COVID Transmissions for 4-19-2021
Impact of J&J pause appears minimal at most—and an end is in sight
Greetings from an undisclosed location in my apartment. Welcome to COVID Transmissions.
It has been 518 days since the first documented human case of COVID-19. 518 is an area code for upstate New York, and thus happens to be the area code for calling Governor Andrew Cuomo, perhaps to ask him why his administration suppressed information on deaths caused by his policy of releasing COVID-19 patients back into nursing homes early in the pandemic.
I’m not saying you should do that. I’m just saying that if you did, the area code would be 518. The rest of the number would be 474-8390.
Today we will discuss an area where Governor Cuomo, and the rest of the United States, is enjoying particular success, however—vaccine uptake!
As usual, bolded terms are linked to the running newsletter glossary.
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Now, let’s talk COVID.
No impact of J&J pause on US daily vaccinations
We’re now almost a week out from the J&J vaccination pause, and I am incredibly relieved to say that it looks like the decision to recommend this pause has not led to a drop in the pace of vaccinations in the US: https://www.cnbc.com/2021/04/16/covid-19-cases-deaths-vaccinations-daily-update.html
For 10 straight days, the pace of vaccinations in the US has stayed above 3 million daily. The overall prevalence of single-shot vaccination (which I recently saw called “halfcination”) is now around 39%, with 25% fully vaccinated in the US overall. Apparently many states are also reaching a 50% rate of first-shot deliveries.
I’m reminded of where Israel, the current world leader in single-dose vaccination, was not too long ago. A 25% full vaccination rate is probably not enough for us to see widespread population effects, but I think in localities with high uptake we may begin to see plummeting case rates.
Unfortunately, it seems that vaccinations in Israel are slowing somewhat. This is disappointing, but they are around 60% having received one dose and 55% of the population fully vaccinated. This seems to result in some population effects that have been documented in Israel, where COVID-19 deaths are negligible each day and the incidence of disease is amazingly low. The pandemic in Israel is, essentially, over.
I mention this because with 39% of the US currently at least one dose in, and an additional 0.5% receiving their first doses each day (approximately 1.6 million), the US is on track to reach the same vaccination prevalence as Israel within 1-2 months. Maybe even faster than that; I’ll show my work for this estimate.
Within 1 month the number of complete vaccinations will be 39%, and I expect at least another 15% of the country will have gotten first doses. I also expect that J&J vaccinations will resume (more on that in a moment), which will speed the increase of complete vaccinations since it is single dose.
So in about a month we might have a 55% single-dose rate and a 39% or higher full vaccination rate in the US; in another month, we might project that 55% will have full vaccination at minimum and 70% will be single-dose. This may be overly rosy, given the possibility of vaccine hesitancy slowing uptake, but at least we have a sense of where things are going.
If Israel is a good model for where things are going, then it looks like case numbers in the US could really start to crash over the next couple of months. You might think that the US would be worse off than Israel, given our tremendous caseload over the history of the pandemic, but actually during the recent case peak in Israel, incidence there was around 77 per 100,000 daily while the US incidence is currently around 22 per 100,000 daily. So, with good vaccine uptake it might be even easier to bring those numbers way down.
J&J vaccinations likely to resume in the US this week or next
According to Tony Fauci, vaccinations using the J&J vaccine are likely to resume, possibly as early as the end of this week: https://www.cnbc.com/2021/04/18/fauci-us-will-likely-resume-use-of-jj-covid-vaccine-with-a-warning.html
Dr. Fauci’s comments also noted that he expects a warning will be added to the label. Frequent readers will note that this was one of the outcomes that I predicted last week when the pause was first announced—a break amounting to perhaps two weeks, with a warning added to the vaccine label to help prevent the undesirable-but-rare clotting outcome. The nature of this label modification will also depend on whether the CDC and FDA now feel confident that they can establish a likely patient profile for this rare outcome. If they can do that, then we may see a full contraindication, saying that this vaccine should not be used in certain people. Since I don’t have the data, I won’t speculate specifically on what that restrictions may be. Watch this space.
Global deaths pass 3 million
News broke over the weekend that global COVID-19 deaths have now passed 3 million. Put in perspective, this is quite a lot lower than the 1918 influenza pandemic, which is thought to have killed up to 50 million, but higher than several other influenza pandemics since then, such as the 1957 H2N2 influenza pandemic or the 1968 H3N2 pandemic—both of which are estimated to have killed around 1 million people. Admittedly, in 1957 and 1968, the world population was substantially lower, but the case-fatality rate for these viruses was also about 1/5th that of COVID-19. Another example is the 2009 H1N1 pandemic, which killed fewer than 600,000 people worldwide. However, that pandemic virus was considered particularly mild.
Also, those pandemics are over. The COVID-19 pandemic is continuing.
Anyway, that context having been provided, let’s drill in a little further to the current global situation. India and Western Asia are seeing high increases in COVID-19 cases. Europe is seeing mixed results, with many countries dropping while others are seeing increases. Central America looks stable or falling, but South America and Canada are seeing a strong wave of cases. Case numbers throughout Africa appear relatively low, but health system reporting in Africa can sometimes be less reliable than other places, so we have to take that with a grain of salt.
Overall, the global situation does not look good to me. Global health inequalities are being driven into sharp relief in the current situation, although there are some surprising exceptions—for example, Canada. Still, I am concerned that the pandemic will drag on for quite some time in economically-burdened countries, making their situations worse and further degrading overall healthcare quality. As the wealthiest countries in the world begin to end their local manifestations, there must be a thought given to the responsibility that these countries have to the rest of the human species. There are many arguments I have seen for why that should happen, but there is only one that I personally care about: it is the right thing to do.
I am eager to see how, in the next 3/4ths of 2021, wealthy countries will step up to make sure that the COVID-19 pandemic really ends.
What am I doing to cope with the pandemic? This:
Fixing a hole
I spent my weekend fixing drywall at my old place so that I can have perhaps a small prayer of getting my security deposit back. Exciting, right?
If you’re interested in such things, I used vinyl spackling to fill these small holes because, as mentioned, they were small. Vinyl spackling is one of two major options you have for drywall repair, the other being joint compound. Joint compound is a bit better for larger repairs, and for joining disparate pieces of drywall. Spackle, on the other hand, is good for small repairs because it dries relatively quickly and can be painted almost immediately.
Truth be told I probably would have used joint compound if the hardware store I walked into hadn’t been 2 minutes from closing time (4 pm on a Sunday?? What?). Joint compound can be substituted for spackle, but you can’t use spackle for everything that joint compound can do. I’d generally rather buy the more versatile thing if I can.
Anyway, that’s probably more than you ever wanted to know about drywall repair.
I assure you all that once things really settle out from my move, this section is going to get more interesting again!
I wanted to respond to a comment from Rreedd that I’ve let sit for some time, because I think this reader has asked some really interesting questions:
Hi John, thank you for producing this newsletter. I have found it to be invaluable- most especially given the hyper-politicization of everything these days.
I’m curious to know how much the virus itself, especially in comparison to other endemic coronaviruses in the area of origin?
If the wet market isn’t the likely point of origin, where else might be an area species overlap that would produce a spillover event?
I’m also curious to get your thoughts on variants and vaccine ‘break-through’. I imagine that in the design phase of vaccine development, a highly conserved protein/epitope/antigen would be the target.
are these true break-through events by these variants or is more likely just an issue of variability of vaccine efficacy among individuals?
How much do we know about how these emerging variants differ from the OG SARS-CoV-2?
And lastly, how are viruses speciated? I know offspring viability tends to be the litmus test for organisms, but when does a variant get its own Wikipedia page?
If you’ve answered any of the above before, apologies! And thank you again for your work.
Kind regards.
These are all good questions. I’ve touched on some before, but done my best to provide pretty comprehensive answers here as well:
Hi there! I’ve wanted to reply to this for quite some time, but with many developments last week I am only getting to it now.
First, I want to thank you for your kind words. I think there has been quite enough sensationalism throughout this pandemic, with some people trying to capitalize on fear of the emergency, and others trying to capitalize on denying it. I would much rather be led by data. I’m glad that that comes through.
Now to your questions. Your first question, I think, has a missing word. I believe you’re asking how much variation there is in SARS-CoV-2 relative to other sarbecoviruses in Asia. It has a pretty high identity with viruses that have been isolated from bats in Asia, particularly in Southeast Asia. However, it has some unusual variations that were somewhat unexpected. These may have come from recombination with another unknown sarbecovirus in bats, or they may have originated during a passage through some other intermediate animal host. The exact way that these variations arose will be a subject of scientific inquiry for many years, I expect.
For your next question, I have to point something out about your terminology. “Wet market” does not mean what most people think it means. In Asia, there are wet markets and dry markets. Dry markets sell dry goods, in other words, things that are not fresh produce and meats. Things like electronics, fabrics, etc. Wet markets sell fresh food. In the West, we would call them food markets. There is an impression that has arisen that live animal markets and wet markets are the same thing, but they are not. Live animal markets, on the other hand, are tightly restricted in China. The Huanan Wholesale Seafood Market in Wuhan happens to trade in both wet foods and live animals, however. I just think it’s important to demystify the terms here.
Anyway, to really answer your question, species spillover events happen a lot more than you’d think. Humans are constantly encroaching on the habitats of other animals in our search for resources. There are a lot of places where human expansion has put people at an interface with wild animals, and the effects generally do not go in a way that favors the health of the local ecology. Sometimes, however, there is blowback on human ecology as well. In many cases, when diseases transfer from wild animals to humans, it is because of humans hunting those animals directly. And indeed, someone may have been hunting bats. People in the US catch diseases hunting squirrels and other small game, and the same may happen in China too.
People also interact with animals incidentally to other activities. For example, Nipah virus, an incredibly deadly virus that I studied during my PhD, passes into humans from bats during the collection of date palm sap. Date palm sap is harvested much in the same way that maple tree sap is collected; it is then fermented and consumed as a kind of wine. Fruit bats like to eat it too, though, and frequently interact with the harvesting vessels. Fruit bats, particularly the Flying Foxes that carry Nipah virus, are often very large, and have a very careful balance of metabolism, food intake, and flight weight. This means that they tend to extract as much nutrient value from their food as they can as quickly as possible, and then spit out or otherwise excrete what is left, also as quickly as possible. The result is a lot of contaminated stuff that is spat out or otherwise discarded right next to something intended for human consumption. Viruses can transfer to humans by this mechanism. Perhaps something similar took place with SARS-CoV-2, either directly from bats or via an intermediate host.
Yet another option is transfer through an intermediate host in an agricultural setting. After the SARS outbreaks of the early 2000s, China put restrictions in place on interactions with wild animals, particularly for consumption purposes. To satisfy demand for wild animals, a project to raise these animals on farms was started. It is possible that in these wild animal farms, there were opportunities for interactions between bats and the animals being raised there. This is also reminiscent of something that happened with Nipah virus.
When Nipah virus first emerged in Malaysia, it was on a pig farm. The pigs were separated into three different buildings based on their age, and in order to make additional money off of the farm’s land, the owners planted mango orchards nearby to the pig enclosures. The mangos were for sale at market. Fruit bats love mangos, and they would chew the fruit and then spit out the pulp (again, maintaining the all-important flight weight). This led to pulp entering one of the pig enclosures, and bringing Nipah virus with it, where it infected the pigs. There, because of the age-related movement of pigs, the virus was supplied with a steady stream of new susceptible hosts. This allowed it to adapt somewhat to the pigs, and eventually facilitated its transfer into humans. It killed almost 40% of those infected.
I could envision something similar happening in a wild animal farm. Perhaps contact with local bats transferred a proto-SARS-CoV-2 into the wild animal population. There, it may have accumulated mutations that made it better-suited to infect a wider group of mammals, and eventually it may have transferred into humans.
Any of these scenarios is plausible. We will need to learn more in order to assess what happened exactly.
Now to your next question, which is a little easier to answer: No, I don’t think we are seeing genuine break-through events, because real-world data, even in the presence of variants, is showing vaccine efficacy that is aligned with the efficacy seen in clinical trials. While I am somewhat concerned about evidence that B.1.351 may be able to cause mild disease at greater rates in vaccinated people (with the AstraZeneca vaccine, specifically) than other variants, I don’t think that these events represent true defeat of the vaccine. The vaccine in question did not have incredibly high efficacy against overall disease to start with, at least not compared to the mRNA vaccines, and the drop was based on a pretty restricted population. Meanwhile, its stellar efficacy against serious disease and death from COVID-19 was not compromised. So I don’t know if I would call this “breakthrough” per se. Instead, I think we are seeing a vaccine that generates slightly incomplete immunity in many patients, and a variant that can also evade immunity slightly. Put that together and you will see some more cases of mild disease.
I’m not very concerned about this because I believe that infection of a vaccinated person with a new variant is quite likely to make them immune to that variant in short order. Human immune systems are extremely adaptable, and can update their memory of a pathogen to reflect changes that have happened in its antigens since the last time the person was exposed to those antigens.
So far, the variants are not wildly different from SARS-CoV-2 as it first emerged in Wuhan. The mutations that are observed are few in number, though some have clear functional consequences. Several are clearly antibody-evasion mutations, but this handful of changes is not likely to compromise an immune response that is composed of antibody and T-cell responses that target varied and disparate parts of the virus. It may allow the virus to survive a little longer in a vaccinated host, perhaps enough to pass on to an unvaccinated person if they should meet one (making it a good idea to keep wearing masks even when vaccinated), but I don’t expect them to break through immunity enough to give a person serious disease as they currently stand.
For what it is worth, I think this is what happens with many human coronaviruses. We are exposed to them as children and develop decent immunity against them, but over time they mutate. Instead of getting seriously ill when exposed to these new variants, we just get a mild cold and our immunity is updated, until the next new variant is seen. If everything goes right with our vaccine-induced immunity, I anticipate that new variants of SARS-CoV-2 will be like common cold viruses, causing disease to a mild extent in some people, no disease in others, and perhaps severe disease in people who have severe levels of immunosuppression.
Now to the next question...”how are viruses speciated?” As it turns out, viruses are speciated by committee. There is a group called the International Committee on the Taxonomy of Viruses, and they convene groups of experts to examine new sequences and new phenomena in order to decide if viruses have made the leap to becoming separate species. Typically this requires quite a dramatic change, and a lot of the work to decide on a new species is done when some strange isolate is found out in the wild and a debate is needed over whether it is part of an existing species or something new.
For variants, the ICTV decides usually whether they are new strains, or just variants of an existing strain. Strain definition is not as stark as species definition. Viral species are rarely very similar to one another. Strains may have a very high level of similarity, but with key differences. Specifically, there are two sorts of differences that can make a strain: first, it may be immunologically distinct. This means if I am immune to variant X, and I am exposed to variant Y, my immunity to variant X doesn’t prevent me from experiencing full-blown disease. If that is the case, then variant X and variant Y will probably be called strain X and strain Y by the ICTV. Another option may be geographic dominance. If variant X is found to dominate on a specific continent, but is unable to overcome variant Y on another continent, and vice versa, ICTV is likely to declare these to be different strains.
It’s not a very hard and fast distinction; the committee has to make a call in each case.
I hope this helps answer your questions!
You might have some questions or comments! Send them in. As several folks have figured out, you can also email me if you have a comment that you don’t want to share with the whole group.
Join the conversation, and what you say will impact what I talk about in the next issue.
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See you all next time.
Always,
JS
Thought you might want to know: Gorski linked back to you again:
https://sciencebasedmedicine.org/christian-elliots-18-reasons-i-wont-be-getting-a-covid-vaccine-viral-antivaccine-misinformation/?utm_source=rss&utm_medium=rss&utm_campaign=christian-elliots-18-reasons-i-wont-be-getting-a-covid-vaccine-viral-antivaccine-misinformation
John,
I would very much appreciate it if you could comment on outbreaks of shingles that are occurring in persons who have been COVID-19 vaccinated.