Novel Coronavirus

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BetteTheRed

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There are 4 people in Alberta in the hospital, under 30, with no known pre-existing conditions. At this point no one knows they won't have a severe case if they get it.
To unconfuse Kimmio:

There are 4 people in Alberta in the hospital [with Covid-19], under 30, with no known pre-existing conditions. At this point no one knows they won't have a severe case if they get it. ["No-one" and "they" refer to generic Albertans, not those specific 4, who definitely have it.]
 

ChemGal

One with keen eye
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To unconfuse Kimmio:

There are 4 people in Alberta in the hospital [with Covid-19], under 30, with no known pre-existing conditions. At this point no one knows they won't have a severe case if they get it. ["No-one" and "they" refer to generic Albertans, not those specific 4, who definitely have it.]
Thanks, I was totally lost about the question.
Yes, there's still the 'young, healthy people only have mild cases' attitude - many do, but no one knows if they would have a mild case, or a severe one until they actually get infected as there are young, healthy people who do end up severely ill.
 

Northwind

Still knitting. Walking the path to health.
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Dr Henry regularly points out that as long as the virus is anywhere, there is a risk of it being spread even when we're in places that haven't see cases of it for some time.

I expect we'll see more young people getting sick sadly. There are stories emerging of parties and gatherings that will likely result in sick people.
 

Mendalla

Eastern Lowland Gorilla
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Ontario had its first death under 20 recently so the young folks really need to be a bit more mindful. They may be less at risk than aging, diabetic, hypertensive apes but that doesn't make them bulletproof.

London is fairing reasonably well now. Most days Middlesex-London Health Unit is reporting under 5 confirmations. Today was only one. Our incidence per 100,000 is well below the provincial rate so we've done fairly well. Can't let our guard down yet, but at least things are looking up as July approaches.
 

ChemGal

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There's an outbreak in a condo building in Calgary. Will be interesting to see if there's any new information about how it's spreading or if it's as simple as something like elevator buttons. Hopefully people there who aren't sick yet can avoid it.
 

KayTheCurler

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I have an eighty year old friend who thinks they are sitting ducks in their fancy condos. She recognises that ONE person carrying the virus could spread it via an elevator button or the stairway handrails. Everyone in the building is over 65 and most have health problems.
 

Mrs.Anteater

Just keep going....
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Nova Scotia hasn’t had a new case in two weeks. Two people remain in hospital, I believe they are no longer active cases but people who had it so badly that they still suffer the fallout.
The atlantic bubble is opening up next week.
 

ChemGal

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I have an eighty year old friend who thinks they are sitting ducks in their fancy condos. She recognises that ONE person carrying the virus could spread it via an elevator button or the stairway handrails. Everyone in the building is over 65 and most have health problems.
If it's just by common touch surfaces though, people can at least mitigate that risk entirely on their own with handwashing, handsanitizer, etc. If it's something like a ventilation system, that control is not there.
 

EasternOrthodox

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Here’s the article, that won’t display,

Subscribe to read | Financial Times

Scientists have identified a new set of 68 genes associated with a high risk of developing severe Covid-19 as geneticists seek to understand why people vary so much in their susceptibility to the illness.

The preprint paper released on Thursday by analytics company PrecisionLife, which used data from UK Biobank, adds to a growing number of genetic clues about vulnerability to the virus.

The phenomenon of some people suffering grave illness while others are infected without symptoms despite being in similar environments has caused widespread puzzlement.

Twelve of the 68 genes identified by Oxford-based PrecisionLife are involved in the heart and blood circulation, including the regulation of calcium levels. This tallies with the observation that the cardiovascular system often undergoes severe stress in patients hospitalised with Covid-19.

Last week an international academic team found two areas of human DNA that differed significantly between 1,600 patients in Spain and Italy who suffered Covid-19 respiratory failure and people who bore no signs of disease.

One set of genes determines blood group: people with group A blood (roughly 30 per cent of the global population) have a higher risk of serious illness than group O, the researchers found.

The second covers genes involved in the ACE2 receptor, a protein on the surface of human cells that the coronavirus uses as an entry point, although their precise connection to Covid-19 remains unclear.

The findings are “just a start”, said Daniel Wilson, an expert in infectious disease genomics at Oxford university. “But they are a pointer to the way human genetic analysis will help to explain why some people get severe Covid and others escape.”

The potential influence of genetic discoveries is huge. They can lead to better drugs to treat Covid-19 because they improve scientists’ understanding of the disease’s biology.

Longer term, decoding a patient’s DNA once infection is confirmed could enable a personal treatment plan to be tailored to their likely genetic response to the virus.

“At some point it may be possible to measure people’s genetic risk score for susceptibility to Covid,” said Prof Rory Collins, chief executive of UK Biobank, which has several projects to match genetic data on its 500,000 participants with their Covid-19 experiences.

“We could then identify particularly vulnerable people who need to be protected if there is an outbreak of the disease nearby,” he added.

Two international consortiums have been formed to co-ordinate the research. Both aim to share all data and analysis openly and release results as quickly as possible.

The Covid-19 Host Genetics Initiative is led by Mark Daly and colleagues at the Institute for Molecular Medicine Finland. The other project, the Covid Human Genetic Effort, is led from the US by Helen Su of the National Institutes of Health and Jean-Laurent Casanova of Rockefeller University.

The US project is searching for variations in single genes that would account for the unusual cases of young and healthy individuals who have a life-threatening response to Sars-Cov-2 infection — and for people who seem to resist infection even when they are exposed multiple times.

“There are people, for example the spouses of someone who is critically ill, sharing a bed with someone and remaining not only asymptomatic but even testing negative,” said Prof Casanova.

Aids researchers have found that genetic mutations on the CCR5 protein, which HIV uses to enter human cells, make some people resistant to infection by that virus. There may be comparable variations in the ACE2 receptor that would affect their susceptibility to Sars-Cov-2.

Scientists are using human DNA in different ways to investigate Covid-19. Some researchers are using genetic data already accumulated for other purposes, such as UK Biobank, and matching it with any information that emerges about the subjects’ Covid-19 experience. Others are obtaining fresh genomes from Covid-19 patients.

There are also different levels of analysis. Top of the range is “whole genome sequencing” which reads all 3bn chemical letters of DNA that store the genetic inheritance of every human being. Next comes “exome sequencing” which just reads the genes that directly make proteins, the most active biological molecules.

The third level — faster and cheaper than the other two — is “genotyping”. It focuses on an array of 500,000 to 1m DNA letters across the genome chosen because they represent hotspots of individual variation.

The largest database of genotyped data is held by 23andMe, the California-based consumer genetics company, which is keen to see it used for Covid-19 research. Its first study got responses from 750,000 people and provided early evidence that those with type O blood were less likely to test positive for infection — a finding confirmed last week by the academic study in Spain and Italy.

“The speed at which we can conduct these studies has increased enormously,” said Joyce Tung, 23andMe’s vice-president of research. Once it could take a decade to understand how a gene influenced a disease, she added. Now it can be done in a matter of months.
 

EasternOrthodox

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I’m finding Covid-deniers or minimizers (“just like the flu”) increasingly irritating. The few that remain,that is.

Just this morning, the guy who reads the medical journals and makes it intelligible, I hear about this minority who can’t shake off the tired feeling for weeks. Another article reports Type 1 diabetes after recovering from Covid.

Here‘s the video

 

EasternOrthodox

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I have an eighty year old friend who thinks they are sitting ducks in their fancy condos. She recognises that ONE person carrying the virus could spread it via an elevator button or the stairway handrails. Everyone in the building is over 65 and most have health problems.
I’m a decade younger and my condo isn’t particularly fancy but I sympathize with your friend.

My condo building doesn’t have air conditioning and I have seen no vents that would bring in air. The heating is electric baseboard. (The climate is mild here in Victoria, BC).

I’m surprised at how few other older people there are in the building. There‘s even a few children.

I‘m getting the impression that it spreads mostly aerosol, indoors. There hasn’t been a spike (yet) from the US protests. it This is sheer guesswork course.
 

ChemGal

One with keen eye
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Here’s the article, that won’t display,

Subscribe to read | Financial Times

Scientists have identified a new set of 68 genes associated with a high risk of developing severe Covid-19 as geneticists seek to understand why people vary so much in their susceptibility to the illness.

The preprint paper released on Thursday by analytics company PrecisionLife, which used data from UK Biobank, adds to a growing number of genetic clues about vulnerability to the virus.

The phenomenon of some people suffering grave illness while others are infected without symptoms despite being in similar environments has caused widespread puzzlement.

Twelve of the 68 genes identified by Oxford-based PrecisionLife are involved in the heart and blood circulation, including the regulation of calcium levels. This tallies with the observation that the cardiovascular system often undergoes severe stress in patients hospitalised with Covid-19.

Last week an international academic team found two areas of human DNA that differed significantly between 1,600 patients in Spain and Italy who suffered Covid-19 respiratory failure and people who bore no signs of disease.

One set of genes determines blood group: people with group A blood (roughly 30 per cent of the global population) have a higher risk of serious illness than group O, the researchers found.

The second covers genes involved in the ACE2 receptor, a protein on the surface of human cells that the coronavirus uses as an entry point, although their precise connection to Covid-19 remains unclear.

The findings are “just a start”, said Daniel Wilson, an expert in infectious disease genomics at Oxford university. “But they are a pointer to the way human genetic analysis will help to explain why some people get severe Covid and others escape.”

The potential influence of genetic discoveries is huge. They can lead to better drugs to treat Covid-19 because they improve scientists’ understanding of the disease’s biology.

Longer term, decoding a patient’s DNA once infection is confirmed could enable a personal treatment plan to be tailored to their likely genetic response to the virus.

“At some point it may be possible to measure people’s genetic risk score for susceptibility to Covid,” said Prof Rory Collins, chief executive of UK Biobank, which has several projects to match genetic data on its 500,000 participants with their Covid-19 experiences.

“We could then identify particularly vulnerable people who need to be protected if there is an outbreak of the disease nearby,” he added.

Two international consortiums have been formed to co-ordinate the research. Both aim to share all data and analysis openly and release results as quickly as possible.

The Covid-19 Host Genetics Initiative is led by Mark Daly and colleagues at the Institute for Molecular Medicine Finland. The other project, the Covid Human Genetic Effort, is led from the US by Helen Su of the National Institutes of Health and Jean-Laurent Casanova of Rockefeller University.

The US project is searching for variations in single genes that would account for the unusual cases of young and healthy individuals who have a life-threatening response to Sars-Cov-2 infection — and for people who seem to resist infection even when they are exposed multiple times.

“There are people, for example the spouses of someone who is critically ill, sharing a bed with someone and remaining not only asymptomatic but even testing negative,” said Prof Casanova.

Aids researchers have found that genetic mutations on the CCR5 protein, which HIV uses to enter human cells, make some people resistant to infection by that virus. There may be comparable variations in the ACE2 receptor that would affect their susceptibility to Sars-Cov-2.

Scientists are using human DNA in different ways to investigate Covid-19. Some researchers are using genetic data already accumulated for other purposes, such as UK Biobank, and matching it with any information that emerges about the subjects’ Covid-19 experience. Others are obtaining fresh genomes from Covid-19 patients.

There are also different levels of analysis. Top of the range is “whole genome sequencing” which reads all 3bn chemical letters of DNA that store the genetic inheritance of every human being. Next comes “exome sequencing” which just reads the genes that directly make proteins, the most active biological molecules.

The third level — faster and cheaper than the other two — is “genotyping”. It focuses on an array of 500,000 to 1m DNA letters across the genome chosen because they represent hotspots of individual variation.

The largest database of genotyped data is held by 23andMe, the California-based consumer genetics company, which is keen to see it used for Covid-19 research. Its first study got responses from 750,000 people and provided early evidence that those with type O blood were less likely to test positive for infection — a finding confirmed last week by the academic study in Spain and Italy.

“The speed at which we can conduct these studies has increased enormously,” said Joyce Tung, 23andMe’s vice-president of research. Once it could take a decade to understand how a gene influenced a disease, she added. Now it can be done in a matter of months.
It's good preliminary work, I didn't go into all the analysis but it jumped out at me that they didn't have enough data to look at those with mild cases - fairly important. I'm also wary of 23andMe being used for a medical study, their science is sketchy for a fair bit of what they promote but maybe for something like this their standards would be greatly increased.
 

EasternOrthodox

Well-Known Member
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It's good preliminary work, I didn't go into all the analysis but it jumped out at me that they didn't have enough data to look at those with mild cases - fairly important. I'm also wary of 23andMe being used for a medical study, their science is sketchy for a fair bit of what they promote but maybe for something like this their standards would be greatly increased.
I noticed the reference to 23andme but had no idea how to evaluate it. I wondered as I‘d never seen any such mention anywhere else. I didn’t know they were sketchy. My sister and I discovered a heretofore unknown half brother on 23andme. Quite interesting, as you might imagine.
 

Mrs.Anteater

Just keep going....
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Here’s the article, that won’t display,

Subscribe to read | Financial Times

Scientists have identified a new set of 68 genes associated with a high risk of developing severe Covid-19 as geneticists seek to understand why people vary so much in their susceptibility to the illness.

The preprint paper released on Thursday by analytics company PrecisionLife, which used data from UK Biobank, adds to a growing number of genetic clues about vulnerability to the virus.

The phenomenon of some people suffering grave illness while others are infected without symptoms despite being in similar environments has caused widespread puzzlement.

Twelve of the 68 genes identified by Oxford-based PrecisionLife are involved in the heart and blood circulation, including the regulation of calcium levels. This tallies with the observation that the cardiovascular system often undergoes severe stress in patients hospitalised with Covid-19.

Last week an international academic team found two areas of human DNA that differed significantly between 1,600 patients in Spain and Italy who suffered Covid-19 respiratory failure and people who bore no signs of disease.

One set of genes determines blood group: people with group A blood (roughly 30 per cent of the global population) have a higher risk of serious illness than group O, the researchers found.

The second covers genes involved in the ACE2 receptor, a protein on the surface of human cells that the coronavirus uses as an entry point, although their precise connection to Covid-19 remains unclear.

The findings are “just a start”, said Daniel Wilson, an expert in infectious disease genomics at Oxford university. “But they are a pointer to the way human genetic analysis will help to explain why some people get severe Covid and others escape.”

The potential influence of genetic discoveries is huge. They can lead to better drugs to treat Covid-19 because they improve scientists’ understanding of the disease’s biology.

Longer term, decoding a patient’s DNA once infection is confirmed could enable a personal treatment plan to be tailored to their likely genetic response to the virus.

“At some point it may be possible to measure people’s genetic risk score for susceptibility to Covid,” said Prof Rory Collins, chief executive of UK Biobank, which has several projects to match genetic data on its 500,000 participants with their Covid-19 experiences.

“We could then identify particularly vulnerable people who need to be protected if there is an outbreak of the disease nearby,” he added.

Two international consortiums have been formed to co-ordinate the research. Both aim to share all data and analysis openly and release results as quickly as possible.

The Covid-19 Host Genetics Initiative is led by Mark Daly and colleagues at the Institute for Molecular Medicine Finland. The other project, the Covid Human Genetic Effort, is led from the US by Helen Su of the National Institutes of Health and Jean-Laurent Casanova of Rockefeller University.

The US project is searching for variations in single genes that would account for the unusual cases of young and healthy individuals who have a life-threatening response to Sars-Cov-2 infection — and for people who seem to resist infection even when they are exposed multiple times.

“There are people, for example the spouses of someone who is critically ill, sharing a bed with someone and remaining not only asymptomatic but even testing negative,” said Prof Casanova.

Aids researchers have found that genetic mutations on the CCR5 protein, which HIV uses to enter human cells, make some people resistant to infection by that virus. There may be comparable variations in the ACE2 receptor that would affect their susceptibility to Sars-Cov-2.

Scientists are using human DNA in different ways to investigate Covid-19. Some researchers are using genetic data already accumulated for other purposes, such as UK Biobank, and matching it with any information that emerges about the subjects’ Covid-19 experience. Others are obtaining fresh genomes from Covid-19 patients.

There are also different levels of analysis. Top of the range is “whole genome sequencing” which reads all 3bn chemical letters of DNA that store the genetic inheritance of every human being. Next comes “exome sequencing” which just reads the genes that directly make proteins, the most active biological molecules.

The third level — faster and cheaper than the other two — is “genotyping”. It focuses on an array of 500,000 to 1m DNA letters across the genome chosen because they represent hotspots of individual variation.

The largest database of genotyped data is held by 23andMe, the California-based consumer genetics company, which is keen to see it used for Covid-19 research. Its first study got responses from 750,000 people and provided early evidence that those with type O blood were less likely to test positive for infection — a finding confirmed last week by the academic study in Spain and Italy.

“The speed at which we can conduct these studies has increased enormously,” said Joyce Tung, 23andMe’s vice-president of research. Once it could take a decade to understand how a gene influenced a disease, she added. Now it can be done in a matter of months.
I don’t really see a benefit of this. Nobody can change their genes. Others might be less at risk, but that’s statistically and they shouldn’t let down their guard. I looks more like a case of too much research money is thrown at researchers and they are researching for researchings sake.
 

Luce NDs

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There is so much unknown about the relationship between the mitochondrial walls and the gateways that form up agonist and antagonist blockage.

Knowing the genetic code is just the surface of the enigma ... but this is easily denied by folks that would rather not know ... the resolution is beyond us ...
 
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