1. The WSJ reports,
Public-health experts generally agree that to reopen society safely, communities need widespread testing so officials can be confident that the number of coronavirus cases in the population is low and people who are positive can be quarantined.
The article is still talking about doorknob effects and how long virus can live on surfaces. Meanwhile, nobody has looked for evidence that people get the virus from surfaces.
Consider two policy objectives. One is to protect the health of people who are vulnerable, primarily the elderly in nursing homes. The other is to protect otherwise less vulnerable people from getting something worse than a mild case of the disease.
We do not have the scientific evidence to determine what is necessary or sufficient to achieve either objective. But “public-health experts generally agree” that testing is the answer. I would feel better about public-health experts if they generally agreed that it would be a good idea to run experiments and carefully evaluate hypotheses before pronouncing them.
2. Javiero is back.
First I want to focus on the Wuhan Commercial Vehicles Show (CCVS) that was held between November 1 and November 4 in the Wuhan International Expo Center. Besides Chinese manufacturers present at the show, including of course Dongfeng Trucks, foreign manufacturers present at the show included Mercedes-Benz, Scania, SAIC-IVECO, Michelin, and Palfinger.
Read the whole thing. I like his detective work. As he points out, his analysis implies that the virus was in Wuhan by early November.
Do we know how common it is for other coronaviruses (or even other respiratory viruses) to spread via commonly touched surfaces? Seems like someone somewhere must have done useful research.
We don’t have to pretend we’re starting from 0. What bugs me is when I hear there’s a question of whether infected people develop immunity or not. Or whether warm weather will slow it down or not. We don’t have to start from scratch. There’s still lefty of research to imply that yes, people will have immunity for some period of time after infection and yes warmer weather will slow it down. The relevant questions are how long will immunity last and how much will warm weather slow it down. Similarly, I suspect there’s evidence somewhere about the ways in which respiratory viruses are spread that we can leverage as a starting point.
There is plenty of evidence of transmission via surfaces. Lab evidence, measurements from surfaces in hospitals, nursing homes, day care centers, and epidemiological evidence, for coronaviruses, other viruses, hepatitis, and more.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828811/
What we don’t know is the relative importance of surface transfers vs social interactions like parties, business meetings, trade shows, and choir practice.
Thanks!
I think I’d argue that it’s the absolute transmittability of both that matter. Let’s say someone is twice as likely to get it from close conversation with an infected person than through contaminated surfaces, but both are highly likely. We wouldn’t conclude that all you need to do is avoid close conversations; we would conclude that people should both avoid close conversations and wash their hands frequently.
Oh the other hand, there are two German studies of the corona on surfaces that conclude that surface transmission is not very important. Streeck, and Drosten, two different studies. Can’t find originals, but there is reporting here.
https://www.corona24.news/c/2020/04/09/the-risk-of-infection-in-the-public-is-extremely-low-the-virus-has-little-resistance-on-surfaces.html
That article is odd in that they say things like, you have little risk while shopping, but they apparently only studied its survival on surfaces. What if spreads through the air in stores? Even at that high, vague level, their claims don’t match up with the evidence.
“We don’t have to pretend we’re starting from 0.”
I agree. We also seem to pretend that we don’t know some of the things we have already learned about this one, like who is at risk, what the fatality rate is, what drugs seem to work, what basic actions can help slow the spread.
I haven’t come across research about your first question (Do previous coronaviruses spread via commonly touched surfaces?). But here is an interesting study of your second question, about evidence of acquired immunity for previous coronaviruses:
Marta Galanti & Jeffrey Shaman (Columbia U.), “Direct observation of repeated infections with endemic coronaviruses” (published 27 April 2020). Here is a link to the article:
https://www.medrxiv.org/content/10.1101/2020.04.27.20082032v1.full.pdf
And here is a summary:
“Background: While the mechanisms of adaptive immunity to pandemic coronavirus SARS-CoV-2 are still unknown, the immune response to the widespread endemic coronaviruses HKU1, 229E, NL63 and OC43 provide a useful reference for understanding repeat infection risk. Methods: Here we used data from proactive sampling carried out in New York City from fall 2016 to spring 2018. We combined weekly nasal swab collection with self-reports of respiratory symptoms from 191 participants to investigate the profile of recurring infections with endemic coronaviruses.
Results: During the study, 12 individuals tested positive multiple times for the same coronavirus. We found no significant difference between the probability of testing positive at least once and the probability of a recurrence for the beta-coronaviruses HKU1 and OC43 at 34 weeks after enrollment/first infection. We also found no significant association between repeat infections and symptom severity but strong association between symptom severity and belonging to the same family.
Conclusion: This study provides evidence that re-infections with the same endemic coronavirus are not atypical in a time window shorter than 1 year and that the genetic basis of innate immune response may be a greater determinant of infection severity than immune memory acquired after a previous infection.”
Note: The N is not large.
Will the Covid-19 virus exhibit different duration of acquired immunity?
My comment was a reply to Dave!
Thanks! Yes, I’ve previously read that coronavirus immunity is typically 1-2 years but that immunity can fade fast in some. This suggests a shorter immunity period than even a year. Maybe I had read the 1-2 years for SARS or MERS antibodies? I don’t remember.
I despair of a world that can’t seem to handle the idea of probability. Everyone wants absolute safety. While we don’t know much about COVID-19 for 100% certain, there’s plenty we can say with enough certainty to make risk management decisions that will move us in the right direction and let us balance safety with living our damn lives.
For example, there are enough data to know our #1 problem is aged care facilities, in many places accounting for 50% of all fatalities. If we want a place to start, it’s the obvious one. Roll out rapid tests for all staff at the start of every shift. Yes, yes I know the tests are not 100% accurate. So long as we understand that, and design the process to compensate, we can still achieve significant reductions in infection rates and deaths.
Similarly, we don’t have enough data on precise modes of transmission, but there’s enough to be gleaned from the patterns of infection to indicate that transmission via surfaces is less much important than aerosol transmission when people are in close quarters and talking loudly, shouting, singing. Enforce masks and physical distancing indoors and nothing more (meanwhile everyone is madly running around disinfecting surfaces – can anyone say “pandemic security theater”?)
Do those two things and we could solve 75% of the problem and get 90% of our lives back.
Testing staff at LTC would be a big win. Based on what I’ve seen in LTC facilities, a big part of the problem is that the staff are usually low paid foreign labor living in dense housing and taking public transport. In addition, the food service model (mass cafeteria style manned by those same people) is a recipe for disaster.
In the Javier article, he mentions Pickaway County Ohio as a current hot spot. That hot spot is due to a prison located there, and tests of every inmate after finding similar widespread infection at the prison in Marion County Ohio. It was not a hotspot until mid-April, and then only because the inmates got tests while the rest of the state you have to be actively very sick or in healthcare to get a test.
I agree with Arnold that too much discussion by public health experts focuses on using tests we do not have, followed by tracking for which we have not budgeted or hired, followed by quarantining in hotels that we have not leased.
Let’s have more essays on how to control the pandemic without mass testing. If Sweden has done this, let’s see what we can copy from them, instead of these fantasy agendas
I just saw a very interesting graph from phone data. It looked at how often people were traveling, etc. Sweden and Nashville have about the same slowdown in social activity despite one being “locked down” and the other not.
So you are allowed to go to a restaurant in Sweden, but few do. It’s almost as if the virus itself, not the government, is the main driver in this change in business activity.
I’d say the average joes have done better that public-health experts than figuring this out.
“I would feel better about public-health experts if they generally agreed that it would be a good idea to run experiments and carefully evaluate hypotheses before pronouncing them.”
Then, the question is, “Why don’t they?” by which I mean, “Why don’t the incentives they face point them towards doing so?” Without any experiments or data, public-health experts usually warn about *potential* dangers and recommend measures that *could* alleviate such dangers. Examples: without testing, community spreading *could* over-run hospitals, and closing “non-essential” businesses might help. Without evidence to the contrary, asymptomatics *could* spread through aerosols, so wearing masks *might* slow spreading. (Note: in both examples *neither* the potential problem nor the proposed solution has been tested.) Indeed, the only way to over-rule these experts’ recommendations is to produce conclusive proof that they are unnecessary or do more harm than good. Examples: the serologic tests showing widespread antibody presence aren’t conclusive enough yet and, besides, it hasn’t been proven yet that antibodies imply immunity. (Both are true, but why is the burden of proof to show that the experts’ hypotheticals aren’t true?) There is no proof yet that risks of wearing a contaminated mask outweigh the potential benefits. (Why don’t experts need to demonstrate that masks are safe and effective?) So, public-health experts are perversely incented to *not* run experiments to evaluate hypotheses. Why risk proving oneself wrong?
Of course, this is a longstanding problem for government interventions more generally. (Note: public-health experts’ recommended measures usually are implemented through government.) It’s almost never required that government interventions demonstrate safety (no unintended consequences) nor efficacy (solves the actual problem) before implementation. (In fact, the Supreme Court has enshrined this “no proof required” standard as the so-called rational basis test.) Imagine if a drug company could say, “This disease might be treatable through pharmaceutical intervention. We are experts in pharmaceutical intervention. Until you can provide definitive proof that our drug doesn’t work, everyone should be required to take it.” That’s the standard facing public-health experts for their non-pharmaceutical interventions.
And, as David Goldhill points out, lockdowns are like a drug with significant toxicity.
Here is some proof of concept evidence that SARS-CoV-2 was transmitted from one person at a location to later person at the same location.
https://www.cdc.gov/mmwr/volumes/69/wr/mm6914e1.htm
Cluster A. A woman aged 55 years (patient A1) and a man aged 56 years (patient A2) were tourists from Wuhan, China, who arrived in Singapore on January 19. They visited a local church the same day and had symptom onset on January 22 (patient A1) and January 24 (patient A2). Three other persons, a man aged 53 years (patient A3), a woman aged 39 years (patient A4), and a woman aged 52 years (patient A5) attended the same church that day and subsequently developed symptoms on January 23, January 30, and February 3, respectively. Patient A5 occupied the same seat in the church that patients A1 and A2 had occupied earlier that day (captured by closed-circuit camera) (5). Investigations of other attendees did not reveal any other symptomatic persons who attended the church that day.
Doesn’t identify the risk probability but establishes the principle.