Why does the coronavirus spread so easily between people?(nature.com)
nature.com
Why does the coronavirus spread so easily between people?
https://www.nature.com/articles/d41586-020-00660-x
162 コメント
Another thread describes him as a retired nurse. Any pointers to his CV?
Both are true. He's a nurse with a doctorate. He actually address this in this video: https://www.youtube.com/watch?v=AAwYFEcvvOc&t=170
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.
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
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.
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.
The endlessly bad/conflicting advice
- 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).
- 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.
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.
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.
It can likely survive up to 9 days on fomites (surfaces and objects), or longer with low temperatures and high humidity.
https://www.news-medical.net/news/20200211/Coronavirus-can-l...
which references:
https://www.who.int/docs/default-source/coronaviruse/situati...
https://www.journalofhospitalinfection.com/article/S0195-670...
https://www.news-medical.net/news/20200211/Coronavirus-can-l...
which references:
https://www.who.int/docs/default-source/coronaviruse/situati...
https://www.journalofhospitalinfection.com/article/S0195-670...
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)"
https://www.evergreenhealth.com/coronavirus
"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)"
https://www.evergreenhealth.com/coronavirus
Because it's both CONTAGIOUS and highly INFECTIOUS.
ngcc_hk(2)
> 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.
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.
> and smokers are less likely to get serious illness from COVID-19.
Source? Genuinely interested
Source? Genuinely interested
https://www.reddit.com/r/COVID19/comments/fdb2g6/new_study_r...
https://www.reddit.com/r/COVID19/comments/fbodxp/study_finds...
https://www.reddit.com/r/COVID19/comments/f8wldm/unlike_appa...
https://www.reddit.com/r/COVID19/comments/ff06im/bulk_and_si...
https://www.reddit.com/r/COVID19/comments/fbodxp/study_finds...
https://www.reddit.com/r/COVID19/comments/f8wldm/unlike_appa...
https://www.reddit.com/r/COVID19/comments/ff06im/bulk_and_si...
If a smoker does get it though, is it more severe?
> Consistent with earlier results, the few smokers who do get diagnosed sem to be more likely to progress to severe illness (3/5 vs ~1/5 expected). https://www.reddit.com/r/COVID19/comments/fdb2g6/new_study_r...
> Consistent with earlier results, the few smokers who do get diagnosed sem to be more likely to progress to severe illness (3/5 vs ~1/5 expected). https://www.reddit.com/r/COVID19/comments/fdb2g6/new_study_r...
Yes, that's also what I said in my original comment.
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.
That sounds unusual since smoking in China seems ubiquitous.
> smokers are less likely to get serious illness from COVID-19
Source? I thought the contrary.
Source? I thought the contrary.
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.
* 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 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
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
What about former smokers?
I imagine that, depending on the mechanism of action, and whether the "increased immunity" remains, there could something reproducible to reduce transmission.
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.
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"
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"
>A: We don't know yet
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).
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).
This article made me get off my digital duff and Google "how do asymptomatic diseases enter the body COVID 19".
This Harvard health blog provides a few explanations. [0]
[0] https://www.health.harvard.edu/blog/as-coronavirus-spreads-m...
This Harvard health blog provides a few explanations. [0]
[0] https://www.health.harvard.edu/blog/as-coronavirus-spreads-m...
"Why does the coronavirus spread so easily between people?" One of the reasons is the transmission from asymptomatic contacts, e.g. https://www.nejm.org/doi/full/10.1056/NEJMc2001468
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)
3. We have no innate immunity to this novel 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)
3. We have no innate immunity to this novel virus
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.
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.
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.
This one is more contagious than a common cold?
It's more contagious than its close relative, SARS.
see point 3
I think 8,000 liters is a bit off?
2,113 gallons / 8,000 liters
1,849 gallons / 7,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3357553/
2,642 gallons / 10,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398662/
2,642 gallons / 10,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448375/
3,000 gallons / 11,356 liters - https://www.nasa.gov/mission_pages/cloudsat/news/air-water.h...
3,963 gallons / 15,000 litres - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398662/
https://www.google.com/search?q=site:ncbi.nlm.nih.gov+liters...
2,113 gallons / 8,000 liters
1,849 gallons / 7,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3357553/
2,642 gallons / 10,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398662/
2,642 gallons / 10,000 liters - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448375/
3,000 gallons / 11,356 liters - https://www.nasa.gov/mission_pages/cloudsat/news/air-water.h...
3,963 gallons / 15,000 litres - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398662/
https://www.google.com/search?q=site:ncbi.nlm.nih.gov+liters...
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
4. Temperatures are ideal in the regions where it's spreading
It’s unclear how much this matters
So are temperatures in the human respiratory system. It’s foolish to just assume warmer temperatures will stop it.
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:
https://www.scientificamerican.com/article/why-do-we-get-the...
https://www.scientificamerican.com/article/why-do-we-get-the...
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.
It's spreading in Australia where it's summer with cozy 30°C
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.
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).
Is there community spread in Australia at this point or are most of those cases imported or directly related to an imported case?
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.
If respected sources waited until they knew the answer, the only available sources would be unreliable.
So if that is the only conclusion, at least there is an authoritative one published.
So if that is the only conclusion, at least there is an authoritative one published.
If they knew the answer, the headline wouldn't be a question, it would be a statement.
The headline is ambiguous. It could be inferred that the question is answered in the article.
A clearer headline would be: "Scientists are trying to understand why the coronavirus spreads so easily between people."
A clearer headline would be: "Scientists are trying to understand why the coronavirus spreads so easily between people."
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.
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.
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.
Just FYI, this is not "deep analysis".
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).
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).
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.
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 ...
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].
[1] http://www.china.org.cn/world/2020-03/08/content_75787774.ht...
[2] https://observer.com/2020/02/bill-melinda-gates-donate-100m-...
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].
[1] http://www.china.org.cn/world/2020-03/08/content_75787774.ht...
[2] https://observer.com/2020/02/bill-melinda-gates-donate-100m-...
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.
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.
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.
Are there any examples of Flu or anything else infecting a cruise ship in a short time period? That was the thing that stood out the most to me.
Norovirus (aka food poisoning) can spread incredibly quickly and is the usual example of "fast moving virus in isolated population".
e.g. https://www.cbsnews.com/news/norovirus-outbreak-hits-royal-c...
e.g. https://www.cbsnews.com/news/norovirus-outbreak-hits-royal-c...
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.
A better example would be norovirus; once that's on a cruise ship, it gets ugly fast.
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.
Not all flus are alike. Some, like H5N1 or Swine Flu were investigated and tracked in great detail, to the point of individual transmission chains.
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.
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.
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.
There doesn't seem to be statistics about how an enthicity affects the virus spread and severity.
From reported cases it looks like certain communities are more endangered than others.
From reported cases it looks like certain communities are more endangered than others.
> From reported cases it looks like certain communities are more endangered than others.
Italians?
I mean, this particular conspiracy theory never seemed at all plausible, but it seems particularly non-plausible _now_.
Italians?
I mean, this particular conspiracy theory never seemed at all plausible, but it seems particularly non-plausible _now_.
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.
Italians have custom to kiss when greeting people, that can increase the spread.
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)
_Is_ kissing people you don't know a thing in Northern Italy? I'd associate it more with France.
speedgoose(3)
Where can one obtain raw (anonymized) data on individual cases? Age, sex, location, infection date, severity, outcome, resolution date? Preferably machine readable?
Edit: thanks for the links, guys!
Edit: thanks for the links, guys!
Unclear if it answers your question explicitly but a friend mentioned on this; https://coronavirustechhandbook.com/
The WhatsApp group is likely to have a source
The WhatsApp group is likely to have a source
You might have luck digging through https://old.reddit.com/r/COVID19/
That's still PII; you need to aggregate to actually anonymize.
Ok. The question still stands?
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.
Don't know but look at places like Kaggle:
* https://www.kaggle.com/brendaso/2019-coronavirus-dataset-012...
* https://www.kaggle.com/kimjihoo/coronavirusdataset
* https://www.kaggle.com/brendaso/2019-coronavirus-dataset-012...
* https://www.kaggle.com/kimjihoo/coronavirusdataset
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.
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.
https://www.youtube.com/user/Campbellteaching/videos