These COVID-19 patients incubate new coronovirus strains


Among the 100 million people worldwide who have suffered from coronovirus infection, scientists are turning to the case of a 45-year-old COVID-19 patient in Boston to understand how the virus is able to outcompete humans. .

During his 154-day illness – the longest one on record – the patient’s body became a crucible of riotous viral mutations. He offered the world the first sight of a significant change in the virus’s spike protein, which sounded an alarm bell when it was later found in strains in the United Kingdom, South Africa and Brazil.

In the UK strain, a genetic change known as N501Y is believed to help increase the infectivity of the virus by about 50%. In South African strains, it may reduce the effectiveness of COVID-19 vaccines and treatments. Trials of its effect on the Brazilian version are still ongoing.

The Boston patient is now seen as an important precursor of the coronovirus with the ability to discontinue newer and more dangerous versions. However, he died during the summer, but the medical file he left is helping experts anticipate the formation of a new immune system, which has been growing for months with patients with compromised immune systems fighting the virus Let’s focus on the role of the population.

The most ill in COVID-19 patients, this population of “long hulls” plays an important role in planting new variants of coronovirus, some of which may alter the trajectory of the epidemic.

The mutation arising from this single patient is “a microcosm of viral development that we are seeing globally,” Dr. Jonathan Z. Lee, an infectious disease specialist at Brigham and Women’s Hospital in Boston, who treated him. “He showed us what can happen” when germs with a germ to change genetic shape stumble upon situations that reward them for doing so.

Indeed, conditions where patients cannot clear the viral infection are “the worst case scenario to develop mutations”, Dr. Dr., an immunologist and founding director of the Ragan Institute in Boston. Bruce Walker said.

As the illness of weeks turns into months, a virus copies itself millions of times. Each copy is an opportunity to make random mistakes. As it harbors new mutations, viruses can occur on those that help antagonize drugs, empty the immune system, and strengthen.

SARS-CoV-2, the coronovirus causing COONID-19, has been an unexpected opposition. Volcker said it is a chance to see its change in near-real-time, and see where and how it mutates in a host can guide the design of vaccines and drugs that do not lose their effectiveness over time .

COVID-19 patients were beginning to fill the beds of Brigham and Women’s Hospital in the spring of 2020, when the Boston patient was first admitted. He had fever, nausea and a whistle in his lungs that provoked “ground glass” the appearance of the new disease, said Lee, who was part of the team that detailed the man’s case in the New England Journal of Medicine.

But COVID-19 was one of his challenges. For 22 years, he suffered from a rare disorder called antiphospholipid syndrome, which caused his immune system to attack his organs and spread dangerous blood clots throughout the body.

To protect his rogue immune system from being killed, the patient needs an arsenal of immunosuppressive drugs. But in his fight against coronavirus, those drugs tied the patient’s punching arm behind his back.

A Boston patient tested positive for SARS-CoV2 infection four different times over 22 weeks. He was hospitalized six times, including in intensive care. Doctors treated her with three courses of the antiviral drug Remedisvir and once with an experimental cocktail of Razenon’s monoclonal antibodies.

Exterior of Brigham and Women's Hospital in Boston

A patient who battled COVID-19 for 154 days was admitted four times during her illness at Brigham and Women’s Hospital in Boston.

(Brigham and Women’s Hospital)

The swab taken from his nose and throat during his second hospital stay provided the first indication of the shocking pace of the virus’s genetic mutations: 30,000 letters of coronovirus, compared to a sample taken during his first hospitalization. The sequence of 11 characters was flipped, and nine such nucleotides were omitted.

His next visit to the hospital landed him in the ICU. The tests showed that 10 more characters were changed in the virus’s genetic code and another one was removed in a span of only five weeks. Three weeks after recovering, he tested positive again and was put on a mechanical ventilator to help him breathe. This time, the researchers found 11 more letter mutations and 24 more deletions in the virus’ genome.

Scientists could not say whether the Boston patient had failed to kick the virus, or whether it was completely altered so that his immune system could not recognize it.

One thing was clear: more than half of the changes occurred in a stretch of the genetic code, which determines the structure of the virus’s spike protein, which protuberance plumps on human cells and initiates an infection. The virus “receptor binding domain” – essentially the key that locks on a human cell – constitutes only 2% of the virus’s genetic code. But 38% of the mutations that occurred during a Boston patient’s long illness focused on just that place.

In late December, British scientists speculated that such a scenario involving an immunological patient somewhere in England may have led to a mutation that isolated the UK strain.

Walker said he fears that there are many more patients, including those with untreated HIV infection. People infected with HIV infected with COVID-19, and drugs that reward SARS-CoV-2 for “escape” mutations, can become the crucible of viral mutations.

Scientists in South Africa share that concern.

“In South Africa, the country with the world’s largest HIV epidemic, one concern is long-term viral replication and intra-host development in the context of HIV infection,” the authors of an early study wrote that alerted the world to a new version Gaya in early December.

COVID-19 patients are treated with oxygen in South Africa

Patients with COVID-19 are treated with oxygen at Tshwane District Hospital in Pretoria, South Africa.

(Jerome Delay / Associated Press)

So far, there is no evidence that patients suffering from HIV are at risk of long-lasting cases of COVID-19. Their explorers stated that even if they were, a long series of immunocompromised patients would have been necessary to produce multiple mutations that differentiated the strain of South Africa.

Scientists are still trying to understand how some mutations like N501Y have reached so many places at once. Has the scale of the epidemic mushroom given the virus many opportunities to change itself? Or are these mutations occurring in very few people, such as Boston patients, and then somehow stopping the ride around the world?

Both factors are presumably at work, and the longer the epidemic heats up, the more likely the virus will have to develop random mutations.

The Boston patient shows why it can be so dangerous. In their case, stretches of the genetic code that were most prone to change the affected structures are designed to recognize COVID-19 vaccines and drugs. There are now indications that changes may reduce the value of those measures.

Tulio de Oliveira, an infectious disease researcher at the University of KwaZulu-Natal, South Africa, sees a pattern in which uncontrolled proliferation and long-term infection work together to increase coronovirus mutations.

Many places where new variants have been identified – including South Africa, Britain and California – experienced waves of split two outbreaks in just a few months. De Oliveira suspects that this is not merely a coincidence.

In the first wave, he said, the spread of the infection gives the virus ample opportunity to take genetic changes that can remain in the body of immune patients. By the time a second wave begins, novel versions incubating in these long-hulls have also started circulating. When they encounter a large number of new hosts, the result is a fertile environment for the strains to establish themselves – if their genetic modification confers some benefit.

D’Olivera said that the best way to prevent more mutations is to both extend vaccination and protect people with compromised immune systems.

“If we keep the virus here and there for a long time, we will give more opportunities to outsource it to us.”

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