clinical trials involving interferon and coronavirus, according to clinictrials.gov. New interferon-based therapies may soon emerge from the studies. British doctors just published a study in The Lancet saying an inhaled version of interferon beta-1a benefited COVID-19 patients. Randomly assigned people who received the drug were twice as likely to fully recover. This is Synairgen’s promising drug SNG001 which was first detailed in mid-July.
Chris Smith started writing about gadgets as a hobby and before he knew it he shared his views on tech topics with readers around the world. Whenever he doesn’t write about gadgets, he can’t miserably stay away from them, even if he tries desperately. But that’s not necessarily a bad thing.
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