Good morning and welcome to COVID Transmissions.
It has been 416 days since the first documented human case of COVID-19.
Some new information today on yet another variant lineage of SARS-CoV-2. This one is different from the UK one.
As usual, bolded terms are linked to the running newsletter glossary.
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Now, let’s talk COVID.
The South African variant
While we have been talking about the UK-identified B.1.1.7 variant that has made many headlines, another SARS-CoV-2 variant has been identified in South Africa; it has since been detected in other countries. This variant, named B.1.351, has a large number of amino acid changes in the spike glycoprotein as well, some of which I find more concerning than those in B.1.1.7.
The CDC has a descriptive page that helps to explain some of the differences between these two variants: https://www.cdc.gov/coronavirus/2019-ncov/more/science-and-research/scientific-brief-emerging-variants.html
You can also read some news about this here: https://www.politico.eu/article/the-south-african-covid-19-variant-what-we-know-so-far/
The reason I am more concerned about the B.1.351 variant is that it contains mutations that seem to be more likely to interfere with preexisting immunity to other variants. That doesn’t mean it will necessarily escape a vaccine, but I wonder if it won’t slightly compromise vaccine effectiveness or result in worsened reinfections in those who are exposed to it.
It isn’t clear, also, if this is a more transmissible variant, but there are indications that it is.
Something that is interesting to note here is that this variant may have emerged in an immunocompromised person or someone who otherwise harbored the infection for a long period of time. Specifically, in the initial report of the new variant, the authors noted the following (caveat: not yet peer-reviewed work):
One hypothesis for the emergence of this lineage, given the large number of mutations relative to the background mutation rate of SARS-CoV-2, is that it may have arisen through intra-host evolution in one or more individuals with prolonged viral replication. This hypothesis is supported by the long branch length connecting the lineage to the remaining sequences in our phylogenetic tree.
The last point is that the virus appears to be less related to its immediate relatives than you would expect if it had passed normally through sequential hosts experiencing typical infections. Instead, it appears to have mutated more than other lineages in a single host or in a small group of hosts. This may have been possible due to prolonged infection, which usually occurs in patients who fail to mount a proper immune response.
This is a matter of great concern because many tens or even hundreds of millions of people worldwide, with a variety of conditions including HIV or immunosuppressive therapy regimens, might be candidates to incubate variants of this type.
To me this illustrates the importance of getting the best possible immunity that we can achieve in as many people as possible as quickly as possible. Getting less-durable or less-robust immunity in patients may not be enough and it may help variants like this to emerge. I don’t want to see that happen.
As for the particulars of this variant’s properties, I am going to need to cover that over several issues because I am just digesting it myself. However, this Twitter thread (and its subthread) was very interesting to me:
Ambulances in LA instructed not to transport patients with a low chance of survival
With the hospital system in Southern California strained to its limits, and nearly 1 in 5 people in LA testing positive for COVID-19 infection, ambulances have been instructed to triage patients before transporting them. Patients who are not likely to survive will not be taken to hospitals.
This is the kind of care rationing that is always raised by US conservatives as a danger of national healthcare systems, except that the US doesn’t have such a system. Instead, the system in the US is just strained to the maximum by a virus that has run out of control.
This shouldn’t be how it is in the wealthiest nation ever to have existed in the history of the world, and I have trouble understanding how exactly we allowed things to get this way.
You can read more details here: https://dailycaller.com/2021/01/05/los-angeles-california-ems-ambulance-transport-patients-low-survival-chances/
What am I doing to cope with the pandemic? This:
Watching: Still Game
I’ve recommended the show before, but earlier in the pandemic my wife and I started watching a BBC TV show about retirees living in Scotland, called Still Game. It is a very sweet comedy about a community of older people who, despite each individual’s flaws, really care about each other. It offers a sense of community that is hard to find in the pandemic and that I think we all miss. The ninth and final season of the show was put into Netflix recently, and we have watched each episode very slowly, since the creators said they would “comedically retire” the main characters at the end of this season.
Last night we finished it, and it is really very sweet. The characters and the town they live in became a character in the show itself, and the ending demonstrates this. It also demonstrates, very effectively, how the affection these characters feel for each other only makes sense if that same affection is shared by the audience. It was pretty powerful. I still recommend the hell out of this show.
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.
My announcement of a plan to change the frequency of “free” issues of this newsletter has led to some feedback from a couple of paid subscribers. It appears that several people who pay to support this newsletter would much prefer that it continue to provide 5 free issues every weekday. My goal in creating an exclusive issue each week was to thank these paid subscribers. Apparently they instead wish to support continued open access, which I think is really generous of them.
I still want to do something to thank paid subscribers. I intend to add, at least once every two weeks, an evening edition of the newsletter that will go only to paid subscribers. This evening edition will expand on topics that have been requested by paid subscribers or provide additional illumination on things I just happen to think are interesting regarding COVID-19.
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See you all next time.
Always,
JS
Hi, John. I'd love to see some expert like, say, a virologist discuss immunity to the viral shell "carriers" of certain vaccines, e. g. the AZ and J&J vaccines for COVID-19. My particular train of thought: they use a viral capsid to carry genetic material into the host cell, which then manufactures viral proteins to sensitize the immune system. They also will generally contain an adjuvant, yes?
So ... the host presumably develops immunity to both the carrier virus and the intended target, and I can't see how the adjuvant can only intensify immunity to the target. Now the patient is immune to the carrier. By itself, immunity to a harmless adenovirus (or whatever type) is fine, but what if you need a booster shot? Wouldn't there be a reasonable chance that the immune system would destroy the pseudo-virions containing the viral genetic material before it entered the patient's cells? OTOH, I don't know a darn thing about the kinetics of the immune system ... if you wait a year for circulating antibodies to drop, would the immune system react too slowly (with memory cells having to proliferate) to prevent re-immunization?
Thanks.
Hey, good news: preprint indicates that the BioNTech vaccine should protect against both the N501Y variants. Not yet tested against E484K.
https://www.snopes.com/ap/2021/01/08/pfizer-study-suggests-vaccine-works-against-virus-variant/