When two brothers got seriously with the Covid-19 at the same time in March, their doctors were baffled. Both were young (29 and 31 years old) and in good health. However, within a few days they may no longer be able to breathe their own and, tragically, one of them died.
Two weeks later, when a couple of brothers beat Covid, either in their twenties, also gave the impression in the Netherlands, geneticists were called to investigate, what they discovered was a trail that led to serious cases, genetic diversifications and gender. Differences with a loss of immunity work, as that can lead in the end to a new technique to treat thousands of patients with coronavirus.
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The common thread of studies is the absence of a substance called interferon that is helping to orchestrate the body’s defense against viral pathogens and can be infused to treat diseases such as infectious hepatitis. Now, more and more evidence suggests that a significant minority of Covid -19 patients are very ill due to an altered reaction to interferon. Former twin studies published Thursday in the journal Science have shown that interferon deficiency may be hidden at a harmful turning point in SARS-CoV-2 infections.
“It looks like this virus has a great trick,” said Shane Crotty, a professor at the Center for Infectious Diseases and Vaccine Research at the La Jolla Institute of Immunology in California. “This wonderful trick is for the initial innate immune reaction for a significant time and, in particular, an early reaction to type 1 interferon.
The paintings highlight the possibility of interferon-based treatments to expand a variety of slow-accumulating Covid-19 treatments, which come with remdesivir and convalescent plasma from Gilead Sciences Inc. , a component of cured patients’ blood that would possibly involve immune factors. .
These remedies offer limited benefits and are sometimes used in very sick hospitalized patients. The option that interferon would possibly help others is exciting, as it is most effective in the early stages of infection, when life-threatening respiratory failure can also simply dozens of studies on interferon remedy are recruiting patients with Covid-19 lately.
‘We believe that time may be a must because only in the early stages can we combat viral waste and protect ourselves from infections,’ said Alexander Hoischen, head of the genomic and immunogenomic generation organization in Radboud. University Medical Center in Nijmegen, analyzed the DNA of the two teams of brothers.
Being male, elderly and having underlying fitness disorders can increase the threat of a potentially fatal Covid-19 to patients, but even within those groups, the severity of the disease varies considerably. -existing degrees of inflammation and immunity, the amount of virus that triggers infection and the genetic makeup of patients.
New Nexus
The role of interferon represents a new link in Covid-19’s complex interaction with the human immune system. Many patients suffer their worst headaches due to an exaggerated immune reaction called cytokine typhoon and can gain advantages from dexamethasone, a reasonable generic. that soothes those typhoons.
“It’s a very attractive disease because very little immunity isn’t good,” said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, on September 10 at an online briefing for Massachusetts General Hospital staff. “Too much immunity is bad. “
According to Yuen Kwok-Yung, Director of Infectious Diseases in the Department of Microbiology at the University of Hong Kong, early or overdue availability of interferon at Covid-19 instances has a primary effect on the severity of the disease. Ideally, the production of the antiviral substance would be triggered when immune cells encounter the genetic mantle of SARS-CoV-2, preventing immediate viral replica within the framework and avoiding complications, he said.
”But the SARS-CoV-2 virus has anti-interferon genes that can prevent or thwart the production or effect of interferon’,’ said Yuen, who measured the effects on human lung tissue. If the reaction to interferon is delayed and the amount of viruses in the frame reaches a peak at a higher level, other portions of the immune formula will be “awakened”.
“Nice place to stay”
This can cause inflammation of the lungs, collateral damage due to an exaggerated reaction of the immune formula to the virus. “It’s deastrous, ” he said.
Some others are known to have trouble fighting infections because they produce antibodies that deactivate their own interferon. On Thursday, a global consortium of researchers said such immune responses to protein could endanger the life of Covid-19 pneumonia in at least 2. 6% of cases. women and 12. 5% of men.
According to the Science study, interferon blocker antibodies gave the impression in 101 of the 987 patients with severe disease, however, in none of the other 663 people with an asymptomatic or benign case. Patients over the age of 65 were also more likely than more young patients to have the autoimmune abnormality, than “clinically silent until patients become inflamed with SARS-CoV-2,” said the organization of more than a hundred scientists.
“Nice stay”
”These effects provide an initial explanation of the excess of men among patients with potentially fatal Covid-19 and the greatest threat to age’, the researchers led through Jean-Laurent Casanova, director of the Laboratory of Human Genetics at Rockefeller University in St. Louis. Giles. de Infectious Diseases in New York, he said, “They also provide a way to identify others who are at risk of a life-threatening Covid-19. “
Genetic research from Covid-19 patients published in the same journal revealed two dozen genetic mutations that remained “silent” until patients became inflamed with SARS-CoV-2. Researchers, many of whom were also concerned about antibodies, sequenced the genomes. 659 patients with life-threatening cases of disease; 3. 5% had genetic diversifications that inhibit interferon production.
These genetic defects were those described by Hoischen and his colleagues in a dozen Dutch centers in the Journal of the American Medical Association two months ago, both teams of siblings had inherited a genetic mutation that altered the reaction to interferon, preventing their immune formula. from the fight against coronavirus until it was replicated for days.
For the Dutch, the effects were cruel. The first, a young father from a city in the south of the Netherlands, suffered from shortness of breath, cough and fever at home for 8 days before being admitted to intensive care and was scheduled to spend 33 days in hospital, 10 of them . on a fan.
Fever that infuriates
His 29-year-old brother succumbed to Covid-19 in an intensive care unit in Rotterdam after being treated for a surprise and fever that rose to 44 degrees Celsius (111 degrees Fahrenheit). When Radboud’s doctors learned of the case of his younger brother, as well as a momentary couple – siblings over 21 and 23 who also had respiratory failure – they sought a genetic cause.
They discovered a mutation that was carried on the X chromosome. Defects on this chromosome are most likely in men, who have only one copy, while women have two.
Mutations in men are rare (occurring in 1 in 10,000 more people) and an unlikely explanation for the vast majority of severe Cases of Covid-19, but scientific studies imply that the diverse bureaucracy of interferon disorder may be the basis of up to 14% of critical patients. and that specific test and remedy can prevent you from serious illness and death.
“If we can get them to our college medical center early enough,” Hoischen said, “our doctors would possibly treat them with interferons. “
Other tactics to succeed over autoimmunity, such as the removal of antibodies opposed to interferon from the blood, called plasmapheresis, can also help patients. On the other hand, patients who produce antibodies opposed to interferon do not administer blood products to treat other patients.
“Rare diseases and maximum non-unusual bureaucracy of the same disease can converge, and we can be informed of others,” Hoischen said. “It’s hope. “
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