Briton Chloe Middleton became one of the youngest victims of the coronavirus in March last year, tells the Daily Mail. The young caregiver was only 21 years old.
Healthy, young and free of any medical conditions, Chloe did not appear to have any of the criteria for the risk of contracting the virus, which about a year ago was just starting to tighten its death grip.
But after the girl was pronounced dead at Wexham Park Hospital in Slough, Berkshire on March 19, 2020, the coroner confirmed that the cause of death was COVID-19.
It was a devastating blow to her family from Beaconsfield, Buckinghamshire, and a powerful wake-up call for millions of young Britons who seemed convinced they were vulnerable to the threat of the coronavirus.
The mother of the unfortunate girl, Diane Middleton, wrote on Facebook an appeal to those who believed that COVID only affects the elderly: “Please think again, this so-called virus took the life of my 21-year-old daughter.”
There is some evidence that the elderly, the frail and the chronically ill are at greatest risk of contracting COVID-19, with nearly 75 percent of the 118,000 deaths in the UK currently occurring in people over 75.
Age and illness weaken the immune system, making it harder for the body to fight the virus and harder to recover from the illness it causes.
But there is also a disturbing fact that some people, like Chloe, simply do not fit the profile of a likely victim of a severe infection. Yes, the case of the deceased girl is rare, rare and the victims are under 30 years old, writes the Daily Mail. But Office for National Statistics data show that just over nine percent of deaths – about 11,000 in total – occur in the 45-64 age group, meaning that many victims are no older than middle age. Some of them have had long-term illnesses or health problems, such as obesity, that have reduced their chances of fighting the virus.
This mystery baffled doctors. But now scientists have found an important clue. The significant differences in the genetic makeup of humans may explain why some are completely infected with the virus, which, given their age and health, they should be able to fight without any major complications, while others hardly show a single symptom.
“We don’t know why these healthy young people are getting so sick with COVID, but one possibility is that they are genetically predisposed to it,” says Professor Eleanor Riley, an expert on the immune system and infectious diseases at the University of Edinburgh. “It is possible that these children have inherited genetic variations from their parents, which puts them at risk.”
In December, a team of scientists from the Roslin Institute in Edinburgh discovered five key genes that increase the likelihood of a COVID-19 patient dying.
Genes carry instructions for every single biological process in our bodies, including how to create cells in the immune system to fight the virus.
The team examined 2,244 critically ill patients with coronavirus, including more than 200 hospitalized in intensive care units. They were terribly ill; three quarters of them could not breathe without mechanical assistance, and more than one in five eventually died.
Blood samples were used to scan the DNA of each patient, and the results were compared with that of healthy individuals to identify any underlying genetic differences that might explain their critical condition.
Scientists have found that out of about 20,000 genes in the human body, critically ill patients are likely to have significant differences in five of them. And they all played an important role in the body’s immune response to infection.
One gene, named TYK2, is critical for making cells in the immune system more inflammatory – or more “evil,” as one researcher described. This is vital to satisfactorily combatting harmful viruses like COVID.
But if the TYK2 gene is defective, this immune response can become overdone, putting patients at risk of severely damaging pneumonia, which is often the real cause of death in COVID.
Another culprit turned out to be IFNAR2, a gene responsible for programming the production of interferon, a molecule that triggers a response from the entire immune system at the first sign of an enemy. When this gene doesn’t work, not enough interferon is released, which gives the virus a head start and allows it to replicate quickly before any resistance appears.
The end result is a rapid fall to life-threatening disease levels. It is unlikely that these results will lead to routine genetic screening of patients, as there is no standard test yet, and even if it were, it would be extremely time-consuming and expensive. But it does give doctors additional clues on how best to treat seriously ill patients.
For example, a new class of drugs called JAK inhibitors, which are already being prescribed to patients with rheumatoid arthritis and other inflammatory conditions, may reduce uncontrolled inflammation caused by disruptions in the TYK2 gene.
A study published last month found the drugs prevent death in patients with severe COVID.
Professor Andrew Easton, a virologist at the University of Warwick, says the discovery of five rogue genes makes sense because there must be some scientific explanation for why healthy young people fall prey to severe infections: “This cannot be just a random event, it must be the main factor. In many cases, we just don’t know what it is. Apart from genetic predisposition, it could also be due to other risk factors that we have not yet identified, such as damage caused by childhood respiratory infections or something else in their medical history that makes them more susceptible to severe infection. “
Our genes dictate more than just the risk of severe COVID infection. They also largely determine our chances of developing sepsis, a fatal complication of COVID and a condition that was already killing about 40,000 people a year in the UK before the pandemic broke out. Sepsis occurs when the immune system accidentally sends infection-fighting chemicals throughout the body, not just to the area of infection. These chemicals cause devastating inflammation and damage healthy tissues and organs, causing them to break down quickly. This is often fatal – sometimes death of patients within 24 hours.
A paper published in January showed that 23 different genes may be associated with an increased susceptibility to sepsis in people infected with viruses or bacteria.
Again, unusual variations in these genes mean that some people, including young, healthy, and healthy adults, may be more likely to become seriously ill and die from sepsis.
Dr. Ron Daniels of the Sepsis Trust says: “From the outset of this pandemic, it was clear that the most critically ill COVID patients were developing sepsis. This includes young people who are critically ill, and it is almost certain that these young healthy people also have a genetic predisposition. ”
While genetics plays an important role, it could also be a simple question about how many viruses are exposed to a virus during infection, according to Professor Eleanor Riley. This is the so-called infectious dose, the amount that must enter the body to cause an infection.
In the case of COVID-19, the virus turned out to be so contagious that scientists believe that several hundred tiny viral particles are enough for the infection to enter the eyes, nose or mouth. With some other viruses, it takes thousands. The higher this infectious dose, the more likely it is to develop serious symptoms of COVID-19 – even in those whose immune systems are operating at full capacity due to their young age.
Perhaps this is why young, healthy doctors, nurses and other healthy key workers died during the first wave, experts say: they were simply more exposed to the virus because of their jobs.
“Maybe they were just unlucky that they received a really heavy dose and breathed it directly into their lungs,” says Professor Eleanor Riley.
And Professor Andrew Easton says, “If someone is exposed to a high dose of infection, the infection is likely to spread much faster.”
And even something as simple as a recent cold can affect the likelihood of COVID in low-risk groups. Most colds are caused by rhinoviruses. But about one in five is associated with members of the coronavirus family – relatives of the COVID virus that are far less destructive.
There are four viruses (229E, NL63, OC43, and HKU1) that scientists say almost certainly each of us has been infected with one or more of them at some point in our lives. Some research suggests that recent exposure to one of these four could mean that the immune system is already tuned in to fight the virus that causes COVID-19.
A 2020 study by the La Jolla Immunology Institute in San Diego, USA, examined blood samples from healthy volunteers who were not infected with COVID-19. Nearly half of these contained cells of the immune system, known as T cells, which were able to recognize and destroy the COVID-19 virus through “cross-reactivity,” where the immune system produces disease-fighting cells in response to an invading organism. proved to be effective against the other.
“It is possible that very sick young COVID patients may not have cross-protection if they have not been exposed to a similar cold virus for a long time,” says Professor Riley.
One of the reasons COVID-19 has become such a difficult adversary is that up to 80 percent of infected people show no symptoms at all, but can still transmit the virus to others.
Scientists at Aarhus University in Denmark think they know why. They studied how the virus behaves in the lungs and found something extraordinary – it looks like it can “hide” from the immune system. As a result, many patients do not see any of the classic signs of the body’s defenses, such as fever or pain, as the virus eludes detection and spreads even further without being noticed. This is a clever mechanism that allows the virus to buy valuable time to establish itself and infect other people.
But there may be a simpler explanation, says Professor Riley. “We do not know if this symptomlessness occurs in most infected people with other infectious viruses, such as the common cold or flu, as we have never tested for this.”
.
