Do you have any source on that? I've always been under the impression that red beard hair was known to be caused by having a single copy of the (mostly) recessive gene that causes red hair. It was always taught as the example to how recessive doesn't always mean that the gene doesn't have an effect.
There might be, but it probably hasn't been studied and would be highly controversial to try to document it. To most people, that will smack of racism and have echoes of incidents where, for example, it was assumed some ethnicities naturally have lower IQs than others.
It’s already widely reported that race is a major risk factor for COVID-19. I doubt fears of looking like a racist are holding people back from reporting that non-racial identifiers contribute to the disease.
Well, I assumed the comment was being downvoted because "sounds racist." But my comment is also being downvoted.
I'm not personally against identifying physical traits that would help serve as a quick-and-dirty visual test of risk assessment and I don't know what's going on with downvotes on HN beyond "there's a pandemic on and voting has been wonky all year, presumably because people are stressed out."
I have a genetic disorder that is predominantly Caucasian. My oldest son has the same thing. It is a Dread Disease.
When I was getting divorced, I did not want to date men who were likely to be carriers because it's homozygous recessive, so if the father is a carrier there is a 50 percent chance the child will be a carrier and a 50 percent chance they will have CF. I am incapable of producing a "normal" child (and didn't know that when I was having kids).
My quick and dirty genetics test to drastically reduce the odds that I was dating a carrier boiled down to "No White Men Allowed." Other ethnicities are dramatically less likely to be carriers.
So it doesn't sound silly to me at all that you could take one look at someone and infer some stats about the odds of their genetic risks for a specific category.
It could also be down-voted because the idea of detecting a gene responsible for blood types visually is just silly?
I have a predominantly Caucasian genetic disorder. The quick-and-dirty visual test for "How high is your risk of being a carrier or having the condition?" is "Are you White?"
Widely reported doesn't mean anything. It just means mainstream journalists thought the story fit their narrative.
Were other confounding factors controlled for? Most of the studies I've seen "widely reported" were using race as a proxy for people with jobs that couldn't be done remotely. Is this still bad? Maybe, but if you're trying to determine if one race in isolation is more susceptible than another from a medical/biological standpoint, that's data I haven't seen "widely reported".
In addition to some other good points made by respondents to your comment, I would wager that the bottleneck for identifying this gene in the general population would be orders of magnitude more significant than just handing out the vaccine based on easily identifiable risk factors (occupation, age range, etc.)
rs35044562. However, the effect is probably very small compared to environmental factors (e.g. disrupted innate immunity due to insulin resistance or obesity).
The highest genetic contribution to any common disease seems HLA-B27 ~ ankylosing spondylitis, closely followed by HLA II ~ type 1 diabetes. But in these cases, still, it just explains around 15% of the variance. After these big contributors, there's a long list of genes that contribute with exponentially diminishing effect sizes. And the overall contribution of genetics never exceeds 50%. It's good to understand some disease factors, but interventions are much simpler from the environmental side of things.
I'm surprised that COVID is not linked to HLA in any meaningful way. Probably the study from Pääbo is not accounting for HLA because of lack of imputed haplotypes. It's a bit of a statistics smell that there's no association whatsoever. Nothing shows up in his chr6 region in the Manhattan plot. All infectious agents have some correlation. That's the whole point of HLA, implementing different strategies against them.
For example, HLA-B57 and B27 tend to be super-responders against HIV. This haplotype seems to be trading more autoimmunity risk in exchange for better protection against rapidly mutating viruses. It expanded quite quickly around Northern Europe around 10000 years ago, probably due to another pandemic.
We don't know, probably it doesn't. I was simply complaining about the lack of HLA correlations in the paper, which is suspicious. Probably they didn't type or impute HLA haplotypes.
My HLA-B27 example was actually a positive one. It gives you higher chances of a good outcome if infected by HIV.
Another paper, with a small sample size, claims HLA-B44 and C01 are susceptible [1].
I work with the Oxford vaccine group, and I am quite interested in this effect, including in vaccinated patients. It's pretty well known bad vaccine efficiency and side effects will correlate very strongly with HLA, and with thymic involution.
Sadly everything is quite chaotic at the minute and it's difficult to get samples and funding for these ideas. If we were more advanced, we would get be classifying vulnerable patients and asking them to shield according to HLA and immunoageing/dysfunction markers.
So as I understand you are involved by the vaccine that AstraZeneca is also behind. So I kind of understand (well, as much as layman can understand, lol) the vaccine that Pfizer and Moderna works. I guess it is a bit better explained on Wikipedia. So their vaccines inject mRNA to our cells which start producing antibodies. While this is brand new kind of vaccine, it's hard to know long term effects of it, but there's a chance that it could cause an autoimmune disease.
When reading about vaccine created by Oxford, the biggest concern seems to be that people could have or develop antibodies for the adenovirus after first dose. I'm guessing someone with HLA-B27 has even a higher chance of doing that. I understand that, but I'm still not understanding how it works. Is it same as the mRNA vaccine, with the difference that the adenovirus is just used to deliver it?
I have collaborators in the vaccine group, but I'm not directly involved in the trial. In fact, I think the Oxford vaccine has 2 potential design issues, 1 of which is shared with all other vaccines.
The first issue is what you pointed out. Adenovirus delivery is potentially more risky. I'm incidentally also HLA-B27, and I will personally stay away from it.
The second issue, shared with all other vaccines, is that IMHO they should not have vaccinated us for the whole spike protein, but just for some fragment. The spike protein contains some mimotopes to confuse the immune system, and I'm worried that this might also be a source of autoimmunity in very rare cases. Naturally, because vaccines had to be rushed, this was not easy to account for.
Nonetheless, they all seem safe. Theoretically, mRNA ones might be safer, unless there's gene transfer/integration of mRNA into cells. But this is a very exotic issue unlikely to cause problems.
Careful, you're starting to sound like a COVID denier. Next thing you'll know you'll be saying restaurants shouldn't be closed for a year and families should be allowed to gather for Thanksgiving!
But please do live in common sense and apply proportionate safeguards: when you notice a changed mole go to the dermatologist. When you cross the road look both ways first, even when you "know" there's nothing coming. And when you're living in a pandemic take sensible measures to reduce the risk to you, and especially to your fellow citizens.
[belatedly saw your later remarks about Neanderthals] - agreed, this new info about genetic heritage doesn't itself warrant acute panic, but it's easy to seem glibly dismissive of all risk. Keep safe, and with luck your local medics will get enough rest that when you arrive at their doors with some non-COVID condition they'll be able to help.
Lucky woman to fall in a high risk category and still live through it. I feel like I understand what you are saying but I would phrase it differently as your statement comes off a bit cavalier about the risk. I would say that while there is a lot of fear about COVID, and much of it justified on the mortality and long term effects that many people are suffering from, do not live in complete fear life can and will prevail. Be cautious on risk, where a mask for your benefits and to minimize the risk to your community etc.
For me when I read your statement it almost comes across as a "well I got wasted and drove home drunk and made it home safely (not self driving vehicle FWIW), therefore I should always go home drunk and maybe advocate that my friends should try it to". Now I'm not saying thats what you are writing but it's a bit unclear.
What you are calling "living in fear" is a temporary circumstance that can prevent permanent consequence. Even if that consequence isn't guaranteed, it's worth the sacrifice to avoid it.
> We're not speaking of the same thing: you assume that by not living in fear I mean not taking any precautions.
I'm only going off of what you said:
> "don't live in fear", even the worse prognosis doesn't automatically leads to death.
> So don't worry too much, even if you're a big risk death isn't guaranteed apparently ;)
It's pretty clear to me that you are saying that we shouldn't try to avoid catching COVID-19, even though it presents a significant mortal risk, because that would be "living in fear".
At least, that is what you were saying until your most recent comment.
> What I mean is don't fret over your Neanderthal great great [...] grandpa that might transmitted you a bad gene for COVID.
I mean, you could have said that in the first place. Instead, you brought up a story about a woman who had cardiac problems, which totally shifted the conversation away from Neanderthal DNA.
If the story you brought up was supposed to be an allegory for people worrying about Neanderthal DNA, then there are a couple things to consider:
1. No one is equating Neanderthal DNA to cardiac disease as a risk factor for COVID-19 mortality.
2. Choosing not to worry about cardiac disease as a risk factor for COVID-19 mortality is clearly a bad idea, even if some people with cardiac disease don't die to COVID-19.
(I'm not trying to be a jerk. I'm about to rush out the door, haven't had enough sleep and I think if we know something about what blood types are impacted, that's useful info.)
Your "high risk" comment seems like an overstatement.
That press release does not give any actual numbers, but links to two studies. I quickly scanned the studies, so may have missed something, but the Denmark one seems to indicate a ~10% higher risk for A/AB than O. While statistically significant, it does not seem like a massive difference. Also, importantly, it states:
This study identifies ABO blood group as a risk factor for SARS-CoV-2 infection but not for hospitalization or death from COVID-19.
Looks like for some 23andme customer, you can go to the Raw Data under your account and search for rs10490770. If that has the "C" variant, then you are almost certain to have the "G" variant of rs35044562 which puts you into the higher risk covid group. (don't take anything here as medical advice, just digging into the data to see if you can find out something helpful).
"A new genome-wide association study has identified a section of chromosome 3 where particular alleles are associated with severed effects after COVID_19 infection. This was then confirmed by a clinical trial of patients. The reported risk SNPs are having Cytosine (C) at position rs10490770 and Guanine (G) at rs35044562. These are in "full linkage disequilibrium", meaning if you have C at the first spot then you almost certainly have G at the second. And you can now check for C at rs10490770 in some 23andMe, Family Finder, and Ancestry raw data files, or directly on 23andMe using Browse Raw Data.
You can search for rs10490770 in your or other people's 23andMe v2,v3,v4, Family Finder and MyHeritage v1, or Ancestry v1,v2 raw data. It's not on the GSA chip, and therefore not on 23andMe v5, FTDNA v2, or MyHeritage v2. It is on Ancestry v1 and v2."
and one region on chromosome 9 that determines ABO blood groups.
Rather than wasting many paragraphs talking about the Neanderthal connection, it would be vastly more useful to determine exactly what these genes do and why they are a risk factor for the disease.
The disease significantly impacts the blood. If we can determine, for example, what blood groups it impacts the worst, that might be meaningful -- a lot more meaningful than "There's a Neanderthal connection."
My general understanding is that studies like this tend to be a case of "We studied what we could get funded for, even if it wasn't exactly what we really wanted to know."
Beyond that, I don't know and don't care about that end of things, really. I'm much more interested in this end of things where I have a smidgen of influence -- that being "What do we see as a priority in discussing the problem on HN?" because HN attracts a lot of brilliant and connected people, so I imagine if we come up with a better mental model for solving the problem here, it will proliferate.
The last author Svante Pääbo's group has been working on Neanderthal genome sequencing for roughly two decades now. It's basic research into the evolutionary history of our species. They certainly didn't secretly want to work on infectious diseases all along.
Besides, where do you get the idea that getting funded to work on the Neanderthal genome is easier than getting funded to work on an ongoing pandemic? Not that Pääbo needs it, as a Max Planck director he doesn't need to apply for grants.
What's happening here is simply that the world's Neanderthal genome experts continue working on Neanderthal genomes, and when they find something that is related to the pandemic it ends up in Nature and the popular press.
Besides, where do you get the idea that getting funded to work on the Neanderthal genome is easier than getting funded to work on an ongoing pandemic?
I stated as clearly as I know how that it is my general understanding, not specific to this article or what is being studied here.
I get the idea from my sister who worked at the CDC for many years and also had multiple rounds of cancer. And before life got in the way and she and I stopped being able to hang on the phone regularly, she used to routinely read the latest cancer research because she worked at the CDC and because she had cancer.
And she used to routinely bitch to me about how "98 percent of it is some variation on the same thing because it's what is trendy and it's what you can readily get funding for. There's almost nothing actually new and interesting in breast cancer research."
She was also patient zero in a cutting edge study and yadda. She was very much an insider in multiple ways and she and I were close at one time, before I was homeless and had no phone for a year or more and before she began working 16 hours a day and had no time talk to anyone regularly, not even our mother.
From the abstract of the paper it sounds like the connection with blood groups was known already [0] and that they actually discovered the link to Neanderthals [1] which makes it understandable that they want to talk about Neanderthals.
[0] "A recent genetic association study identified a gene cluster on chromosome 3 as a risk locus for respiratory failure after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A separate study (COVID-19 Host Genetics Initiative)2 comprising 3,199 hospitalized patients with coronavirus disease 2019 (COVID-19) and control individuals showed that this cluster is the major genetic risk factor for severe symptoms after SARS-CoV-2 infection and hospitalization."
[1] "Here we show that the risk is conferred by a genomic segment of around 50 kilobases in size that is inherited from Neanderthals and is carried by around 50% of people in south Asia and around 16% of people in Europe."
Other studies have pointed to higher risk for A and B blood types / lower risk for O blood types. That's much easier data to gather, since you don't actually have to pinpoint specific genes, just do a blood type test on people who get severe covid.
For this research - just because you've identified a gene linked to risk, doesn't mean you can say anything about why or how that happens. We likely don't know much about this area of the genome - how it's expressed, etc. and so they went with the angle we DID know - that it's inherited from neanderthal. No doubt more research in this area will be done now that they've found a region of interest.
Your quote is wrong. From the first paragraph, the sentence immediately following your quote: "the region on chromosome 3 is the only region that is significantly associated with severe COVID-19 at the genome-wide level". The chr9 region is not associated.
The quote was grabbed because it said what that gene was associated with -- blood groups -- and the disease is known to impact blood. I am not finding anything in the article that explains what chromosome 3 does.
If anyone can cast some light on what chromosome 3 does, that would be cool. (Maybe it's in the article and bad eyesight plus lack of sleep is causing me to miss it?)
My main point was just: What do these genes actually do in the body? We should be looking at that. It's a much more important question than where these genes come from.
> The quote was grabbed because it said what that gene was associated with -- blood groups -- and the disease is known to impact blood.
The sentence following your quote says a new study suggests genes determining blood groups are NOT associated with COVID severity. If you want to criticize the paper, at least quote something that the paper actually supports. As to your main point, others are working on the functional part. The authors just report a finding with their expertise. Not every scientific paper immediately solves a practical problem.
You're complaining about the world's Neanderthal genome experts [0] continuing to work on the Neanderthal genome ...
There is no claim here of a novel finding of immediate biomedical significance; rather this builds on top of other people's biomedically relevant work, which is cited in the abstract.
No, not really. I'm more complaining about what the world chooses to focus on.
When the pandemic started, there were numerous articles on the front page of HN about ventilators and how to build your own and nonsense like that and I was critical of that as well. And it soon turned out that ventilators weren't really a good solution.
Neanderthal experts can study whatever they want to study, but their research is being connected to this pandemic and given that we are in lock down number two, I think we have more urgent issues than where these genes came from and I wish people in general -- the world at large -- would focus on that.
Granted, I'm short of sleep and no doubt saying things somewhat ham-handedly.
This could be a useful piece of the puzzle, or it could be entirely useless, but we don't get to say that now - only time will tell. This is how research works. Computers came out of research into weaving and loom technology. If you had said we need technology to interconnect the globe, you wouldn't have funded research into weaving. Yet here we are.
I have a genetic disorder. I have been getting better for nearly two decades while the world attacks and dismisses me as a lunatic and teller of tall tales for the crime of talking on the internet about it sometimes.
I got better by looking at what we know about how the genetic defect impacts cell function in my body and learning a lot about cell function and connecting the dots between the micro -- molecules misprocessed at the cellular level -- and the macro -- dysfunction in certain tissues and how the body handles and mishandles food, among other things.
I'm not capable of setting aside twenty years of life experience in order to fit myself neatly into the Overton Window, especially when short of sleep.
It never ceases to amaze me how much negative attention my comments get, like it's just incredibly important for people who think they know more about science than I do to quash my ability to give my 2 cents.
My stellar credentials include being a homemaker for two decades and spending nearly six years homeless. Everyone on the planet is more than welcome to look at my comments, decide quietly to themselves that I'm an idiot who knows nothing, downvote it and move the fuck on rather than lecturing me about the crime of having thoughts about the pandemic and what I think we should be looking at if we actually want to solve it and not treat it like we are looky-loos at a zoo seeking entertainment in the deaths of our fellow human beings.
Science also includes critical thinking, critique of what has been done, rigorous discussion and a whole lot of other things beyond just dicking around with exploring whatever catches our fancy for funsies.
I'm not sure why, but you're taking my comment as a personal attack. I was not personally attacking you, or trying to quash your 2 cents. You gave your 2 cents, and I disagree with the main thrust of what you said, so I gave my 2 cents on the topic. That's all that's happened, you're not being run out of town on a rail for speaking outside the overton window - you just suggested that this research was a waste of time and I argued that it does not seem to me to be a waste of time.
It seems like you have some resentment because you don't feel your personally acquired knowledge is being valued correctly? That may be the case generally, but it's not the case here, I assure you.
> The highest carrier frequency occurs in Bangladesh, where more than half the population (63%) carries at least one copy of the Neanderthal risk haplotype and 13% is homozygous for the haplotype.
As a Bangladeshi now living outside of the country, I am not sure what to make of it. We didn't have any proper lockdown AFAIK. In a country with huge amount of poor populace, it's almost impossible to do mandate people to stay in home when they don't have means to live. Thus COVID is very widespread, although not reported because of lack of testing. Even with all that, COVID didn't cause much harm to the population. Albeit, all of it is ancedotal.
Probably helps that Bangladesh’s population pyramid tends to towards the young. So there just aren’t that many old people to get sick and die. Of course, this disease is just subtle enough that it might fly under the radar without statistics to bring its havoc to light.
Average age Bangledesh: 27, USA, 37, also, my bet is the curve drops hard at the older echelons, and since 85% of deaths are among the elderly, COVID just finds it hard to kill a lot of people in those places.
Most researchers seem to put the identical ancestors point (also known as the all common ancestors point or the genetic isopoint) for humans at somewhere in the last 20k years.
That's the point where every single human alive either had no descendants who are alive today or everyone alive today is their descendant.
Since the Neanderthals were extinct long before the identical ancestor point, it follows that if anyone alive today is descended from Neanderthals, then everyone alive today is descended from Neanderthals.
The naming question: is there a word or term for when person A is a descendant of person B but does not have any genes from B?
I've heard of someone using the term "homeopathic descendant" for this, but I think that was offered as a joke.
The visual analogy that comes to mind is representing each person in the first generation as a randomly selected half deck of playing cards, second generation is a random selection of their parents cards, and so on.
Thanks for the link. One should weight the Corona impact with the the age distribution for each country. And for a lot of countries this correlates very well. Interestingly, Japan has very few Corona problems despite having one of the oldest population.
Many fear nuclear war, but I'm now more fearful of future bioweapon viruses that can incapacitate targeted populations leaving the attacking nation relatively unharmed. The new "strategic warfare". Feels like Pandora's box is open.
Viruses engineered to kill people do not spread as fast. It needs a host, a living one to be able to spread effectively unless you bomb a whole country at once with bio-bombs. You might as well use nuclear weapons then. Ebola has a very high death rate but doesn't spread as fast. A virus doesn't have some internal goal to kill humans. It'd rather not kill the host, it'd rather spread as far and wide as it can; speaking from the evolutionary standpoint.
A well engineered bioweapon would be a virus that goes undetected for a few months and then happens to kill the host due to complications. That can wipe out an entire country or possibly the whole human race. I don't think this is possible biologically.
> A well engineered bioweapon would be a virus that goes undetected for a few months and then happens to kill the host due to complications. That can wipe out an entire country or possibly the whole human race. I don't think this is possible biologically.
"Killing the host" is not some natural thing that happens with Viruses. It's a complex process of immune system + dosage. It's not like virus has any evolutionary interest in demobilizing the host. It goes against the evolutionary pressure. That's why I said "happens to kill the host", due to complications.
Article says it's only killed a million people damn man we allow tobacco to be sold every day I even own a tobacco farm let me tell you it kills a lot more than this coronavirus. Yet if I keep lobbying they'll let me keep selling this poison to the masses laughing my ass off. Part of the lobbying that I do is to ensure that every single tobacco death is counted correctly so many slips on a pack of cigarettes and dies and they market tobacco as the death it's my job to make sure that that is corrected. Imagine all of the covid deaths they're marking just because shortage of supply. There's no me to lobby for covid ensuring every death marked by the virus is actually by the virus. I keep seeing stories where a person dies from something completely unrelated to virus yet the doctors blamed covid.
Actually, tobacco was only the first in a line of fear-mongering tactics centered around the idea that merely breathing can cause death and despair all around you. [0] It may have began with cigarettes, but here we are now with COVID-19.
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[ 3.2 ms ] story [ 151 ms ] thread> that is inherited from Neanderthals and is carried by around 50% of people in south Asia and around 16% of people in Europe.
(I have a red beard and 23andme confirmed my Neanderthal genes)
I'm not personally against identifying physical traits that would help serve as a quick-and-dirty visual test of risk assessment and I don't know what's going on with downvotes on HN beyond "there's a pandemic on and voting has been wonky all year, presumably because people are stressed out."
When I was getting divorced, I did not want to date men who were likely to be carriers because it's homozygous recessive, so if the father is a carrier there is a 50 percent chance the child will be a carrier and a 50 percent chance they will have CF. I am incapable of producing a "normal" child (and didn't know that when I was having kids).
My quick and dirty genetics test to drastically reduce the odds that I was dating a carrier boiled down to "No White Men Allowed." Other ethnicities are dramatically less likely to be carriers.
So it doesn't sound silly to me at all that you could take one look at someone and infer some stats about the odds of their genetic risks for a specific category.
I have a predominantly Caucasian genetic disorder. The quick-and-dirty visual test for "How high is your risk of being a carrier or having the condition?" is "Are you White?"
Were other confounding factors controlled for? Most of the studies I've seen "widely reported" were using race as a proxy for people with jobs that couldn't be done remotely. Is this still bad? Maybe, but if you're trying to determine if one race in isolation is more susceptible than another from a medical/biological standpoint, that's data I haven't seen "widely reported".
The highest genetic contribution to any common disease seems HLA-B27 ~ ankylosing spondylitis, closely followed by HLA II ~ type 1 diabetes. But in these cases, still, it just explains around 15% of the variance. After these big contributors, there's a long list of genes that contribute with exponentially diminishing effect sizes. And the overall contribution of genetics never exceeds 50%. It's good to understand some disease factors, but interventions are much simpler from the environmental side of things.
I'm surprised that COVID is not linked to HLA in any meaningful way. Probably the study from Pääbo is not accounting for HLA because of lack of imputed haplotypes. It's a bit of a statistics smell that there's no association whatsoever. Nothing shows up in his chr6 region in the Manhattan plot. All infectious agents have some correlation. That's the whole point of HLA, implementing different strategies against them.
For example, HLA-B57 and B27 tend to be super-responders against HIV. This haplotype seems to be trading more autoimmunity risk in exchange for better protection against rapidly mutating viruses. It expanded quite quickly around Northern Europe around 10000 years ago, probably due to another pandemic.
My HLA-B27 example was actually a positive one. It gives you higher chances of a good outcome if infected by HIV.
Another paper, with a small sample size, claims HLA-B44 and C01 are susceptible [1].
I work with the Oxford vaccine group, and I am quite interested in this effect, including in vaccinated patients. It's pretty well known bad vaccine efficiency and side effects will correlate very strongly with HLA, and with thymic involution.
Sadly everything is quite chaotic at the minute and it's difficult to get samples and funding for these ideas. If we were more advanced, we would get be classifying vulnerable patients and asking them to shield according to HLA and immunoageing/dysfunction markers.
[1] https://www.mdpi.com/1422-0067/21/15/5205
So as I understand you are involved by the vaccine that AstraZeneca is also behind. So I kind of understand (well, as much as layman can understand, lol) the vaccine that Pfizer and Moderna works. I guess it is a bit better explained on Wikipedia. So their vaccines inject mRNA to our cells which start producing antibodies. While this is brand new kind of vaccine, it's hard to know long term effects of it, but there's a chance that it could cause an autoimmune disease.
When reading about vaccine created by Oxford, the biggest concern seems to be that people could have or develop antibodies for the adenovirus after first dose. I'm guessing someone with HLA-B27 has even a higher chance of doing that. I understand that, but I'm still not understanding how it works. Is it same as the mRNA vaccine, with the difference that the adenovirus is just used to deliver it?
The first issue is what you pointed out. Adenovirus delivery is potentially more risky. I'm incidentally also HLA-B27, and I will personally stay away from it.
The second issue, shared with all other vaccines, is that IMHO they should not have vaccinated us for the whole spike protein, but just for some fragment. The spike protein contains some mimotopes to confuse the immune system, and I'm worried that this might also be a source of autoimmunity in very rare cases. Naturally, because vaccines had to be rushed, this was not easy to account for.
Nonetheless, they all seem safe. Theoretically, mRNA ones might be safer, unless there's gene transfer/integration of mRNA into cells. But this is a very exotic issue unlikely to cause problems.
Her cardiologist told her "stay home, because if you get COVID you will die".
She caught it in march or April, stayed in bed for 15 days.
She fully recovered. I saw her this summer, if she didn't tell me I wouldn't have guessed she had it.
So don't worry too much, even if you're a big risk death isn't guaranteed apparently ;)
Say bye to your karma then
That doesn't change the risk calculation.
My point was: don't live in fear.
[belatedly saw your later remarks about Neanderthals] - agreed, this new info about genetic heritage doesn't itself warrant acute panic, but it's easy to seem glibly dismissive of all risk. Keep safe, and with luck your local medics will get enough rest that when you arrive at their doors with some non-COVID condition they'll be able to help.
For me when I read your statement it almost comes across as a "well I got wasted and drove home drunk and made it home safely (not self driving vehicle FWIW), therefore I should always go home drunk and maybe advocate that my friends should try it to". Now I'm not saying thats what you are writing but it's a bit unclear.
Risk factors are about probabilities, not certainties. Anyone who has even rudimentary exposure to statistics will understand this.
One single heartwarming anecdote does not invalidate the fact that the odds didn't work out for 1.4 million people world wide.
Why do you think that cardiologist made it in the first place?
Is it possible that the cardiologist's prediction was sane even though it was wrong in this case?
What I mean is don't fret over your Neanderthal great great [...] grandpa that might transmitted you a bad gene for COVID.
I'm only going off of what you said:
> "don't live in fear", even the worse prognosis doesn't automatically leads to death.
> So don't worry too much, even if you're a big risk death isn't guaranteed apparently ;)
It's pretty clear to me that you are saying that we shouldn't try to avoid catching COVID-19, even though it presents a significant mortal risk, because that would be "living in fear".
At least, that is what you were saying until your most recent comment.
> What I mean is don't fret over your Neanderthal great great [...] grandpa that might transmitted you a bad gene for COVID.
I mean, you could have said that in the first place. Instead, you brought up a story about a woman who had cardiac problems, which totally shifted the conversation away from Neanderthal DNA.
If the story you brought up was supposed to be an allegory for people worrying about Neanderthal DNA, then there are a couple things to consider:
1. No one is equating Neanderthal DNA to cardiac disease as a risk factor for COVID-19 mortality.
2. Choosing not to worry about cardiac disease as a risk factor for COVID-19 mortality is clearly a bad idea, even if some people with cardiac disease don't die to COVID-19.
https://www.nature.com/articles/s41467-020-19623-x
(I'm not trying to be a jerk. I'm about to rush out the door, haven't had enough sleep and I think if we know something about what blood types are impacted, that's useful info.)
That press release does not give any actual numbers, but links to two studies. I quickly scanned the studies, so may have missed something, but the Denmark one seems to indicate a ~10% higher risk for A/AB than O. While statistically significant, it does not seem like a massive difference. Also, importantly, it states:
This study identifies ABO blood group as a risk factor for SARS-CoV-2 infection but not for hospitalization or death from COVID-19.
https://www.wikitree.com/g2g/1067199/new-clinical-study-link...
"A new genome-wide association study has identified a section of chromosome 3 where particular alleles are associated with severed effects after COVID_19 infection. This was then confirmed by a clinical trial of patients. The reported risk SNPs are having Cytosine (C) at position rs10490770 and Guanine (G) at rs35044562. These are in "full linkage disequilibrium", meaning if you have C at the first spot then you almost certainly have G at the second. And you can now check for C at rs10490770 in some 23andMe, Family Finder, and Ancestry raw data files, or directly on 23andMe using Browse Raw Data.
You can search for rs10490770 in your or other people's 23andMe v2,v3,v4, Family Finder and MyHeritage v1, or Ancestry v1,v2 raw data. It's not on the GSA chip, and therefore not on 23andMe v5, FTDNA v2, or MyHeritage v2. It is on Ancestry v1 and v2."
So you can search your 23andMe data for rs10490770 by going to https://you.23andme.com/tools/data/
More information and options are at https://customercare.23andme.com/hc/en-us/articles/115004310...
Rather than wasting many paragraphs talking about the Neanderthal connection, it would be vastly more useful to determine exactly what these genes do and why they are a risk factor for the disease.
The disease significantly impacts the blood. If we can determine, for example, what blood groups it impacts the worst, that might be meaningful -- a lot more meaningful than "There's a Neanderthal connection."
Beyond that, I don't know and don't care about that end of things, really. I'm much more interested in this end of things where I have a smidgen of influence -- that being "What do we see as a priority in discussing the problem on HN?" because HN attracts a lot of brilliant and connected people, so I imagine if we come up with a better mental model for solving the problem here, it will proliferate.
Besides, where do you get the idea that getting funded to work on the Neanderthal genome is easier than getting funded to work on an ongoing pandemic? Not that Pääbo needs it, as a Max Planck director he doesn't need to apply for grants.
What's happening here is simply that the world's Neanderthal genome experts continue working on Neanderthal genomes, and when they find something that is related to the pandemic it ends up in Nature and the popular press.
I stated as clearly as I know how that it is my general understanding, not specific to this article or what is being studied here.
I get the idea from my sister who worked at the CDC for many years and also had multiple rounds of cancer. And before life got in the way and she and I stopped being able to hang on the phone regularly, she used to routinely read the latest cancer research because she worked at the CDC and because she had cancer.
And she used to routinely bitch to me about how "98 percent of it is some variation on the same thing because it's what is trendy and it's what you can readily get funding for. There's almost nothing actually new and interesting in breast cancer research."
She was also patient zero in a cutting edge study and yadda. She was very much an insider in multiple ways and she and I were close at one time, before I was homeless and had no phone for a year or more and before she began working 16 hours a day and had no time talk to anyone regularly, not even our mother.
If someone prefers their papers as PDFs, there is also one available on the website (I for one hate the mess that these "web papers" are): https://www.nature.com/articles/s41586-020-2818-3.pdf
[0] "A recent genetic association study identified a gene cluster on chromosome 3 as a risk locus for respiratory failure after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A separate study (COVID-19 Host Genetics Initiative)2 comprising 3,199 hospitalized patients with coronavirus disease 2019 (COVID-19) and control individuals showed that this cluster is the major genetic risk factor for severe symptoms after SARS-CoV-2 infection and hospitalization."
[1] "Here we show that the risk is conferred by a genomic segment of around 50 kilobases in size that is inherited from Neanderthals and is carried by around 50% of people in south Asia and around 16% of people in Europe."
For this research - just because you've identified a gene linked to risk, doesn't mean you can say anything about why or how that happens. We likely don't know much about this area of the genome - how it's expressed, etc. and so they went with the angle we DID know - that it's inherited from neanderthal. No doubt more research in this area will be done now that they've found a region of interest.
If anyone can cast some light on what chromosome 3 does, that would be cool. (Maybe it's in the article and bad eyesight plus lack of sleep is causing me to miss it?)
My main point was just: What do these genes actually do in the body? We should be looking at that. It's a much more important question than where these genes come from.
The sentence following your quote says a new study suggests genes determining blood groups are NOT associated with COVID severity. If you want to criticize the paper, at least quote something that the paper actually supports. As to your main point, others are working on the functional part. The authors just report a finding with their expertise. Not every scientific paper immediately solves a practical problem.
There is no claim here of a novel finding of immediate biomedical significance; rather this builds on top of other people's biomedically relevant work, which is cited in the abstract.
[0] https://en.wikipedia.org/wiki/Svante_P%C3%A4%C3%A4bo
When the pandemic started, there were numerous articles on the front page of HN about ventilators and how to build your own and nonsense like that and I was critical of that as well. And it soon turned out that ventilators weren't really a good solution.
Neanderthal experts can study whatever they want to study, but their research is being connected to this pandemic and given that we are in lock down number two, I think we have more urgent issues than where these genes came from and I wish people in general -- the world at large -- would focus on that.
Granted, I'm short of sleep and no doubt saying things somewhat ham-handedly.
I got better by looking at what we know about how the genetic defect impacts cell function in my body and learning a lot about cell function and connecting the dots between the micro -- molecules misprocessed at the cellular level -- and the macro -- dysfunction in certain tissues and how the body handles and mishandles food, among other things.
I'm not capable of setting aside twenty years of life experience in order to fit myself neatly into the Overton Window, especially when short of sleep.
It never ceases to amaze me how much negative attention my comments get, like it's just incredibly important for people who think they know more about science than I do to quash my ability to give my 2 cents.
My stellar credentials include being a homemaker for two decades and spending nearly six years homeless. Everyone on the planet is more than welcome to look at my comments, decide quietly to themselves that I'm an idiot who knows nothing, downvote it and move the fuck on rather than lecturing me about the crime of having thoughts about the pandemic and what I think we should be looking at if we actually want to solve it and not treat it like we are looky-loos at a zoo seeking entertainment in the deaths of our fellow human beings.
Science also includes critical thinking, critique of what has been done, rigorous discussion and a whole lot of other things beyond just dicking around with exploring whatever catches our fancy for funsies.
It seems like you have some resentment because you don't feel your personally acquired knowledge is being valued correctly? That may be the case generally, but it's not the case here, I assure you.
It’s the modern era’s equivalent of musicians and artists courting wealthy patrons, in order to keep funding flowing.
Black holes, Dinosaurs, Neanderthals, ...
As a Bangladeshi now living outside of the country, I am not sure what to make of it. We didn't have any proper lockdown AFAIK. In a country with huge amount of poor populace, it's almost impossible to do mandate people to stay in home when they don't have means to live. Thus COVID is very widespread, although not reported because of lack of testing. Even with all that, COVID didn't cause much harm to the population. Albeit, all of it is ancedotal.
Racism and inequality are awful.
That brings to mind a naming question.
Most researchers seem to put the identical ancestors point (also known as the all common ancestors point or the genetic isopoint) for humans at somewhere in the last 20k years.
That's the point where every single human alive either had no descendants who are alive today or everyone alive today is their descendant.
Since the Neanderthals were extinct long before the identical ancestor point, it follows that if anyone alive today is descended from Neanderthals, then everyone alive today is descended from Neanderthals.
The naming question: is there a word or term for when person A is a descendant of person B but does not have any genes from B?
I've heard of someone using the term "homeopathic descendant" for this, but I think that was offered as a joke.
https://mumbaimirror.indiatimes.com/coronavirus/news/sero-su...
https://www.telegraph.co.uk/news/2020/06/03/exclusive-corona...
A well engineered bioweapon would be a virus that goes undetected for a few months and then happens to kill the host due to complications. That can wipe out an entire country or possibly the whole human race. I don't think this is possible biologically.
All it needs is a long period when the host is contagious and asymptomatic. That way it spreads easily before killing the host.
> A well engineered bioweapon would be a virus that goes undetected for a few months and then happens to kill the host due to complications. That can wipe out an entire country or possibly the whole human race. I don't think this is possible biologically.
"Killing the host" is not some natural thing that happens with Viruses. It's a complex process of immune system + dosage. It's not like virus has any evolutionary interest in demobilizing the host. It goes against the evolutionary pressure. That's why I said "happens to kill the host", due to complications.
[0] https://en.wikipedia.org/wiki/Passive_smoking