“A lot of people get very sick or die from COVID-19, while others are walking around not knowing they have it. Why?”
Researchers at Stanford University are trying to solve the mystery of mild illness with Covid-19 for some lucky people who, unlike other patients, get the disease “on foot”.
Another study confirms the link between COVID-19 mild illness and previous infections with seasonal coronaviruses such as those that cause the common cold, and Stanford University researchers are trying to explain why.
So if you have been infected with another coronavirus strain in the past, you may be unknowingly more likely to have mild symptoms of COVID-19.
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This is shown by the scientific data of a new study by Stanford University, a fact that is attributed to specific “memory” cells of our immune system.
A lot of people get very sick or die from COVID-19, while others are walking around not knowing they have it. Why?
Why is this happening?
These cells are activated faster when they come in contact with SARS-CoV-2, the virus that causes COVID-19 infection, as those who have “fought” in the past with a coronavirus strain “remember” the battle.
This mobilization also seems to be an explanation for the fact that children have milder symptoms when they have COVID-19 than adults, as they are more often affected by seasonal infections.
The cells thrown into battle
When T lymphocyte receptors detect a peptide on the surface of a cell “foreign” to the body, such as a protein from a pathogen, these cells are activated and proliferate to destroy all the cells that contain these sequences. peptides.
Some of these T lymphocytes will “store” in their memory the information from this battle, ready in case they meet the specific peptides again to act immediately.
How does this whole process relate to the coronavirus?
Study author and postdoctoral fellow Vamsee Mallajosyula confirmed for the first time that certain parts of the SARS-CoV-2 sequence are identical to similar parts of the peptides of one or more coronavirus strains that cause one or more of the four most common clusters.
The research methodology
The researchers first assembled a group of 24 different peptide sequences that were either unique to proteins made from SARS-CoV-2 or also found in similar proteins made from one or more (or even all) of seasonal infections; coronavirus strains.
Analyzing blood samples from donors who were not infected with the coronavirus-causing SARS-CoV-2 virus, but who may have been infected with another common cold-induced coronavirus strain, and determining the number of T lymphocytes that targeted each peptide, found that T lymphocytes targeting SARS-CoV-2 peptides that were common to those of other coronavirus strains were more likely to proliferate than those lymphocytes targeting peptides found only in SARS-CoV-2.
This means that in the past they had encountered a milder strain of the coronavirus – and had proliferated in response – while several of these cells were “memory cells”.
But how is mild illness explained?
Going a step further in research and understanding this attack, they analyzed samples from patients who had contracted COVID-19 infection.
They concluded that those with mild symptoms also had more memory T lymphocytes that acted directly against common SARS-CoV-2 peptides compared to other coronavirus strains.
“It may be that patients with severe COVID-19 hadn’t been infected, at least not recently, by gentler coronavirus strains, so they didn’t retain effective memory killer T cells,” said Dr Mark Davis, senior study author.
In contrast, the T lymphocytes of seriously ill patients targeted peptides that are unique to SARS-CoV-2, starting from scratch their “battle” with the virus, without having any previous “memory”.
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“Sniffles and sneezes typify the daycare setting,” he said, “and coronavirus-caused common colds are a big part of the reason. As many as 80% of kids in the United States get exposed within the first couple of years of life.”
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