I upvoted this just because of the nature.com link - but after I actually read it, I am disapointed. Summary:
Q: Why does the coronavirus spread so easily between people?
A: We don't know yet
The results presented not verified by experiments yet.
"But some researchers are cautious about overstating the role of the activation site in helping the coronavirus to spread more easily. “We don’t know if this is going to be a big deal or not,” says Jason McLellan, a structural biologist at the University of Texas at Austin"
That's a gross oversimplification of the article. They have identified proteins and associated host-cell enzymes and can postulate why this combination would result in greater spread (and additionally why other organs are affected).
It's really not hard to grasp why it would spread quickly. This virus harbors in the respiratory system of an infected patient. The viral infection invades cells and releases more of the virus.
This is so contagious because:
1. Everyone breaths in nearly 8000 liters of air each day
2. Virus are so small that they stay suspended in air for a while, some estimates are 30min (think how smoke stays afloat)
Article lists multiple leading experts working round the clock on this, all saying they're not sure why the virus is so contagious.
But some random person of uncertain credentials says "It's really not hard to grasp why it would spread quickly".
If you have some kind of expert credentials with serious evidence, then it would be great to hear it. Otherwise your opinions are just unhelpful, potentially dangerous noise - and the internet has no shortage of those already.
> Authoritative expert opinions that require belief are worse and more dangerous than a random person's honest analysis
Really? Believing multiple named doctors' opinions from a well-known journalistic source on a technical issue is more dangerous than believing a random stranger who I know nothing about other than their username? On the balance of risks, I'll take the doctors, thanks.
What they're trying to figure out is how it spreads so quickly when other viruses of the same family do not. Also this is an RNA virus (like most viruses), and RNA is not a stable molecule, especially compared to DNA. The ability of the virus to attach to and invade cells is also not an absolute. Our adaptive immune system can and does recognize the virus as a threat. What you flippantly described as "not hard to understand" is actually very hard to understand for the domain experts actually working in this field..
Your points suggest that every respiratory virus should be highly contagious, but don't explain why this one is more contagious than other similar viruses.
Yes, all good conjecture that is likely accurate, but wildly important to not only proceed based on these assumptions and to get definitive proof of the mechanisms
Why is there so much general confidence warmer temps will reduce spread? Is it really warm temps = more daylight = more UV bouncing around breaking up virus particles in the air? Does it make any difference at all for the majority of folks who spend almost all waking hours inside?
I think there's probably an aspect of wishful thinking, and I certainly wouldn't say that there's anything like general confidence in the idea. Actually, I've only heard this stated as fact by politicians and similar; experts are mostly WAY more cautious about it.
it is because the warmer weather is what stopped SARS-COV in 2002 from spreading this far. the western world was lucky in that ignoring it the first time was an okay strategy. SARS-COV-2 is making its way around the globe right now and hopefully has the same limitations or this may get out of control. ignoring is the most dangerous option at this point. please watch this video by 3blue1brown https://www.youtube.com/watch?v=Kas0tIxDvrg a math professor in the US about the situation.
But maybe the main reason that SARS died out by the summer was not primarily because of the temperature but had more to do with the fact that it wasn't as nearly contagious and they were able to contain it with social distancing?
I don't know if there is such confidence among specialists, but among non specialists the arguments I have heard are based on assumed similarities with the common flu. These arguments may or may not apply , and there is still disagreement and unanswered questions on why the flu is seasonal:
I believe its something along the lines that when there is more moister in the air, the water droplets grab the floating particles and fall to the ground. Thus higher humidity often slows the impact of airborne virus, hence we have a flu season.
85 cases in Australia. And how many of those are imported?
In a binary sense, yes it “is spreading”. Even an R0 of 0.1 is “spreading”. But there is hardly enough data to say it is spreading widely in Australia.
The virus spread in summer/tropical vs winter/non-tropical regions is orders of magnitude different. But this is also not definitively causal. Just extremely highly correlated.
Yup, the counter to it is India. With almost all of the 43 cases imported even after more than 17000 tests seem to indicate that it's not spreading there (it could be a variety of factors including under-testing).
There does seem to be some secondary spread in Australia however this seems to be from close contact with people who have been overseas. We are a little late to the game having established effective screening and information sharing early On. There is a expectation that the next few weeks will show a marked increase in community spread.
Well, to be fair, its not meant to be a textbook or a journal article where being super explicit matters much more. It's a fun article for laypeople like us.
I encourage everyone who wants to stay up to date to follow the daily video updates from Dr John Campbell. He’s a (semi) retired academic doctor who specialises in respiratory diseases.
He looks at it from a scientific and pragmatic point of view, without typical media hyperbole. He’ll often get info from doctors on the ground. He’s been posting videos on COVID-19 since January.
I've been watching these for about the last 10 days. He's very calm and reasoned. And he continually to reiterates that we need to be more proactive instead of being reactive. I wish our governments in the West would take his advice.
Question for a virologist, but does it actually spread so easily between people? The article asks a loaded question, but is it "justifiably loaded"?
Given the background prevalence of influenza it might be hard to compare, but does it actually spread more easily than influenza does? Is that a conclusion we can already take? For sure it seems to be spreading faster than SARS did, but I don't know if SARS was considered "easy" in this regard either.
The W.H.O. director said 4 days ago "Covid-19 does not transmit as efficiently as influenza" (https://news.ycombinator.com/item?id=22488862). So, I'm also confused and unsure how to rectify this.
I saw that thread as well and there were so many comments about how he cannot be trusted and that they are an institution bought by the Chinese.
I don't know. I might just be horribly, horribly naive. That is not meant to be sarcastic, but an actual possibility. But I really do feel like if we cannot trust institutions like the WHO, then we have zero facts and everyone can just come up with their own facts/form their own beliefs about this disease. I guess the one thing everyone is on the same page about is that we should wash our hands more frequently ...
It appears China did actually donate $20 million to the WHO[1], but I'm not sure what this means. I've seen claims that they've walked back statements immediately following the donations, and whether or not that's true seems to be mostly opinion. I'm sure it influenced the WHO but how much is difficult to say.
Maybe I'm grossly naive too, but it seems incredibly myopic to assume that everything coming out of the WHO is now immediately suspect when the facts are pretty clear that we just don't know much about this virus and probably won't for quite some time. There have been one or two early papers coming out questioning how transmissible the virus is, but I think the data is just too limited.
Without the World Health Organization, we're left with the CDC... and not much else.
FWIW the Gates Foundation was also going to donate $20 million to the WHO[2].
HN can be very disappointing. Software developers in general can be disappointing because we usually have enough information to make us dangerous and we also succumb to conspiracy theories.
WHO currently represents the scientific consensus.
I'd rather be on the side of the scientific consensus rather than entertain unfounded accusations of corruption promoted by random weirdos on YouTube.
one of the features of influenza is the neuraminidase protien [sialidase].
our cells have a "fuzz" of molecules around them refered to as a glycocalyx, and the influenza virus can digest its way through the glycocalyx, using the neuraminidase.
coronavirus doesnt have this feature to assist in fusion and entry.
Norovirus is the bane of my existence as a parent of 3 small children. One kid throwing up? Great. Expect everyone in the family to have it within three or four days.
The tricky thing about my comparing with influenza is that "it's just the flu". Even if an influenza infection would spread with comparable ease on a cruise ship (and maybe it doesn't), I'm guessing it would not be investigated, reported or even remarked.
H1N1 pandemic from 2009 has infected 1.4 billion people, with only a 0.02% mortality rate.
Based on those numbers alone we can be pretty sure that it would have infected everyone on a boat.
If this coronavirus will have the same spread, we could be talking of 19,600,000 to 42,000,000 deaths, or even more if the infections happen all at once and overwhelm the hospitals.
So let's hope it's not as contagious as H1N1 or we're fucked.
I guess it could be worse. We could be talking of the Spanish flu, which killed more than 1% of the world population.
AFAIK cruise ships are notorious for spreading infections diseases between the thousands relatively tightly packed on board for weeks at a time. Though usually these are digestion related diseases and usually less severe.
With flu probably about 50% of passengers have been vaccinated. Another 30% or so may already have some level of immunity. With covid nobody (or relatively few people who have had it by now) has immunity and there is no vaccine.
We do have numerous examples of noroviruses infecting a lot of people on cruise ships.
The R0 of the disease is more of a statistical problem. IMHO the question is actually not straightforward. To answer that question implies that the data that we have is representative, or that the current disease model is accurate. The number of asymptomatic carriers, suspected, confirmed, false negatives, deaths, (deaths falsely attributed to other diseases), etc are not known at this point.
Most droplet born viruses are very contagious (e.g. efficiently infect a target). It wouldnt surprise me if the covid-19 virus is so contagious because symptoms are slow to develop.
SARS was effectively stopped because fever developed quickly so it could be easily detected.
Rubeola, pertussis, and TB are all incredibly infectious (R0 > 10) because they are truly airborne. They essentially can survive and still be very infectious in a desiccated form that can float in the air for a long time.
Molecularly you can look at the ID 50 (infectious dose) required to start an infection.
Epidemiologically speaking there can be broader causes like temperature stability, length of illness, severity of illness, amount of virus production, induction of coughing, etc etc.
My bet is on non molecular epidemiological reasons
IIRC SARS was also most contagious after the victim was experiencing severe symptoms.
This had a couple effects:
1. It meant that it didn't spread as quickly because people were already bedridden during the worst phase
2. It was most dangerous to medical personnel. In fact, one of the top experts was infected while treating patients and it was considered a big deal. If an expert following top protocols to the letter could get infected then there was cause for worry.
- dont wear masks, save them for the actual sick. For a disease most people dont know they have and incubates for days seems like the advice should be “wear a mask if you have a cough”.
- dont cough on your clothing, cough into tissues, toss them and wash your hands. This seems almost impossible given most people seem to cough multiple times a minute. Why not teach them to contain the spray. Eg Best: Dont go out. Next best: wear a mask. As a last restort, cough into your shirt (as in pull the collar up over your mouth an cough down inside the shirt so the spray is contained inside it).
Masks are currently in short supply. At this point it's more important for medical personnel to have access to masks, than it is for individuals. Because if the hospitals get overwhelmed, we're all screwed — this being a classic tragedy of the commons.
Also it's pretty hard to wear a mask correctly. I've seen plenty of people wearing surgical masks with their nose out. If you aren't going to wear that mask correctly, then what's the freaking point?
And even if you can train yourself to wear a mask correctly, to properly dispose of it, etc, the price of masks, even surgical ones, has gone through the roof and even if you can afford to wear a new one each day or two, the supply of masks isn't reliable.
So I'm afraid that at this point, even if you have a cough, the best you can do is to isolate yourself, because masks are in short supply and expensive.
Can't tell if you're listing good advice to follow (in contrast to "the endlessly bad/conflicting advice") or listing examples of bad advice that shouldn't be followed.
>Most droplet born viruses are very contagious (e.g. efficiently infect a target).
Is that your own co-relation?
For e.g. Influenza Type B versus Influenza type C. Type C is not as contagious and the seasonal flu vaccine does not cover it.
>Rubeola, pertussis, and TB are all incredibly infectious (R0 > 10) because they are truly airborne. They essentially can survive and still be very infectious in a desiccated form that can float in the air for a long time.
Being contagious doesn't directly co-relate to being equally harmful. For e.g. Most healthy adults can easily deal with TB. The numbers shift, but approximately over 40% of the Indian population is infected with TB.
Impressive, a gene analysis shows that SARS-Cov2 is the first known SARS virus that has genes for docking at furin activation sites. And furin sites are not only in the lungs, but also in the liver and small intestines. This may explain why there are actual cases with liver failures.
> Their experiments have shown that the spike protein binds to a receptor on human cells — known as angiotensin-converting enzyme 2 (ACE2) — at least ten times more tightly than does the spike protein in the SARS virus. Veesler’s team has also found this, which suggests that the receptor is another potential target for vaccines or therapies. For example, a drug that blocks the receptor might make it harder for coronavirus to enter cells.
First, let me say that although the government doesn't formally recognize me as a doctor, I watch a lot of medical stuff on TikTok so I'm basically getting my MD 7 seconds at a time.
That aside, this seems dubious to me; if anything it's likely better to take ACE inhibitors now so that your body makes more ACE2 receptors before you get the virus. One of the ways the virus kills people is by detroying their ACE2 receptors, which your lung cells need in order to function. Downregulating them is unlikely to prevent the virus from getting into your cells, rather it will just leave your cells with less healthy ones left over after the virus destroys the ones it uses to enter your cells.
As evidence from this epidemic, smoking cigarettes upregulates your ACE2 receptors, and smokers are less likely to get serious illness from COVID-19. Of course if they do get seriously ill then they're more likely to die, but this is probably just because of the lung damage caused by smoking. At the very least it seems irresponsible to put out a statement like this without saying that all the available evidence currently points the opposite way, as does the evidence from the SARS epidemic.
Anecdotally, it would make sense, right? Back when I used to smoke, whenever there was the flu season I went full blown bronchitis most of the time, while the rest of my family had only mild symptoms. Smoking is already known to aggravate any flu symptoms to the point of escalating to a more serious condition.
I've been watching the firehose of pre-prints, raw data and community analysis at reddit.com/r/COVID19 and
* Initially it looked like maybe smoking was a notable risk factor.
* Then some data from a different population seemed to indicate maybe smoking was protective.
* Then further analysis indicated that all this data was likely skewed by upstream sampling bias (like pretty much all CV19 data so far).
* The latest speculation is that maybe smoking makes one less likely to catch CV19 but if you've are a heavy smoker currently (or recently), once you have CV19 your outlook is worse (but nowhere near as bad as being over 60 or immuno-compromised). This was based on a more recent study which seemed to have better data because it went narrow and deep on a few cases, however, it has the disadvantages of small sample size.
* My best guess is that the last bullet might be directionally correct but effect size is small enough that it could easily be swamped by other factors.
In general, us "armchair analysts" obsessively scraping the raw data sources and modeling on it quickly realize that all of the data is very noisy since different regions are using different criteria for what counts as a "case", "severe" and even "hospitalization". Plus no country is sampling the population in a consistent way because they have different criteria to get a test (which can also change daily and by area). For example, Italy's numbers look really troubling in terms of severity and progression until you look at the median ages of who they are testing, which skews 13 years older than their overall population.
From what I remember from skimming one of those submissions on /r/COVID19, it wasn't smoking that was considered possibly preventive, but nicotine (by blocking something the virus uses to enter the body). Nicotine is most commonly ingested through smoking, but there are other ways that also don't carry the health damage and addiction of smoking.
I was curious if anything comes out of it, but I guess there's still nothing significant.
I noticed this smoker effect early on! Data from China was showing about 20% of the infected population was smokers, while smoking is closer to 60% in Chinese men (by cursory google search). The death rates were much higher for infected smokers, but they were curiously underrepresented.
This has a really interesting double effect if you think about it. In places with lots of smokers, fewer people will get the disease, but a larger proportion will die from it. Both of those effects will magnify the death rate.
Edit: assuming the protection is additive and not proportional to existing rates across ages
I imagine that, depending on the mechanism of action, and whether the "increased immunity" remains, there could something reproducible to reduce transmission.
The data was small but seemed to be worse for former smokers. That’s hard to judge though, because former smokers are likely to have quit due to health problems. I haven’t seen any useful stats on infection rates but I think that’s an interesting idea.
Where can one obtain raw (anonymized) data on individual cases? Age, sex, location, infection date, severity, outcome, resolution date? Preferably machine readable?
it probably is not available to random folks on Hacker News. I doubt this sort of information is being widely disseminated, with centralized collection, due to the rapidly evolving nature of the epidemic, and, as mentioned, the PII issues.
I'm not a medical person, so I thought I'd pass this along ... information from a major King Country hospital, citing the CDC (and an eye-opener for me ... see site for more helpful details).
"1 person out of 200 people who are exposed to a COVID-19 positive individual, will become COVID-19 positive (0.5% transmission rate in the general public)"
Very encouraging to see such deep analysis available to the general public.
As a layperson, I feel I know very little about how SARS-CoV-2 spreads from person to person, especially given that asymptomatic persons are communicable.
If you really want to understand what's going on with CV19 you can try reading the pre-print papers posted at www.reddit.com/r/COVID19 which is a heavily moderated science-focused sub. The analyses posted by users down thread often contain links to even more recent source data.
I've learned an enormous amount there (and also how inaccurate media headlines can be in a complex, rapidly-evolving situation like this).
I got no skin in US or PRC but I'd like to point out that US screwed up their handling on Covid.19 while China, having the largest outbreak, seems to manage to keep things under control.
You can argue the technique, but you can't argue the result.
Seeing your nickname has "_hk" (hong kong?) I would imagine there's some sentiment against PRC? Let's remove that sentiment for now since virus does not select people based on race nor political ideology.
China's messed up handling and initial cover-up is why anyone else had an opportunity to mess up their national response in the first place... Remember the doctor who was silenced by the police? They could have stopped it if they didn't have such strong state culture against realizing facts contradictory to their plans.
Really, the virus does select people for political ideology. Governments with denialist streaks tend to get selected.
(Don't think that the US got it right either, I just don't want China's huge initial mistake to be forgotten in light of their recent draconian efforts.)
I've got quite a few fellow Iranians that debunked the health minister Covid.19 infection as political drama to show that "hey, I'm the health minister and I got covid.19, it's not bad" while they covered up the initial infection numbers that was denied by local lawmakers at Qom.
These are not apple to apple "handling the situation" but the goal is the same: downplay, restore order, lie if necessary.
You know that China is most likely lying about their infection numbers. They have to "save face" and all that. I don't know which is worse, not testing, or actively lying.
Is it not obvious? For all its various faults, the US government isn't known for endless constant censorship of the press and social media for anything it doesn't like. There's no US equivalent to the Great Firewall.
China will censor "Winnie the Pooh" because it must tame any criticism of its Dear Leader, meanwhile you can compare Trump to any number of fictional or real characters and nothing will happen.
US capitalists are constantly involved in censoring and shaping of the press. There is no need for a Great Firewall since all enterprises are privately owned and voluntarily censor as much as is needed [1]
China does not even censor "Winnie the Pooh", feel free to look it up on Baidu. If you have believed this obvious lie, what else have you believed? Consider that perhaps the dominant group in your country have an incentive to lie to you about a threat to their profits.
> US capitalists are constantly involved in censoring and shaping of the press. There is no need for a Great Firewall since all enterprises are privately owned and voluntarily censor as much as is needed [1]
Ah yes, the many popular social media platforms that censor all criticism and mockery of Trump, such as:
Untrue. You will be jailed, harassed, ridiculed, or killed in the Western world for questioning holocaust evidence because doing so would completely undermine the ideological basis of leadership in the West.
You will be ridiculed by your peers, not the government, because the reality of the holocaust is very well documented, and deniers are suspected of motivated reasoning. But jailed or killed? I highly doubt that. They aren't comparable in the slightest.
Personally I would want as many sources as possible, but I think it's safe to say that the Chinese authoroties, in the beginning at least, have not been the bastion of truth.
Then again, nor have the US been entirely open about the situation. But that's more the ramblings of an old senile man.
Indonesia, for the longest time, boasted (yes, they, the govt, the health minister, literally boasted) to have zero Covid.19. The moment the country found out that they have 2 Covid.19, they acted as-if the current administration was "ready" and threw an elaborate press conference detailing the steps to track down the infected patients only to be ousted by the patients themselves.
This is the news about how the Indonesian government "was ready to track" and ensure "proper steps" were taken:
Essentially they're saying that "no, the govt didn't track down coronavirus, we went to the hospital and check ourselves as soon as we heard about our dance partner who was positive".
You need to talk to the locals regarding these news to learn the nuances/truth. We can't rely on NYTimes, BBC, or any international medias.
I can understand why Government "tries" to act as if they're ready because they don't want the citizens to be panicking and creating further chaos. They (the govt) have no choice but to lie.
Italy has the second oldest (on average) population after Japan. I saw a statistic today that said that the average age of Italian victims is currently 81.
As far as I know Italy also has a hospital culture that is extremely open, e.g. it is common for patients (non-ICU I guess) to get home-cooked meals brought by friends and family instead of having a hospital meal. That means that if there is community spread, the very weakest of the elderly, those already hospitalized, will be more exposed than in countries where hospital visits are less common. An extremely cynical view would be that this increases deaths early on but frees up valuable beds for the peak of the wave. (It's painful to just write this)
This has nothing to do with being racist, unless it's racist to acknowledge that we do have different genetic material.
The more we know the better we can protect ourselves. For example why Russia has so few cases, when they are sharing border with China?
I read somewhere that Asian males have large number of receptors that the virus uses to infect, but I consider this unreliable given that from other sources we still don't exactly know how the virus spreads.
>Don't you know it's not good to be racist? That it's bad? That we shouldn't discriminate racially, it's bad. Judging people on their religion is bad. It's bad to judge people by their skin color, their social background, or their nationality.
Evaluating the impact that race-specific genetics may or may not have on a disease is not "judging" anyone. We are still in the early days of understanding this disease, with many unanswered questions, but eventually information like this could be helpful to improving our models and predictions.
Edit: you explained elsewhere that this is an attempt at humor by quoting a French movie. While I prefer more serious content on HN, I understand others may disagree. At the very least, would you please make it clear when you are quoting?
>In biological taxonomy, race is an informal rank in the taxonomic hierarchy, below the level of subspecies. It has been used as a higher rank than strain, with several strains making up one race.[1][2] Various definitions exist. Races may be genetically distinct populations of individuals within the same species,[3] or they may be defined in other ways, e.g. geographically, or physiologically.[4] Genetic isolation between races is not complete, but genetic differences may have accumulated that are not (yet) sufficient to separate species.[5] The term is recognized by some, but not governed by any, of the formal codes of biological nomenclature.
What they mean is that race is not well-defined among phylogenists/pop geneticists and thus a largely irrelevant concept to the scientific community at large
Physiological implications of variations in the genetics between Africans, Europeans, Inuit, Pacific Islanders, South East Asians, Native Americans, etc are a very relevant reality to medical researchers, who are part of the scientific community.
These concern only about a handful of genes that have been the subject of very intense selective pressure and has little to do with how phylogeny classifications are done with entire genomes at large. Not only that, this selective pressure often results in evolutionary convergence (all populations in malarial latitudes have some modicum of resistance to malaria, not just Africans) and the resulting shared traits don't say anything about populations are classified.
There are population differences that matter for medical purposes. That some of them overlap with some definitions of race is more of a "broken clock is right twice a day" happenstance.
People who use the concept of races, by using the concept of races.
But it's cultural differences I guess, races and racism is bad in my culture, see the movie quote that is making fun of that, and it seems like in yours races and racism do not seem obviously related. I will not try to convince you, you got my point of view. If you write an international scientific paper, please don't use races, thank you very much.
>In biological taxonomy, race is an informal rank in the taxonomic hierarchy, below the level of subspecies. It has been used as a higher rank than strain, with several strains making up one race.[1][2] Various definitions exist. Races may be genetically distinct populations of individuals within the same species,[3] or they may be defined in other ways, e.g. geographically, or physiologically.[4] Genetic isolation between races is not complete, but genetic differences may have accumulated that are not (yet) sufficient to separate species.[5] The term is recognized by some, but not governed by any, of the formal codes of biological nomenclature.
As your link points out, and as is widely acknowledged among the phylogeny and popgen communities, there is no single definition of race and the notion is largely discredited in modern classifications.
As the summary says, it's an informal and arbitrary term. In non-human biology, I haven't seen it used for anything except pet categorization for laymen.
It's true that "race" is not used with the relative level of consistency and precision as other terms are, like "species", but it's important to remember that all of these categorisations have edge cases and grey areas. Saying that it is "arbitrary" is not helpful here, and can imply that it is "wholly arbitrary" which is wrong.
That's a false equivalence. Some terms are well-defined in phylogeny, and even among the murkier concepts (like species) almost all of them are clearer than race which basically covers a hodge-podge of sometimes contradictory concepts no one ever seems to agree on.
It is arbitrary enough as to be utterly irrelevant in modern genomics. Some people cling to it, usually doctors who haven't gotten the memo, old school taxonomists who don't want to let go of their traditional systems, and of course Pioneer Fund recipients. But popgen/phylogeny researchers avoid using it because of how little information it conveys due to its being so poorly defined.
My first reaction was to think "gosh that's a bit racist". Then I remembered that people of African or Indian origin are more susceptible to sickle cell anaemia [https://en.wikipedia.org/wiki/Sickle_cell_disease#Epidemiolo...], so perhaps it's not after all. I have zero medical expertise in any area, so I have no idea, but I don't think it's without merit as a question. I appreciate it could be used as a stick by racist people, though.
I don't think that your example of Sickle Cell (SCD) is a good comparison to the original quote:
> how an ethnicity affects the virus spread and severity … certain communities are more endangered than others.
SCD is a genetic disease. It is prevalent in specific regions where malaria is common because SCD protects against malaria. There aren't a suite of genes which make people more susceptible to SCD, there's a single inherited gene which causes SCD. You can't catch SCD from another person unless you inherited their genes.
COVID-19 is a flu virus transmitted from person to person. There's no single gene which makes people more likely to catch or transmit flu. There may be multiple genes which increase susceptibility, but once you start talking about a suite of genetics, ethnicity essentially stops being a factor. (Unless those genes directly influence a survival trait for the local area, such as skin color.) There is too much genetic variation within ethnic groups compared to global variation to single out any groups due to genetics.
Thanks for the extra detail. The reason I'd even heard of it is because my wife was tested for it while pregnant, because she has some African ancestry. It's the only case I know of where that kind of racial origin affected susceptibility to any kind of condition.
Do you know if there are any known patterns for certain groups having different levels of protection against respiratory viruses? I'm trying to phrase this carefully, as I'm genuinely interested, and don't want to come off as some Infowars-style nutjob.
I tried to quote a classic French movie but the comedy may have been lost in translation. Anyway, if you don't want to sound racist, you can say ethnicity or ethnic group.
Edit: English is not my native language, and after reading up about race vs ethnicity, I think the word race was correct here. Ethnicity we can derive from the countries themselves although that could be messed up by tourists.
I can no longer edit my post, but showing both would be useful.
Sickle-cell anemia is heritable, not transmitted. The interesting thing is that they're less susceptible to malaria, because sickle-cell anemia has protective effects against it. And malaria is a transmissible disease.
Q: Why does the coronavirus spread so easily between people?
A: We don't know yet
The results presented not verified by experiments yet.
"But some researchers are cautious about overstating the role of the activation site in helping the coronavirus to spread more easily. “We don’t know if this is going to be a big deal or not,” says Jason McLellan, a structural biologist at the University of Texas at Austin"