Dr. Megan Ranney has learned a lot about COVID-19 since she started treating patients with the disease in the emergency room in February.
But there’s one question you still can’t answer: how sick are some patients as it is to others?
Advanced age and underlying medical disorders represent the sole component of the phenomenon, said Ranney, who has noticed that patients of ages, education and physical prestige adhere to many other trajectories.
“Why is one 40-year-old man in poor health and another doesn’t even want to be admitted?”asked Ranney, associate professor of emergency medicine at Brown University.
In some cases, according to new and provocative research, other people, specifically men, succumb because their immune formula is affected by friendly fire. Researchers hope this discovery will expand treatments for these patients.
In a foreign science study, 10% of the nearly 1,000 COVID patients who developed life-threatening pneumonia had antibodies that defuse key proteins from the immune formula called interferons. These antibodies, called autoant antibodies because they attack the framework itself, have not been discovered in total, in 663 other people with mild or asymptomatic COVID infections. Only 4 of the 1,227 healthy people had autoantibodys. The study, published on 23 October, was conducted through COVID Human Genetic Effort, which includes two hundred study centres in 40 countries.
“This is one of the main vital things we’ve learned about immune formula since the start of the pandemic,” said Dr. Eric Topol, executive vice president of studies at Scripps Research in San Diego, who was not concerned about the new study. “It’s a decisive discovery. “
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In a brief clinical examination through the same team, writers noted that another 3. 5% of critically ill patients had mutations in the genes that control interferons related to virus control. Since the framework comprises 500 to 600 of these genes, it is imaginable that researchers will notice more mutations, said Qian Zhang, lead writer at the time of examination.
Interferons serve as the body’s first line of defense against infections, sound the alarm, and trigger an army of virus-fighting genes, said virologist Angela Rasmussen, associate researcher at Columbia University’s Mailman School of Public Health’s Center for Infection and Immunity.
“Interferons are like a chimney alarm and a sprinkler formula, all in one,” said Rasmussen, who is not worried about new studios.
Laboratory studies show that interferons are suppressed in some other people with COVID-19, through the virus itself.
Interferons are especially vital to the framework of new viruses, such as the coronavirus, which the framework has never encountered, said Zhang, a researcher at the Rockefeller University Infectious Diseases Human Genetics Laboratory in St. Giles.
When he becomes inflamed with the new coronavirus, “his body deserves alarms to sound,” Zhang said. “If you don’t sound the alarm, you may have viruses in giant amounts. “
Significantly, the patients did not produce autoantibodies in reaction to the virus, but appeared to have had them even before the pandemic began, said Paul Bastard, director of the antibody study, also a Rockefeller University researcher.
For reasons researchers don’t understand, autoant antibodies never caused a challenge until patients became inflamed with COVID-19, Bastard said. One way or another, the new coronavirus, or the immune reaction it triggered, turns out to have set them in motion. .
“Before COVID, his condition was silent, ” said Bastard. “Most of them had never been sick. “
Bastard said he now wonders if interferon autoanti-devices also increase the threat of other viruses, such as influenza. Among the patients in his study, “some of them had contracted influenza in the past, and we’re investigating whether autoantibodys can have had an effect on the flu. “
Scientists have long known that viruses and immune formula compete in a type of arms race, with viruses evolving to evade the immune formula and even suppress their response, said Sabra Klein, professor of molecular microbiology and immunology at Johns Hopkins Bloomberg School. .
Antibodies are often the heroes of the immune formula, protecting the body against viruses and other threats. But sometimes, in a phenomenon known as autoimmune disease, the immune formula turns out and creates autoantibodies. This occurs in diseases such as rheumatoid arthritis, when antibodies attack the joints, and type 1 diabetes, in which the immune formula attacks the insulin-producing cells in the pancreas.
Although doctors do not know the precise reasons for autoimmune diseases, they have observed that situations occur after a viral infection. Autoimmune diseases are more common as other people age.
In an unforeseen discovery, 94% of the patients in the study with these autoantibodies were men. About 12. 5% of men with life-threatening COVID pneumonia had interferon autoantibodies, compared with 2. 6% of women.
This is unexpected, given that autoimmune diseases are much less unusual in women, Klein said.
“I’ve been reading the sexual differences in viral infections for 22 years, and I don’t think reading autoantibodys thinks that would be a threat to COVID-19,” Klein said.
The study can help explain why men are more likely than women to become seriously ill with COVID-19 and die, Klein said.
“You see a lot more men dying at 30, only at 80,” he says.
Akiko Iwasaki, professor of immunobiology at Yale Medical School, noted that several genes from the immune system’s reaction to viruses are discovered on the X chromosome.
Women have two copies of this chromosome, with two copies of the gene, which gives them a backup in case a copy of a gene becomes defective, Iwasaki said.
However, men only have one copy of the X chromosome, so if there is a defect or destructive gene on the X chromosome, they do not have another copy of that gene to properly solve the problem, Iwasaki said.
Bastard noted that a woman on the test who developed autoantic antibodies has a rare genetic disease in which she has an X chromosome.
Scientists have struggled to understand why men have a greater threat of hospitalization and death by COVID-19. When the disease first gave the impression in China, experts hypothesized that men were more likely to smoke because they were much more likely to smoke than the Chinese. Woman.
Researchers temporarily detected that men in Spain were also more likely to die of COVID-19, even though men and women smoke at about the same rate, Klein said.
Experts hypothesized that men could run a greater threat because they are less likely to wear masks in public than women and are more likely to retain medical care, Klein said.
But differences in behavior between men and women only provide one component of the response. Scientists say it is imaginable that the hormone estrogen protects women, while testosterone would possibly put men at greater threat. Interestingly, recent studies have shown that obesity poses a much greater threat to men with COVID-19 than to women, Klein said.
However, they have their own form of coVID-19 suffering.
Studies show that women are 4 times more likely to revel in long-term symptoms of COVID, which last weeks or months, adding fatigue, weakness and some form of intellectual confusion known as “mental fog,” Klein noted.
As women, “maybe we and we are less likely to die, but then we’ll have all those long-term complications,” she says.
After reading the studies, Klein said, she would like to know if patients who are seriously ill from other viruses, such as influenza, also harbor genes or antibodies that disable interferon.
“There’s no evidence of that in the flu,” Klein said. “But we don’t look. With COVID-19, we could have discovered a very new disease mechanism that we can also locate and provide in a number of diseases.
Scientists say the new test solves a component of the mystery of why patient outcomes can vary so much.
Researchers say that some patients may have overcome exposure to other coronaviruses and that patients who become seriously ill may also have inhaled higher doses of the virus, for example, after repeated exposure to inflamed colleagues.
Although doctors have sought links between disease outcomes and blood type, they have produced conflicting results.
Evaluating patients for interferon autoanticorps may only help to find out which patients are most likely to be very ill, said Bastard, also affiliated with the Necker Hospital for Sick Children in Paris. Hospitals in Paris can now evaluate patients at the request of a doctor, he said.
Although only 10% of patients with life-threatening COVID-19 have autoantibodys, “I think we give the check to everyone who enters,” Bastard said. Otherwise, “we would not know who is at risk of serious illness. “form of disease. “
Bastard said he hoped his discoveries would lead to new life-saving therapies. It notes that the framework produces many types of interferons. Giving these patients another type of interferon, an interferon that is not disabled through their genes or autoanticorps, can simply fight them. the virus.
In fact, a pilot examination of 98 patients published Thursday in the respiratory medicine with lancet revealed the benefits of an inhaled form of interferon. In the UK industry-funded examination, patients hospitalized by COVID randomly assigned to obtain beta-1a interferon were more than twice as likely as others enough to resume their normal activities.
Researchers want to verify these findings in a much broader study, said Dr. Nathan Peiffer-Smadja, a researcher at Imperial College London who was not concerned about the study but wrote an adjunct editorial. Future studies deserve to check patients’ blood for genetic mutations and self-anti-anti-interferon antibodies to see if they respond from others.
Peiffer-Smadja notes that inhaled interferon can paint more than an injected form of the drug because it is administered into the lungs. While injected editions of interferon have been used for years to treat other diseases, the inhaled edition is still experimental and not marketed. Available.
And doctors want to be careful with interferon right now, because an examination conducted through the World Health Organization found that no advantages are gained from the injected form of the drug in COVID patients, Peiffer-Smadja said. mortality rates in patients receiving interferon, this location was possibly due to chance. Administering interferon later in the course of the disease may also simply announce a destructive immune reaction called cytokine storm, in which the immune formula does more harm than the virus.
Scientists around the world have introduced more than a hundred interferon clinical trials, according to Clinicaltrials. gov, a database of studies through the National Institutes of Health.
Until larger studies are completed, doctors say, bastard’s effects will replace the way they treat COVID-19.
Dr. Lewis Kaplan, president of the Society of Critical Care Medicine, said he treats patients for their symptoms, not their threat factors.
“If he’s a little sick, he’s treated a little carefully,” Kaplan said. “If he’s sick, he gets a lot of attention. But if a COVID patient has high blood pressure, diabetes and obesity, we don’t say, “They have threat factors. “Let’s put them in the ICU. “
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Dr. Megan Ranney has learned a lot about COVID-19 since she started treating patients with the disease in the emergency room in February.
But there’s one question you still can’t answer: how sick are some patients as it is to others?
Advanced age and underlying medical disorders represent the sole component of the phenomenon, said Ranney, who has noticed that patients of ages, education and physical prestige adhere to many other trajectories.
“Why is one 40-year-old man in poor health and another doesn’t even want to be admitted?”asked Ranney, associate professor of emergency medicine at Brown University.
In some cases, according to a new and provocative research, some other people, specifically men, succumb because their immune formula is affected by friendly fire. Researchers hope this discovery will expand treatments for these patients.
In a foreign science study, 10% of the nearly 1,000 COVID patients who developed life-threatening pneumonia had antibodies that defuse key proteins from the immune formula called interferons. These antibodies, called autoant antibodies because they attack the framework itself, have not been discovered in total, in 663 other people with mild or asymptomatic COVID infections. Only 4 of the 1,227 healthy people had autoantibodys. The study, published on 23 October, was conducted through COVID Human Genetic Effort, which includes two hundred study centres in 40 countries.
“This is one of the main vital things we’ve learned about immune formula since the start of the pandemic,” said Dr. Eric Topol, executive vice president of studies at Scripps Research in San Diego, who was not concerned about the new study. “It’s a decisive discovery. “
Dr. Megan Ranney has learned a lot about COVID-19 since she started treating patients with the disease in the emergency room in February.
But there’s one question you still can’t answer: what makes some patients sicker than others?
Advanced age and underlying medical disorders represent the sole component of the phenomenon, said Ranney, who has noticed that patients of ages, education and physical prestige adhere to many other trajectories.
“Why is one 40-year-old man in poor health and another doesn’t even want to be admitted?”asked Ranney, associate professor of emergency medicine at Brown University.
In some cases, provocative new studies show that other people, especially men, succumb because their immune systems are affected by friendly fire. The researchers hope that this discovery will expand the treatments aimed at these patients.
In a foreign science study, 10% of the nearly 1,000 COVID patients who developed life-threatening pneumonia had antibodies that defuse key proteins from the immune formula called interferons. These antibodies, called autoant antibodies because they attack the framework itself, have not been discovered in total, in 663 other people with mild or asymptomatic COVID infections. Only 4 of the 1,227 healthy people had autoantibodys. The study, published on 23 October, was conducted through COVID Human Genetic Effort, which includes two hundred study centres in 40 countries.
“This is one of the main vital things we’ve learned about immune formula since the start of the pandemic,” said Dr. Eric Topol, executive vice president of studies at Scripps Research in San Diego, who was not concerned about the new study. “It’s a decisive discovery. “
In a brief clinical examination through the same team, writers noted that another 3. 5% of critically ill patients had mutations in the genes that control interferons related to virus control. Since the framework comprises 500 to 600 of these genes, it is imaginable that researchers will notice more mutations, said Qian Zhang, lead writer at the time of examination.
Interferons are the body’s first line of defense against infections, sound the alarm and trigger an army of virus-fighting genes, said virologist Angela Rasmussen, associate researcher at Columbia University’s Mailman School of Public Health’s Center for Infection and Immunity.
“Interferons are like a chimney alarm and a sprinkler formula, all in one,” said Rasmussen, who is not worried about new studios.
Laboratory studies show that interferons are suppressed in some other people with COVID-19, through the virus itself.
Interferons are especially vital to the framework of new viruses, such as coronavirus, which the framework has never found, said Zhang, a researcher at Rockefeller University’s Human Genetics Laboratory for Infectious Diseases in St. Louis. Giles.
When he becomes inflamed with the new coronavirus, “his body deserves alarms to sound,” Zhang said. “If you don’t sound the alarm, you may have viruses in giant amounts. “
Significantly, patients did not produce autoantiantibodys in reaction to the virus. Instead, they gave the impression that he had it even before the pandemic began, said Paul Bastard, leader of the antibody study, also a researcher at Rockefeller University.
For reasons researchers don’t understand, autoantic antibodies have never caused a challenge until patients have become inflamed with COVID-19, Bastard said. One way or another, the new coronavirus, or the immune reaction it triggered, turns out to have caused them to move.
“Before COVID, his condition was silent, ” said Bastard. “Most of them had never been sick. “
Bastard said he now wonders if interferon autoanti-devices also increase the threat of other viruses, such as influenza. Among the patients in his study, “some of them had contracted influenza in the past, and we’re investigating whether autoantibodys can have had an effect on the flu. “
Scientists have long known that viruses and the immune formula compete in a type of arms race, with viruses evolving to evade the immune formula and even suppress its response, said Sabra Klein, professor of molecular microbiology and immunology at Johns. Hopkins Bloomberg School. .
Antibodies are usually the heroes of the immune formula, protecting the body from viruses and other threats, but sometimes, in a phenomenon known as autoimmune disease, the immune formula results in and creates autoantiantibodys. , when antibodies attack the joints, and type 1 diabetes, in which the immune formula attacks insulin-producing cells in the pancreas.
Although doctors do not know the precise reasons for autoimmune diseases, they have observed that situations occur after a viral infection. Autoimmune diseases are more common as other people age.
In an unforeseen discovery, 94% of the patients on the test with these autoantiantibodys were men. Approximately 12. 5% of men with life-threatening COVID pneumonia had interferon autoantibodys, compared to 2. 6% of women.
This is unexpected, given that autoimmune diseases are much less unusual in women, Klein said.
“I’ve been reading the sexual differences in viral infections for 22 years, and I don’t think reading autoantibodys thinks that would be a threat to COVID-19,” Klein said.
The study can help explain why men are more likely than women to become seriously ill with COVID-19 and die, Klein said.
“You see a lot more men dying at 30, only at 80,” he says.
Akiko Iwasaki, professor of immunobiology at Yale Medical School, noted that several genes from the immune system’s reaction to viruses are discovered on the X chromosome.
Women have two copies of this chromosome, with two copies of the gene, which gives them a backup in case a copy of a gene becomes defective, Iwasaki said.
However, men only have one copy of the X chromosome, so if there is a defect or destructive gene on the X chromosome, they do not have another copy of that gene to properly solve the problem, Iwasaki said.
Bastard noted that a woman on the test who developed autoantic antibodies has a rare genetic disease in which she has an X chromosome.
Scientists have struggled to understand why men have a greater threat of hospitalization and death by COVID-19. When the disease first gave the impression in China, experts hypothesized that men were more likely to smoke because they were much more likely to smoke than the Chinese. Woman.
Researchers temporarily detected that men in Spain were also more likely to die from COVID-19, even though men and women smoke at about the same rate, Klein said.
Experts hypothesized that men might be at greater risk because they are less likely to wear masks in public than women and more likely to delay medical care, Klein said.
But differences in behavior between men and women provide only one component of the response. Scientists say it is imaginable that the hormone estrogen protects women, while testosterone may expose men to a greater threat. Interestingly, recent studies have shown that obesity poses a much greater threat. for men with COVID-19 than for women, Klein said.
However, they have their own form of coVID-19 suffering.
Studies show that women are 4 times more likely to revel in long-term symptoms of COVID, which last weeks or months, adding fatigue, weakness and some form of intellectual confusion known as “mental fog,” Klein noted.
As women, “maybe we are less likely to die, but then we will have all these long-term complications,” she says.
After reading the studies, Klein said, he would like to know if patients who are seriously ill with other viruses, such as influenza, also harbor genes or antibodies that disable interferon.
“There’s no evidence of that in the flu,” Klein said. “But we don’t look. With COVID-19, we could possibly have discovered a very new disease mechanism that we can also locate in various diseases.
Scientists say the new test solves a component of the mystery of why patient outcomes can vary so much.
Researchers say that some patients may have overcome exposure to other coronaviruses and that patients who become seriously ill may also have inhaled higher doses of the virus, for example, after repeated exposure to inflamed colleagues.
Although doctors have sought links between disease outcomes and blood type, they have produced conflicting results.
Detecting interferons in patients can only help to find out which patients are most likely very ill, said Bastard, also affiliated with the Necker Hospital for Sick Children in Paris. Verification takes approximately two days. Hospitals in Paris can now evaluate patients at the request of a doctor, he said.
Although only 10% of patients with life-threatening COVID-19 have autoantibodys, “I think we give the check to everyone who enters,” Bastard said. Otherwise, “we would not know who is at risk of serious illness. “form of disease. “
Bastard said he hoped his discoveries would lead to new life-saving therapies. It notes that the framework produces many types of interferons. Giving these patients another type of interferon, an interferon that is not deactivated through their genes or autoanticorps, can simply fight them. the virus.
In fact, a pilot examination of 98 patients published Thursday in the journal Lancet Respiratory Medicine discovered the benefits of an inhaled form of interferon. In the UK industry-funded study, hospital COVID patients randomly assigned to obtain beta-1a interferon were more than twice as likely as others to resume their normal activities sufficiently.
Researchers want to verify these findings in a much broader study, said Dr. Nathan Peiffer-Smadja, a researcher at Imperial College London who was not concerned about the study but wrote an adjunct editorial. Future studies deserve to check patients’ blood for genetic mutations. and autoanticorps opposed to interferon, to see if they respond from others.
Peiffer-Smadja notes that inhaled interferon can paint more than an injected form of the drug because it is administered into the lungs. While injected editions of interferon have been used for years to treat other diseases, the inhaled edition is still experimental and not marketed. Available.
And doctors want to be wary of interferon right now, as an examination conducted through the World Health Organization did not discover advantages of the injected form of the drug in COVID patients, Peiffer-Smadja said. mortality rates in patients receiving interferon, this location was possibly due to chance. Giving interferon later in the course of the disease can also inspire a destructive immune reaction called cytokine storm, in which the immune formula does more harm than the virus.
Scientists around the world have introduced more than a hundred interferon clinical trials, according to Clinicaltrials. gov, a database of studies from the National Institutes of Health.
Until larger studies are completed, doctors say, the effects of Bastard will supersede the way they treat COVID-19.
Dr. Lewis Kaplan, president of the Society of Critical Care Medicine, said he treats patients for their symptoms, not their threat factors.
“If he’s a little sick, he’s treated a little carefully,” Kaplan said. “If he’s sick, he gets a lot of attention. But if a COVID patient has high blood pressure, diabetes and obesity, we don’t say, “They have threat factors. “Let’s put them in the ICU. “
In a brief clinical examination by the same team, the writers noted that another 3. 5% of critically ill patients had mutations in genes that control interferons related to virus control. Given that the framework comprises 500 to 600 of those genes, it is conceivable that researchers will notice more mutations, said Qian Zhang, lead writer at the time to examine.
Interferons are the body’s first line of defense against infections, sound the alarm and trigger an army of virus-fighting genes, said virologist Angela Rasmussen, associate researcher at Columbia University’s Mailman School of Public Health’s Center for Infection and Immunity.
“Interferons are like a chimney alarm and a sprinkler formula rolled into one,” said Rasmussen, who is not concerned in the new studies.
Laboratory studies show that interferons are suppressed in some other people with COVID-19, through the virus itself.
Interferons are especially vital to the framework of new viruses, such as coronavirus, which the framework has never found, said Zhang, a researcher at Rockefeller University’s Human Genetics Laboratory for Infectious Diseases in St. Louis. Giles.
When he becomes inflamed with the new coronavirus, “his body deserves alarms to sound,” Zhang said. “If you don’t sound the alarm, you may have viruses in giant amounts. “
Significantly, patients did not produce autoantibodys in reaction to the virus, but appeared to have had them even before the pandemic began, said Paul Bastard, leader of the antibody study, also a researcher at Rockefeller University.
For reasons researchers don’t understand, autoant antibodies never caused a challenge until patients became inflamed with COVID-19, Bastard said. One way or another, the new coronavirus, or the immune reaction it triggered, turns out to have set them in motion. .
“Before COVID, his condition was silent, ” said Bastard. “Most of them had never been sick. “
Bastard said he now wonders if interferon autoanti-devices also increase the threat of other viruses, such as influenza. Among the patients in his study, “some of them had contracted influenza in the past, and we are investigating whether autoantiantibodys can just have an effect on the flu. “
Scientists have long known that viruses and immune formula compete in a type of arms race, with viruses evolving to evade the immune formula and even suppress their response, said Sabra Klein, professor of molecular microbiology and immunology at Johns Hopkins Bloomberg School. .
Antibodies are usually the heroes of the immune formula, protecting the body against viruses and other threats, but sometimes, in a phenomenon known as autoimmune disease, the immune formula results and creates autoantibodies. This happens in diseases like rheumatoid arthritis. , when antibodies attack the joints and type 1 diabetes, in which the immune formula attacks the insulin-producing cells in the pancreas.
Although doctors do not know the precise reasons for autoimmune diseases, they have observed that situations occur after a viral infection. Autoimmune diseases are more common as other people age.
In an unforeseen discovery, 94% of the patients on the test with these autoantiantibodys were men. Approximately 12. 5% of men with life-threatening COVID pneumonia had autoanticorps interferon, compared to 2. 6% of women.
This is unexpected, given that autoimmune diseases are much less unusual in women, Klein said.
“I’ve been reading the sexual differences in viral infections for 22 years and I don’t think reading autoantibodys thinks that would be a threat to COVID-19,” Klein said.
The study can help explain why men are more likely than women to become seriously ill with COVID-19 and die, Klein said.
“You see a lot more men dying at 30, only at 80,” he says.
Akiko Iwasaki, professor of immunobiology at Yale Medical School, noted that several genes from the immune system’s reaction to viruses are discovered on the X chromosome.
Women have two copies of this chromosome, with two copies of the gene, which gives them an endorsement in case a copy of a gene becomes defective, Iwasaki said.
However, men only have one copy of the X chromosome, so if there is a defect or destructive gene on the X chromosome, they do not have another copy of that gene to properly solve the problem, Iwasaki said.
Bastard noted that a woman in the test who developed autoantibodies has a rare genetic disease in which she has an X chromosome.
Scientists have struggled to find out why men have a greater threat of hospitalization and death by COVID-19. When the disease made the first impression in China, experts hypothesized that men were more likely to smoke because they were much more likely to smoke than the Chinese. Woman.
Researchers temporarily detected that men in Spain were also more likely to die of COVID-19, even though men and women smoke at about the same rate, Klein said.
Experts hypothesized that men might be at greater risk because they are less likely to wear masks in public than women and more likely to delay medical care, Klein said.
But differences in behavior between men and women provide only one component of the response. Scientists say it is imaginable that the hormone estrogen protects women, while testosterone may expose men to a greater threat. Interestingly, recent studies have shown that obesity poses a much greater threat. for men with COVID-19 than for women, Klein said.
However, they have their own form of coVID-19 suffering.
Studies show that women are 4 times more likely to revel in long-term symptoms of COVID, which last weeks or months, adding fatigue, weakness and some form of intellectual confusion known as “mental fog,” Klein noted.
As women, “maybe we and we are less likely to die, but then we’ll have all those long-term complications,” she says.
After reading the studies, Klein said, he would like to know if patients who are seriously ill with other viruses, such as influenza, also harbor genes or antibodies that disable interferon.
“There’s no evidence of that in the flu,” Klein said. “But we don’t look. With COVID-19, we could have discovered a very new disease mechanism that we can also locate and provide in a number of diseases.
Scientists say the new test solves a component of the mystery of why patient outcomes can vary so much.
Researchers say that some patients may have overcome exposure to other coronaviruses and patients who became seriously ill may also have inhaled higher doses of the virus, for example, as a result of repeated exposure to inflamed colleagues.
Although doctors have sought links between disease outcomes and blood type, they have produced conflicting results.
Evaluating patients for interferon autoanticorps may only help to find out which patients are most likely to be very ill, said Bastard, also affiliated with Necker Hospital for Sick Children in Paris. Verification takes approximately two days. Hospitals in Paris can now evaluate patients at the request of a doctor, he said.
Although only 10% of patients with life-threatening COVID-19 have autoantibodys, “I think we give the check to everyone who enters,” Bastard said. Otherwise, “we would not know who is at risk of serious illness. “form of disease. “
Bastard said he hoped his discoveries would lead to new life-saving therapies. It notes that the framework produces many types of interferons. Giving these patients another type of interferon, an interferon that is not deactivated through their genes or autoanticorps, can simply fight them. the virus.
In fact, a pilot examination of 98 patients published Thursday in the respiratory medicine with lancet revealed the benefits of an inhaled form of interferon. In the UK industry-funded examination, patients hospitalized by COVID randomly assigned to obtain beta-1a interferon were more than twice as likely as others enough to resume their normal activities.
The researchers want to verify those findings in a much larger study, said Dr Nathan Peiffer-Smadja, a researcher at Imperial College London who was not concerned about the study but wrote an accompanying editorial. Future studies deserve to check the blood of patients in search of genetic mutations and autoanticating antibodies opposed to interferon, to see if they respond to others.
Peiffer-Smadja notes that inhaled interferon can paint more than an injected form of the drug because it is administered into the lungs. While injected editions of interferon have been used for years to treat other diseases, the inhaled edition is still experimental and not marketed. Available.
And doctors want to be wary of interferon right now, because an examination conducted through the World Health Organization did not discover advantages in the injected form of the drug in COVID patients, Peiffer-Smadja said. mortality rates in patients receiving interferon, this location was possibly due to chance. Administering interferon later in the course of the disease may also simply announce a destructive immune reaction called cytokine storm, in which the immune formula does more harm than the virus.
Scientists around the world have entered more than one hundred clinical trials for interferon, according to Clinicaltrials. gov, a database of studies through the National Institutes of Health.
Until larger studies are completed, doctors say, bastard’s effects will replace the way they treat COVID-19.
Dr. Lewis Kaplan, president of the Society of Critical Care Medicine, said he treats patients for their symptoms, not their threat factors.
“If he’s a little sick, he’s treated a little carefully,” Kaplan said. “If he’s sick, he gets a lot of attention. But if a COVID patient has high blood pressure, diabetes and obesity, we don’t say, “They have threat factors. “Let’s put them in the ICU. “
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