Tuesday, March 24, 2020

The effect of quarantine on the spread of coronavirus

The R0 of a virus is the number of people each person infects, assuming the whole population is susceptible (i.e. no herd immunity).  It's not a fixed number for each virus, as it depends not only on how inherently contagious the virus is, but also on the behavior of the population in question.  You will therefore see ranges rather than fixed numbers for R0.  Social distancing is an attempt to bring down the R0, so is the wearing of masks.  If you can get the R0 down below 1, the virus will die out, as there are not enough new cases to replace the old ones. 

Highly infectious viruses with high R0 values include measles (12-18) and chickenpox (5-10).  Flu is much lower, in the range 1-2.5. 

R0 estimates for the new coronavirus vary widely, with the most commonly reported range 2-3.  But in the case of the Diamond Princess cruise ship, we have a worst-case scenario of crowding.  Interestingly, the R0 value increases over time from the 2-3 range to as high as 11.  The latter high number appears to have happened after the implementation of quarantine of passengers to their individual rooms.  Couples and families were then stuck together in a small space, giving it to each other.  But once everyone who was going to get it had gotten it, the rate of spread dropped.

In this graph, the vertical dashed line is the beginning of the quarantine to individual rooms.  The horizontal dashed line is the reproduction number of 1, the point where spread will die out.

Source here

Note that five days after the ship's version of social distancing was implemented, transmission had dropped dramatically.  And by 10 days after, transmission had dropped below 1.

If we look instead at the graph of daily new cases, a number we're getting from various countries in quarantine now, we see an initial increase over a few days, followed by a slow decline. 


Italy, by comparison, looks like this, with the vertical line placed on 3/18, the point where my one FB friend in Italy tells me that they really started tightening down movement in public.

The good news is that Italy has had two consecutive days of decline.  Yes, I know the data aren't perfect; it could be under-testing.  But it could also be the beginning of the end, paralleling the decline on the Diamond Princess.  The bad news is that the decline in new cases was pretty slow on the ship. 

France has technically been on lockdown since 3/17, a week ago.  But the French are not exactly rule-followers, and there were initially several days where the police were first giving out a small fine, then a larger one. But people are even now still reporting that they are seeing some groups of people still gathering on the street, against the rules.  Every day the rules get tightened a little more.  I'm going with 3/19 as the point where people started to take it seriously, although there is some wiggle room there.

I will definitely be watching France over the next few days.

Is it bad to take ibuprofen if you have coronavirus? What about elderberry (sambucus) syrup?

There have been articles circulating on FB about both of these, and I've been asked about them.

Ibuprofen

Ibuprofen is an NSAID, or non-steroidal anti-inflammatory drug.  It is known to reduce levels of IL-6, the inflammatory cytokine that is elevated in severe cases of covid-19 (more here). So you'd think it would actually help prevent severe symptoms, as the anti-IL6 drug Actemra does.  This is also theoretically the mechanism of action of chloroquine and derivatives.  It reduces IL-6 levels and therefore the severe inflammation that threatens to kill the patient.

But one doctor in France observed four young covid-19 patients whose symptoms worsened after taking ibuprofen, and raised an alarm.  It is entirely possible that they would have worsened without ibuprofen.  At this point, we have no controlled trials of any kind on this question.  We just don't know.

On one hand, it doesn't make a lot of sense that an anti-inflammatory would worsen a disease that appears to cause an over-reaction of the immune system.  On the other hand, there have been rare but real cases of bad reactions in children given aspirin (another NSAID) for fevers.

At this point, the French Minister of Health is recommending against NSAIDs for fevers, but the European Medicines Agency has put out a press release stating "There is currently no scientific evidence establishing a link between ibuprofen and worsening of COVID‑19. EMA is monitoring the situation closely and will review any new information that becomes available on this issue in the context of the pandemic."

So the short answer is that we don't know.

Elderberry

Elderberry / Sambucus syrup has been sold as an alternative treatment for the flu for many years.  I first became aware of it when I as in grad school and researching flu.  Someone gave me a bottle and asked me to test it to see if it interfered with flu's ability to infect cells.  I did and it didn't.  But the claim of at least some proponents of taking sambucus for flu is not so much that it blocks infection directly, but raises the immune response, which then fights off the flu.

This is at least plausible, but by no means certain. There is at least one report that human immune cells produce increased levels of IL-6 and other pro-inflammatory cytokines when they are removed from the body and exposed to sambucus syrup.

Given that severe cases of covid-19 have elevated IL-6, it makes sense to avoid sambucus/elderberry if you think that you might have the virus.  However, there have been no reports of adverse reactions to elderberry in actual covid-19 patients.

How is the covid-19 pandemic different from the H1N1 pandemic in 2009?

An infectious disease is classified as a pandemic when it is widespread across multiple countries.  There is also usually a requirement that it have a certain degree of severity.  There are many cold viruses that are worldwide, but are not normally considered pandemic because their symptoms are mild.

The H1N1 flu, or "swine flu" because it came from pigs, was declared a pandemic in early 2009, and it lasted for about a year and a half.  At the time, epidemiologists were worried about this particular flu because the last time a flu virus classified as H1N1 spread worldwide was 1918.  Here is a graph of life expectancy in the US.  Note that neither WWI or WWII killed enough Americans to make a noticeable blip in the graph.  But because that H1N1 strain killed large numbers of young adults who would normally live many more years, it is really obvious in the graph.

US Life Expectancy
So when a new variety of H1N1 started to spread rapidly, more rapidly than normal seasonal flu, epidemiologists took notice. The virus also disproportionately affected young people, just like in 1918.  Because it was a flu, though, we already had structures in place to put a vaccine into production quickly.  The US has huge flocks of chickens in undisclosed locations that lay eggs that we can grow the virus in to make flu vaccine. So the flu vaccine machine swung into action, and there were lots of news reports telling people to be sure to get their flu shot that year.  I remember getting mine.

There were some localized quarantines and school closures, especially early on, but it eventually became apparent that even though the virus was spreading rapidly, it was not like the 1918 version in terms of disease severity.  It was actually less fatal than the regular seasonal flu.  In the end, the case fatality rate was 0.03%, compared to about 2% for the 1918 flu.  Those most at risk of death from the 2009 flu were young children and pregnant women (pregnancy suppresses the immune system). So even though it infected somewhere in the neighborhood of 15% of the world's population, deaths were probably less than half a million worldwide.  By comparison, the 1918 flu infected about a quarter of the world's population, and killed somewhere between 1 and 6 percent of all people alive at the time.

The vaccine probably helped.  We know that it's not hugely effective, but it's better than nothing.  Even if your immune system didn't get activated enough to create full immunity, it might be enough to reduce disease severity.  

Now if we look at the current pandemic, we have a coronavirus instead of a flu virus.  We have never successfully created a human coronavirus vaccine, so we don't know if it's even possible to do so.  We know that there are four human coronaviruses that cause mild symptoms, and two human coronaviruses (SARS and MERS) that are horrible.  SARS has a 10% fatality rate, and MERS has a 34% fatality rate.  So right from the beginning, the CDC and WHO were watching what was going on in China with this new virus.

The new coronavirus is officially called SARS 2, which I think is rather confusing, so I'm going with "new coronavirus" or "this virus," or "covid-19 virus."  Covid-19 is the name of the disease, rather like AIDS is a disease caused by HIV. 

The fatality rate of the this new coronavirus is not as bad as SARS or MERS (thank goodness!).  It's fatality is far worse than the H1N1 flu virus, though. It may be in the neighborhood of the 1918 flu that everyone was afraid of in 2009. I have another post about trying to understand the case fatality rate here, and I concluded that it might be in the neighborhood of 2%, which is roughly what it was for the 1918 flu.

The insidious thing about this virus, compared to SARS and MERS, is that about half of the people, even older people, who get it have no symptoms.  So they spread it without even knowing.  With SARS, we were taking temperatures at airports, and if you had a fever, you couldn't get on the plane.  MERS made people so sick that they couldn't spread it if they wanted to. So those diseases were relatively easy to control. 

This new virus has an unusually wide spread of responses from different people infected.  Half have no symptoms, but roughly 20% get very ill and need medical attention, and 1-2% die. There is a lot of concern that if 20% of the world's population gets it, and 20% of those need medical attention, that means 4% of all humans are going to need the attention of the medical system.  Because it's spreading so quickly, all those people are going to need medical help at about the same time.  That's going to overwhelm the medical system.  The medical professionals are gearing up for things to get much worse, but there's only so much they can do. 

The covid-19 virus is spreading rapidly, probably more rapidly than the 1918 flu.   Numbers have come down in China and South Korea, but all of Europe and the US are still on the rise, both in terms of cases and of deaths. 

We don't know yet how much it will spread.  That depends on so many factors, like social distancing and whether or not we can come up with a vaccine.  It will probably not be as bad as the 1918 flu, but it's already worse than the 2009 flu. 

 It isn't the end of the world.  The human race has survived far worse bouts of infectious disease.  But it is a reminder that we are more vulnerable than we think we are. 
 


Monday, March 23, 2020

About me

I will transfer this to a real about page the next time I go back to the house with internet access, but for now:

I am a semi-retired academic biologist with a background in virology and immunology.  I'm not a medical professional of any kind. When the coronavirus started gaining steam, I posted a few thoughts on Facebook about the science of it, and found that there was a sudden intense interest in all things related to viruses and the immune system. So I kept posting, making my posts public.  But FB is not well-suited to organizing information,  and I've started to get a lot of friend requests from people I don't know. So on 3/22/20, I copied all my previous FB posts into this blog. I will continue to cross-post to this blog and my FB, so if you are my FB friend,  you can ignore this blog and see everything I post there. And if you were sent here by one of my FB friends (most of which are my former students) you can follow just the blog. 

Stay safe and isolate on!

Sunday, March 22, 2020

Diabetes and Covid-19

We've know for awhile that people with various pre-existing conditions are at higher risk of death from coronavirus.  In the original report from the Chinese CDC, people with diabetes had a 3x higher case fatality rate than the general population.  But people with diabetes tend to be older, so it might just be correlation with age. A recently posted preprint matched diabetic covid-19 patients with controls that were similar in age and other health problems. The result was that the diabetics fared worse. They had roughly double the risk of acute respiratory distress, heart damage, kidney damage, and secondary infection. The mortality of diabetic patients was 35%, compared to 20% for matched controls. Median age was 66. 

This makes a lot of sense,  because diabetes comes with increased inflammation,  including increased IL-6, which appears to be a major driver of severe covid-19 disease. 

The prevalence of diabetes is about the same in China and the US, although it's not evenly distributed here.

Stay safe and isolate on!

https://papers.ssrn.com/sol3/JELJOUR_Results.cfm?form_name=journalBrowse&journal_id=3526432&Network=no&lim=false

Coronavirus spread through the air vs on surfaces

I went looking for research on methods of spread of coronavirus, and came up with this interesting study comparing actual spread of SARS in hospital wards with models of airborne only, surfaces only, or some combination. Covid-19 is similar but not identical. They concluded that spread was about 60% through the air / 40% through touch (either surfaces or being touched by medical personnel).

This image shows actual spread in a standard hospital ward, with the bed labeled "1" as the index case.  The other beds are labeled with the probability that its occupant contracted the virus. 




Will covid-19 decrease in the summer?

(Original FB post March 12)

For those looking for a bit of good news regarding covid-19, this is a figure from a paper that has been submitted, but not yet reviewed. It makes the case that the virus spreads most easily in a narrow range of climate conditions (5-11C (41-52F) average temp). I think their case makes a lot of sense. Aside from the correlation between the largest outbreaks and a narrow temperature band, many viruses, including other coronaviruses, are strongly seasonal. The virus was expected to be severe in nearby areas to the south of China, like Bangkok, which had the first case outside of China. But as of today, there has been only one death in Bangkok, compared to 30 in Washington state. Bangkok has had highs of about 90F for the month of Feb.
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I'm a bit surprised that the virus appears not to be spreading rapidly in colder climates. We know that heat kills the virus, but not cold.

Update 3/22/20:

Examples that fit this theory:

  • The hottest US states (Arizona, New Mexico) still do not meet the requirement of  >6 deaths to get a circle on the map, although many more states in the yellow zone now do.
  • Mexico (only 2 official deaths, but I'm not sure how much testing is being done there)

Counter-examples to the theory (i.e. hot climates with more than 6 deaths):

  • Indonesia has 48 deaths
  • Brazil has 25 deaths
  • The Philippines have 25
  • Ecuador has 14
  • Malaysia has 10
  • Australia has 7

Ambiguous cases: 

  • Spain has had 1756 deaths, and it is in the light orange area. 
  • Algeria has 17, mostly clustered in the cooler part of the country, which is orange on the map
Given that the numbers in the counter-examples are low compared with cooler countries, I think this theory is still reasonable.  But only time will tell.

See also this post: https://coronavirusandcovid19.blogspot.com/2020/03/the-mostly-non-fatal-coronaviruses.html

Social distancing in 1918

From a 2007 analysis of how social distancing affected the spread of the 1918 flu. The death rate in St. Louis was about half that of Philadelphia. From the article:

"We noted that, in some cases, outcomes appear to have correlated with the quality and timing of the public health response. The contrast of mortality outcomes between Philadelphia and St. Louis is particularly striking (Fig. 1). The first cases of disease among civilians in Philadelphia were reported on September 17, 1918, but authorities downplayed their significance and allowed large public gatherings, notably a city-wide parade on September 28, 1918, to continue. School closures, bans on public gatherings, and other social distancing interventions were not implemented until October 3, when disease spread had already begun to overwhelm local medical and public health resources. In contrast, the first cases of disease among civilians in St. Louis were reported on October 5, and authorities moved rapidly to introduce a broad series of measures designed to promote social distancing, implementing these on October 7. The difference in response times between the two cities (≈14 days, when measured from the first reported cases) represents approximately three to five doubling times for an influenza epidemic. The costs of this delay appear to have been significant; by the time Philadelphia responded, it faced an epidemic considerably larger than the epidemic St. Louis faced. Philadelphia ultimately experienced a peak weekly excess pneumonia and influenza (P&I) death rate of 257/100,000 and a cumulative excess P&I death rate (CEPID) during the period September 8–December 28, 1918 (the study period) of 719/100,000. St. Louis, on the other hand, experienced a peak P&I death rate, while NPIs were in place, of 31/100,000 and had a CEPID during the study period of 347/100,000."

https://www.pnas.org/content/pnas/104/18/7582/F1.large.jpg
Full article here: https://www.pnas.org/content/104/18/7582#F1

Covid-19 and blood type

File this one under "biology is complicated and strange." I found a paper claiming that people with blood type O had 2/3 of the risk of contracting covid-19 in China. I was skeptical, but apparently SARS is similar. The antibodies to A and B antigens found in the bloodstream of people with type O reduce binding of SARS to its receptor.
https://academic.oup.com/glycob/article/18/12/1085/1988773

Monoclonal antibody to IL-6 to treat covid-19

This looks promising. We know that the virus increases levels of the anti-inflammatory cytokine IL-6. Early results are coming out that treating patients with an IL-6 monoclonal antibody, normally used for rheumatoid arthritis, helps. But you don't want to know how much it costs.

https://www.pharmaceutical-technology.com/news/roche-actemra-coronavirus-complications/
In South Korea, schools were closed on Feb 23, and on March 10, their total cases started to level off. That's 16 days of social distancing, if we take school closure as a marker of it. Presumably some of that time was because people who were exposed beforehand had to go through the incubation period. And there was also some transmission within households and between those considered essential.

Italy closed schools on March 4, so not yet 16 days, and cases there are still increasing at more or less the same rate. But the next few days will be telling. ETA: 5 days later, Italy's daily case numbers and daily death numbers are still increasing. There are anecdotal reports that both are probably being undercounted, as the system there is overwhelmed.

ETA: China has been in lockdown for almost 2 months, and is now starting to get back to normal.

No photo description available.
Covid-19 and excess blood clotting: Several Chinese hospitals have reported that their patients are showing signs of excess blood clotting. In one, 5% of those hospitalized for covid-19 had a stroke (blood clot in the brain.) In another hospital, 25 random infected patients were screened for pulmonary embolism (clot in the lungs) and 10 came back positive. That's 40%. And more recently I saw a report of the bloodwork of hospitalized patients showing that most of them had excess clotting, although the degree to which this is so depends on the severity of disease. D-dimers are used as a marker of clotting in the blood, and the first graph here (A) shows levels in patients. Normal is <0.5. Many also had elevated levels of cardiac troponin, a marker of a heart attack or other damage to the heart tissue (which can be caused by a clot in the heart.) The second graph (B) shows these levels. This test is time-dependent. That is, the levels spike a certain number of hours after you have a heart attack. But clearly heart damage is a problem in some patients.

I suspect that this is at least part of the reason why deaths are higher in older people. Pretty much all of us are gradually building up atherosclerosis as we age, which means narrower passageways in the blood vessels. Older people are also more likely to form blood clots in general, and except in cases of clotting disorders, blood clots are uncommon in children.

Source of the graphs: https://www.thelancet.com/…/PIIS0140-6736(20)30566…/fulltext

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The (mostly) non-fatal coronaviruses:

There are four of them, and as you can see from the graph published (and continuously updated) by the CDC, they are strongly seasonal in the US.

OC43 and 229E have been around for awhile. They were first identified as two out of many viruses that cause the common cold in the 1960s. Unfortunately, according to a longitudinal study done on a group of medical students in the 60's, 229E can be contracted multiple times by the same person, even if they still have antibodies from their last infection. (source in comments). As far as we can tell, SARS and MERS are not like this. That is, survivors appear to be immune to reinfection.

NL63 first transferred to humans in 2004, and uses the same receptor as the covid-19 virus. Interestingly, it prefers children to adults, which kinda shoots down the theory that the receptor is the reason covid-19 avoids children.

HKU1 passed from mice to humans in 2005. It has a different receptor from the covid-19 virus.

The seasonality of all four of these gives me some hope that our current virus will give us a break for the summer, which will give us some time to work on a vaccine.

The CDC respiratory virus surveillance page (the source of the graph) is here: https://www.cdc.gov/surveillance/nrevss/index.html

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What is the case fatality rate (CFR)?

The original report out of China in late February said 2%, with the highest-risk age group at 15% for over 80. But it turns out that that number was derived from just dividing deaths into total cases, in the middle of the epidemic. Obviously some of the newly infected people hadn't had time to die, and so this makes the fatality late look lower than it is. If you do the same calculation for China now, it's 4%.

Apparently this is a common thing to do, even if it is mathematically questionable. In 2003, when SARS 1 was just starting, the WHO estimated its fatality rate at 4%, because they were doing the math in the middle of the epidemic. The actual CFR for SARS is about 10%. (source for 4% estimate in comments)

Another way epidemiologists do the calculation of fatality rate is to divide deaths into total resolved cases (dead plus recovered). The problem with this is that some people die a few days after diagnosis, but nobody is recovered that quickly. So this method overstates the fatality rate, especially early in the progress of the epidemic. Using this method, China is at 4.5%.

However, we know that there are many cases that are not being counted as official, so the actual fatality rate is almost certainly lower than 4%.

South Korea has been testing more extensively than any other country. They have done a bit over 300,000 tests, 2.9% of which have come back positive. The age group that contains the highest number of cases is 20-29. So that gives a clue that South Korea is actually seeing the hidden cases that other countries are missing. Their CFR is 1% if you use the method that undercounts, and 5.5% if you use the method that overcounts. Just by eyeballing the graph of how the "high" number changed for China over time, I'm guessing about 2.5%. Which means that the bad math may have come up with the correct answer, just by chance.

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Moderate handwashing works

"Findings: Moderate-frequency handwashing predicted a lower personal risk of coronavirus infection (age-adjusted incidence rate ratio (aIRR) =0·65, p=0.03) although results for even higher levels of hand hygiene were not significant. For household index cases, overall practice of respiratory hygiene (aIRR =0·61, p=0.01) and handwashing after coughing or sneezing (aIRR = 0·35, p=0.02) were associated with lower risk of onwards transmission."


https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3551360

What percentage of covid-19 cases are hidden and/or asymptomatic?

Yesterday I pointed out that South Korea appears to be finding more of the mild or asymptomatic cases that other countries are missing. But they've tested at most 0.6% of their total population. Their official website says you are eligible for testing if you have fever and/or respiratory symptoms within 14 days of being in contact with a known case. So if you are totally asymptomatic in South Korea, you're not being tested.

But there are a few instances of testing a whole population that give us some interesting data.

First, is the town of Vò in the region of Veneto, Italy. Vò was one of two initial outbreak locations in northern Italy. Upon finding their first two "obvious" cases in late February, including one death, the town and surrounding area was tested in its entirety.

Unfortunately the numbers being reported are not entirely consistent, but the best I can reconstruct is this:

On 2/28, it was reported that there were 133 positive tests out of 6800. Presumably this is the region of Veneto, not the town of Vò, because there are only about 3000 people in Vò.

That's a ratio of 67 hidden cases for each known one. There's obviously a lot of room for error bars. If it just so happened that three people had obvious cases, it would be 44, and if they had only one, it would be 133. It's not great statistically, but it's a rough estimate. This is at the very beginning of the outbreak. Of the 133, 100 were described as asymptomatic. Presumably some of those were actually in the incubation period and developed symptoms over time, but I haven't seen any clarification on that.

In the past few days, more news out of Vò has been released. Out of 3000 people tested in Vò, 66 were positive. That's a ratio of 33 hidden cases for each of the two positive cases in Vò. Those 66 people were quarantined, the town was blockaded from the world, and is now free of the virus.

Another relevant case is that of the cruise ship Diamond Princess, which was quarantined in early February off the coast of Japan, with 3711 on board. As people needed hospitalization, they were removed from the ship, and in early March, all the passengers were removed and quarantined on land. By Feb 20, there were 634 confirmed cases; 328 (52%) were asymptomatic. That's out of 3063 tested. Surprisingly, the asymptomatic cases skew older, although that might be an artifact of who was tested. Older people were tested first, and if you look at just those in their 60's and 70's, they're 58% asymptomatic.

As of March 15, the cases have increased to 712. I'm not seeing any data on whether any of the the previous asymptomatic cases eventually developed symptoms, or were truly asymptomatic for the duration.

To date 7 passengers have died. The case fatality rate on the ship was 2.3%, close to the 2.5% I estimated yesterday, although the average age was 58, higher than that of most countries. This suggests that my estimate is a little bit high.

Putting together what we know about Vò and the Diamond Princess, it appears that most of the hidden cases in Vò were not totally asymptomatic, which is good news. The bad news is that more than half of people who are infected at any given time are asymptomatic.

Because the US is still not testing very much, we are more like Vò than the cruise ship, with the actual number infected at 30-60 times the official numbers. That means the US currently has roughly 400-800K infected, with a bit over half asymptomatic, the official 13.8K in bad enough shape to have attracted attention, and the remaining few hundred thousand experiencing mild symptoms.

Assuming a 2% CFR, 8-16K currently infected people will die. Of course, transmission is still happening, so all these numbers are expected to go up.

But remember the town of Vò, which defeated the virus in a few weeks by testing everyone and quarantining the positives, regardless of symptoms. If we could do that, the virus would be stopped in its tracks.

Source: https://www.medrxiv.org/content/10.1101/2020.03.05.20031773v2.full.pdf

Are all of us going to get it?

tldr: no.

There are a few pathogens that are so contagious, almost everyone in a population gets it, if they haven't been vaccinated. Measles is like that, so is chickenpox. But in most cases, it's only a fraction.


The human genome is 99.9% the same for all of us, but most of the 0.1% difference is in genes related to infection. We are all descended from people who managed to not die of rampant infectious disease.


For example, about 1% of Americans are immune to contracting HIV, and another 10% have a gene that allows them to keep the virus at low enough levels to remain asymptomatic for decades. 20% of the population is immune to the stomach flu. For a long time, the pathogen Mycobacterium leprae was thought to be two pathogens, because there are two ways the human immune system can respond to it, and each person's immune system picks one or the other. If your immune system picks the wrong one, you have chronic leprosy.


To make things even more complicated the immune system changes with age. Children are more susceptible to allergies; adults are more susceptible to chronic inflammation, and that inflammation is probably a factor here.


People tend to think that this is mostly about how "strong" your immune system is, but in both the HIV and stomach flu, the resistance gene is a change in the virus receptor.


With covid-19, we already know that older people are more susceptible to becoming infected, as are those with certain blood types.


We also have the case of the cruise ship, where a group was probably all exposed to some degree, as they were locked up for a month with infected people. If we look at just those over 50, about 80% never got the virus at all. 10% got it, but didn't have symptoms. 9-ish% got it and were sick but survived, and about 0.2-0.3% got it and died.


It's possible that if the 80% who didn't get it had been exposed to a higher dose, they might have gotten it. I suspect that part of the reason the Chinese doctor died of it at 34 was that he was probably exposed to a massive dose of virus, while simultaneously experiencing high stress from being a whistleblower and extreme sleep deprivation from caring for too many very sick patients.


But there is also most likely a genetic difference in how different people's immune systems are responding, and how the virus is interacting with their cells.


How many people will become infected depends on how well we socially distance and quarantine the exposed and infected, how the virus responds to warming temperatures, etc. But it is unlikely to be everyone. Given the case of the cruise ship, it's probably not even going to be the majority.


ETA: If 20% of us get it, and 2% of those that get it die, that's still 1.3 million Americans dead. So not as bad as it could be, but still bad.

Masks to prevent the spread of coronavirus

Tldr: Even a homemade mask is better than nothing.

The idea is that the main mode of spread of this virus is through tiny droplets of moisture breathed out of the lungs of an infected person. If you breathe on a mirror or outside on a freezing day, you can see the moisture, otherwise the fine mist is invisible. If you inhale enough virus particles, they can establish an infection.

If you've ever worn an N95 mask, it's pretty obvious that they at least partially block movement of that moisture, since it gets pretty humid in the mask from your own breathing. But there have been plenty of studies showing that as long as you're using them correctly, they block the relevant sized particles, and also reduce risk of respiratory infections.

In general, the N95 are better than the surgical-type masks, but the surgical masks are better than nothing. Wearing a mask does not bring your risk of infection to zero, but it reduces it by 50-75%, depending on the study. Given that the new virus has an R0 around 2-3 (i.e. each person infects 2 or 3 others), this level of reduction of transmission could bring that rate down to below 1, which would mean the virus would die out, even without lockdowns. That’s even more true if both the transmitter and potential transmittee are both wearing masks, because if you are infectious, the mask traps the virus particles that you’re breathing out.

I suspect that part of the reason the virus hasn’t taken hold in Japan is that it’s very common for people to wear surgical masks in public. Japan has had only 33 covid-19 deaths out of a population of 126 million people, despite having a high population density, proximity to China, and the second-oldest population in the world. I also suspect that the Japanese wash their hands a lot more than we do in the US, so I’m not willing to say it’s only the masks. But given the data, it’s hard to see how it wouldn’t make a significant difference.

So that brings us to the question of the shortage of masks. Medical professionals are running out, and obviously they should get first dibs on newly produced masks. But there has actually been a study done on the effectiveness of homemade masks, and there are lots of webpages out there with instructions to make them. There are even groups collecting handmade ones to be used by medical professionals. The epidemiologists have been predicting “the big one” for years, although most of them thought it would be flu. So that raises the question of whether or not a mask made out of a tea towel would offer any protection. The study measured particle transmission across the masks, not infection. The study was done in the Netherlands, and compared the European equivalent of an N95 mask, a surgical mask, and the handmade mask.

The result was that the tea towel mask pretty consistently filtered out half to 2/3 of particles for everyone, including children. The surgical masks filtered between half and 90%, depending on the person, and the N95 masks filtered at least the 95% that they’re rated for, and quite a bit more for some people. The commercial masks worked much better for adults than children, which makes sense given the mask design.

In the studies of transmission of actual infections, rather than particles in a lab, the difference between N95 and surgical masks is less pronounced. Unfortunately, no one has tested the tea towel mask against actual infection. But even in the worst case here, filtering out half of the viruses should make a real difference for infectivity.

Tea towels are made out of woven material, with little holes in it, whereas N95 masks are made out of a felted fabric. If you look closely at a high-grade furnace filter, rated for virus filtration, it is made of a similar material, and I suspect if you disassembled one, you could repurpose the material as face masks that would be better than a tea towel. But as you might suspect there is no literature on this, and I haven’t tried it myself. I think if I were going to try, I would layer the furnace filter material with something sturdier, as it is pretty thin and might tear easily.

The fit of the mask is as important as the material itself, as contaminated air can go around a loose-fitting mask. The idea is that when you breathe, the fabric should pull in and out as the air passes through it. I own one mask that is made out of molded rubbery material, with replaceable filter pads. It’s clearly much better than even a well-fitted N95 mask, because it creates a truly air-tight seal around the face. So if you happen to have one of those lying around, go for it.

I wore an N95 mask for my one excursion to the store post-social-distancing, even though there are no known cases in my town. Part of my strategy is to try to normalize it. I'm not someone who cares what people think of me, but it still feels a little weird. Hopefully those who want to wear a mask but feel social pressure against it will be emboldened if they are not the first.

Finally, if you have or make a mask, don't forget to disinfect it. The virus particles stick to the material. 10% bleach, 30+% alcohol, or lysol are all fine.

Coronavirus food safety

Although the main method of transmission is through inhalation, there is growing evidence of a fecal-oral route.

The ACE2 receptor is expressed in the lining of the mouth, esophagus, and intestines. So imagine that you're chewing contaminated food. The virus attaches to the cells lining your mouth, gets inside, and that's the beginning of infection.

Fortunately, this virus is very sensitive to heat, so even lightly cooked food is not a problem. I'm attaching graphs of heat inactivation.

It is also killed by acid. Vinegar and lemon juice are both more than acidic enough to do the trick. Most shelf-stable salad dressings are acidic enough to kill any virus on your salad.

To be on the safe side, I have been disinfecting everything that comes into my house, including food. I wipe down the outside of packages with alcohol, and put produce through a soapy water bath. It wouldn't be a bad idea to splash some vinegar into the soapy water, too.

If you're getting take-out, I'd wipe down the outside of the package. And if the food has cooled during delivery, reheat it. I would not eat any take-out that was not either hot or acidic.

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Coronavirus has a half-life of about an hour in its airborne (aerosolized) form

Half-life of virus in aerosol form (floating around in the air) is shorter than on surfaces. Think one day, or a little less, compared to 3 days, to get rid of it completely.

Because UV light kills it, it would most likely die faster outside than indoors.

Source: 
https://www.nejm.org/doi/10.1056/NEJMc2004973

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Anosmia as a marker of "hidden" coronavirus infection

Plausible:
"here is potential that if any adult with anosmia but no other symptoms was asked to self-isolate for seven days, in addition to the current symptom criteria used to trigger quarantine, we might be able to reduce the number of otherwise asymptomatic individuals who continue to act as vectors, not realising the need to self-isolate."