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Why some get it worse than others

The home for all non-political Coronavirus (Covid-19) discussions on The Lemon Fool
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This is the home for all non-political Coronavirus (Covid-19) discussions on The Lemon Fool
onthemove
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Why some get it worse than others

#428031

Postby onthemove » July 16th, 2021, 10:50 am

At least part of the answer would appear to be the absence of 'killer T cells' (distinct from antibodies), from previous coronavirus infections.

" https://www.sciencedaily.com/releases/2 ... 140959.htm
Study ties milder COVID-19 symptoms to prior run-ins with other coronaviruses
...
As the pandemic progressed, Davis mused: "A lot of people get very sick or die from COVID-19, while others are walking around not knowing they have it. Why?"
...
Many of these killer T cells were in "memory" mode, he added.

"Memory cells are by far the most active in infectious-disease defense," Davis said. "They're what you want to have in order to fight off a recurring pathogen. They're what vaccines are meant to generate.""


This information maybe some reassurance to the poster on another thread who expressed concern that their antibody levels were lower than they would have liked.

Also this information does backup the idea that hiding away from infections in general is not always a good idea. It would seem from the research above that it's prior infections from (most likely) a coronavirus variant of common cold that may actually be providing quite a degree of protection - so much so that some people (I've heard estimates of up to 30%) don't even know they've got covid.

I genuinely hope that we as a society don't overreact. Letting colds and flu, etc, do the rounds, caught at work or in crowded trains, planes, etc, could be beneficial. We may already be seeing the benefits with fewer serious covid cases than may have otherwise been the case.

Some more background info on T cells vs antibodies for anyone wondering what's the difference...

"Killer cells
Alongside antibodies, the immune system produces a battalion of T cells that can target viruses. Some of these, known as killer T cells (or CD8+ T cells), seek out and destroy cells that are infected with the virus. Others, called helper T cells (or CD4+ T cells) are important for various immune functions, including stimulating the production of antibodies and killer T cells.

T cells do not prevent infection, because they kick into action only after a virus has infiltrated the body. But they are important for clearing an infection that has already started. In the case of COVID-19, killer T cells could mean the difference between a mild infection and a severe one that requires hospital treatment, says Annika Karlsson, an immunologist at the Karolinska Institute in Stockholm.
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T cells could also be more resistant than antibodies to threats posed by emerging variants. Studies by Sette and his colleagues have shown that people who have been infected with SARS-CoV-2 typically generate T cells that target at least 15–20 different fragments of coronavirus proteins1. But which protein snippets are used as targets can vary widely from person to person, meaning that a population will generate a large variety of T cells that could snare a virus. “That makes it very hard for the virus to mutate to escape cell recognition,” says Sette, “unlike the situation for antibodies.”
...
...
https://www.nature.com/articles/d41586-021-00367-7 "

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Re: Why some get it worse than others

#428057

Postby Lanark » July 16th, 2021, 12:02 pm

There is a strong correlation with vitamin D levels, but no-one has yet proven a causal link.

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Re: Why some get it worse than others

#428094

Postby onthemove » July 16th, 2021, 1:49 pm

Lanark wrote:There is a strong correlation with vitamin D levels, but no-one has yet proven a causal link.


The vitamin D correlation was based on observational studies.

The study I linked to went a little bit further...

"The researchers analyzed blood samples taken from healthy donors before the COVID-19 pandemic began, meaning they'd never encountered SARS-CoV-2 -- although many presumably had been exposed to common-cold-causing coronavirus strains. The scientists determined the numbers of T cells targeting each peptide represented in the panel.

They found that unexposed individuals' killer T cells targeting SARS-CoV-2 peptides that were shared with other coronaviruses were more likely to have proliferated than killer T cells targeting peptides found only on SARS-CoV-2."


This is investigating a causal mechanism - identifying T cells present in blood samples taken prior to the sars-cov-2 pandemic, which show an ability to target aspects of the sars-cov-2 virus - through a mechanism by which T cells are well known to operate.

This is more than simple correlation. This is looking at how the presence of those prior T cells can help combat a sars-cov-2 infection.

"They found that, sure enough, COVID-19 patients with milder symptoms tended to have lots of killer-T memory cells directed at peptides SARS-CoV-2 shared with other coronavirus strains. Sicker patients' expanded killer T-cell counts were mainly among those T cells typically targeting peptides unique to SARS-CoV-2 and, thus, probably had started from scratch in their response to the virus."


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