COVID Get Vaccinated Against the Covid Delta Variant

[PeroK]

Today.
https://www.businessinsider.com/vac...eaths-but-older-relatively-few-uk-data-2021-6

At least 95% of people in the vulnerable groups have been fully vaccinated. We have approximately equal numbers of deaths from the 95% vaccinated against the 5% unvaccinated. So, it appears to be about 20 times more dangerous to be unvaccinated.

 

[Fra]

Thanks for the great explanations!

The T-cell system is definitely part of the adaptive immune system even though they show more cross-reactivity than antibodies. The innate immune system is capable of recognizing broad classes of pathogens, for example, it can recognize lipopolysaccarides from all gram-negative bacteria or dsRNA from all classes of RNA viruses.

If found this interesting stuff as well, suggesting some T-cells does not learn, and behave a bit like innate system?

Invariant natural killer T cells: bridging innate and adaptive immunity
"Invariant natural killer T (iNKT) cells are a subset of lymphocytes that bridge the innate and adaptive immune systems
...
Functionally, iNKT cells most closely resemble cells of the innate immune system, as they rapidly elicit their effector functions following activation, and fail to develop immunological memory. iNKT cells can become activated in response to a variety of stimuli and participate in the regulation of various immune responses. Activated iNKT cells produce several cytokines with the capacity to jump-start and modulate an adaptive immune response.
...
Here, we review the innate-like properties and functions of iNKT cells and discuss their interactions with other cell types of the immune system.
"
-- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616393/

I recall also various reports that correlate severe Covid-19 disease with either underactive, or overreacting T-cell system, and that it was speculated in a tv documentary that some hospital staff that was very sick in the early panedmic might have been so beacuase they received a high dose of virus during transmission as they was treating subjects without knowing they were infected. So probably a race condition of kickstarting the immune system vs virus spread in the subject, where a high contamination dose gives the virus a lead??

Makes me wonder, although very risky to administer, would it in principe work to "vaccinate" someone by exposting them with the real virus, but perhaps a few virus molecules only; small enough so that one can presume that the immune system would beat the virus in the rac but still allow an initiation of adaptions?

/Fredrik

 

[atyy]

I recall also various reports that correlate severe Covid-19 disease with either underactive, or overreacting T-cell system, and that it was speculated in a tv documentary that some hospital staff that was very sick in the early panedmic might have been so beacuase they received a high dose of virus during transmission as they was treating subjects without knowing they were infected. So probably a race condition of kickstarting the immune system vs virus spread in the subject, where a high contamination dose gives the virus a lead??

Makes me wonder, although very risky to administer, would it in principe work to "vaccinate" someone by exposting them with the real virus, but perhaps a few virus molecules only; small enough so that one can presume that the immune system would beat the virus in the rac but still allow an initiation of adaptions?

People used try innoculation with small doses of small pox to give immunity against severe disease. It worked but was risky. Things improved after it was understood that immunity to small pox could be obtained with cow pox, with a much lower risk. https://en.wikipedia.org/wiki/Inoculation

I also came across this interesting article "Exposure to SARS-CoV-2 generates T-cell memory in the absence of a detectable viral infection". https://www.nature.com/articles/s41467-021-22036-z

 

[Ygggdrasil]

Thanks for the great explanations!
If found this interesting stuff as well, suggesting some T-cells does not learn, and behave a bit like innate system?

Invariant natural killer T cells: bridging innate and adaptive immunity
"Invariant natural killer T (iNKT) cells are a subset of lymphocytes that bridge the innate and adaptive immune systems
...
Functionally, iNKT cells most closely resemble cells of the innate immune system, as they rapidly elicit their effector functions following activation, and fail to develop immunological memory. iNKT cells can become activated in response to a variety of stimuli and participate in the regulation of various immune responses. Activated iNKT cells produce several cytokines with the capacity to jump-start and modulate an adaptive immune response.
...
Here, we review the innate-like properties and functions of iNKT cells and discuss their interactions with other cell types of the immune system.
"
-- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616393/

Ah yes, I forgot about iNKT cells. You are correct that those do fit between innate and adaptive immunity, as you said.

I recall also various reports that correlate severe Covid-19 disease with either underactive, or overreacting T-cell system, and that it was speculated in a tv documentary that some hospital staff that was very sick in the early panedmic might have been so beacuase they received a high dose of virus during transmission as they was treating subjects without knowing they were infected. So probably a race condition of kickstarting the immune system vs virus spread in the subject, where a high contamination dose gives the virus a lead??

Yes, I've heard people hypothesize such a model for the disease, where for typical asymptomatic and mild cases, adaptive immunity is able to ramp up before viral load gets too high whereas in severe cases, viral load gets too high before the adaptive immune response can kick in either due to high initial viral load or because of impaired immune response (e.g. due to old age or underlying conditions). If you're interested in reading up more on the adaptive immune response to COVID-19, here's a good source (though it's from Feb and we've learned more since then): https://www.cell.com/cell/pdf/S0092-8674(21)00007-6.pdf

Makes me wonder, although very risky to administer, would it in principe work to "vaccinate" someone by exposting them with the real virus, but perhaps a few virus molecules only; small enough so that one can presume that the immune system would beat the virus in the rac but still allow an initiation of adaptions?

Although potentially feasible, one problem with such approach is that your vaccinated individuals are likely infectious for some period after "vaccination."

 

[artis]

@Fra brought up an interesting point here that I have also read elsewhere, maybe also @Ygggdrasil can comment.
I won't publish the source for this because it is in Russian and not from an authoritative source , nevertheless the guy saying these things is rather well known and not your typical anti vaxxer or conspirator.
So the point of argument is basically this. "It is far better to (not accounting for risk factors) develop natural immunity from the disease than to ramp up antibodies via vaccine"

The argument then goes like this. If the virus doesn't mutate or doesn't do it strongly enough then sure get a vaccine and have your antibodies and be happy , much like has been the case with tick-borne encephalitis.
But if the virus does mutate and that mutation is severe enough to transform the virus or it's function (the way it attaches and the success of it) considerably then a high antibody rate against a previous virus form like one would have from a vaccine might be detrimental in some cases as the large portion of antibodies present will tend to fight off the intruder but will be unsuccessful and spend energy in the process and slow down the capability of the naive T cells and the non-memory part of the immune system to fight off the virus. Also could a factor be the different level of antibody present for each individual after the vaccine as some develop a high level/large amount of them while others develop "just enough" to be considered "positive"What are your thoughts on this take , could it indeed be the case?Also I am searching but find it hard to get any valid information about the immune response to newer variants like the Delta from those that have had the real virus and developed natural immunity , which is my case. I wonder what are the effectiveness ratio between a natural immunity versus the best of current vaccines aka the Pfizer , Moderna etc ?

 

[pinball1970]

@Fra brought up an interesting point here that I have also read elsewhere, maybe also @Ygggdrasil can comment.
I won't publish the source for this because it is in Russian and not from an authoritative source , nevertheless the guy saying these things is rather well known and not your typical anti vaxxer or conspirator.
So the point of argument is basically this. "It is far better to (not accounting for risk factors) develop natural immunity from the disease than to ramp up antibodies via vaccine"

The argument then goes like this. If the virus doesn't mutate or doesn't do it strongly enough then sure get a vaccine and have your antibodies and be happy , much like has been the case with tick-borne encephalitis.
But if the virus does mutate and that mutation is severe enough to transform the virus or it's function (the way it attaches and the success of it) considerably then a high antibody rate against a previous virus form like one would have from a vaccine might be detrimental in some cases as the large portion of antibodies present will tend to fight off the intruder but will be unsuccessful and spend energy in the process and slow down the capability of the naive T cells and the non-memory part of the immune system to fight off the virus. Also could a factor be the different level of antibody present for each individual after the vaccine as some develop a high level/large amount of them while others develop "just enough" to be considered "positive"What are your thoughts on this take , could it indeed be the case?Also I am searching but find it hard to get any valid information about the immune response to newer variants like the Delta from those that have had the real virus and developed natural immunity , which is my case. I wonder what are the effectiveness ratio between a natural immunity versus the best of current vaccines aka the Pfizer , Moderna etc ?

High levels of natural immunity were thought to have been acquired in Brazil

https://www.bmj.com/content/372/bmj.n394

 

[engineer12]

The first is a complicated question to say the least. I will try to address it in pieces.
(1) Natural infection produces a wide range of antibodies (both to different parts of the virus, and of varying efficacy). The quicker the infection clears (if it is asymptomatic and limited to the upper airway), the less time the body has to respond...the humoral immune system (e.g. the part that develops antibodies and T-cell receptors) needs time to start producing antibodies, and then start improving them (immune cells undergo a process called somatic hypermutation to produce much higher affinity / avidity ones). If the infection is short, that doesn't happen.

There is a phenomenon called "antibody-dependent enhancement" where (in some viruses, most notably dengue) previous infection with one serotype (which is really a different virus, 65% homology with each other in dengue, subtypes 1-4) can cause severe disease (e.g. dengue hemorrhagic fever).

That phenomenon can happen in other contexts (indeed, one reason that RSV (respiratory syncitatal virus) vaccines have not been successful is that several first-generation versions (1960s) induced ADE)). It was a known phenomena that was VERY carefully tested for in the Coronavirus vaccines, and was not observed.

The Delta variant seems to be more capable to reinfect recovered people who had previous Beta or Gamma strain infections (<a href="https://www.cell.com/cell/pdf/S0092...m/retrieve/pii/S0092867421007558?showall=true">at least in pseudovirus neutralization assays</a>).

There have been documented reinfection cases in HCW in Brazil,

 

[PeroK]

It looks like the UK is all-in with the Delta variant. In the past four weeks we have gone from about 2,000 positive tests per day to over 20,000 per day (26,000 today).

The government's plan remains to open up on July the 19th and is already saying "we have to learn to live with COVID". It may turn out to be an interesting experiment!

 

[Fra]

If you're interested in reading up more on the adaptive immune response to COVID-19, here's a good source (though it's from Feb and we've learned more since then): https://www.cell.com/cell/pdf/S0092-8674(21)00007-6.pdf

Really nice and broad summary paper!
/Fredrik

 

[Fra]

There is a phenomenon called "antibody-dependent enhancement"

Wow, I never heard of this before. I read up on this and it seems to be a a trojan horse method for viruses to hide and ride on the antibodies. The level of sophistication of survival and evolution from the virus perspective is impressive.

I have in previous projects tried to understand things from the perspective of a single cell, and was amazed. But even the virus perspective seems rich.

Would it be fair to say that the emergence of mutations that employ ADE, is not exactly a coincidence?

/Fredrik

 

[pinball1970]

It looks like the UK is all-in with the Delta variant. In the past four weeks we have gone from about 2,000 positive tests per day to over 20,000 per day (26,000 today).

The government's plan remains to open up on July the 19th and is already saying "we have to learn to live with COVID". It may turn out to be an interesting experiment!

Hopefully it will be with people under 30 who are a lot less likely to get very sick.
We are in exponential now? BUT deaths are in v low levels. The vaccine is working.

 

[atyy]

It looks like the UK is all-in with the Delta variant. In the past four weeks we have gone from about 2,000 positive tests per day to over 20,000 per day (26,000 today).

The government's plan remains to open up on July the 19th and is already saying "we have to learn to live with COVID". It may turn out to be an interesting experiment!

Hopefully it will be with people under 30 who are a lot less likely to get very sick.
We are in exponential now? BUT deaths are in v low levels. The vaccine is working.

https://www.bbc.com/news/health-57667987
Covid: NHS plans booster jab for those 50 and over before winter

UK looks to be in excellent shape with good plans!

 

[artis]

Well I guess being careful is wise always but for someone who has had a natural infection of the UK/other variant or the vaccine there should be no serious case even if the Delta infects you.
I am ofcourse talking about people with no serious background conditions that might otherwise affect an outcome

 

[OmCheeto]

Hopefully it will be with people under 30 who are a lot less likely to get very sick.
We are in exponential now? BUT deaths are in v low levels. The vaccine is working.

Looks exponential to me

Very nice that the case fatality rate has dropped nearly an order of magnitude, due to the vaccinations.

 

[Fra]

Well I guess being careful is wise always but for someone who has had a natural infection of the UK/other variant or the vaccine there should be no serious case even if the Delta infects you.
I am ofcourse talking about people with no serious background conditions that might otherwise affect an outcome

Given the big grey area of long COVID, which is a much larger fraction of people than those that die there are still some concerns I think? We rarely see the nice graphs on this stuff. Media mainly focuses also on death numbers and ICU occupation.

I would still opt not to get it, even if I have to drink beer at home for another year.

From one of the references ine the nice summary paper Yggdrasil recommended...

Multi-organ impairment in low-risk individuals with long COVID​

"Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection has disproportionately affected older individuals and those with underlying medical conditions. Research has focused on short-term outcomes in hospital, and single organ involvement. Consequently, impact of long COVID (persistent symptoms three months post-infection) across multiple organs in low-risk individuals is yet to be assessed.
...
In a young, low-risk population with ongoing symptoms, almost 70% of individuals have impairment in one or more organs four months after initial symptoms of SARS-CoV-2 infection. There are implications not only for burden of long COVID but also public health approaches which have assumed low risk in young people with no comorbidities."
-- https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1

/Fredrik

 

[PeroK]

Given the big grey area of long COVID, which is a much larger fraction of people than those that die there are still some concerns I think? We rarely see the nice graphs on this stuff. Media mainly focuses also on death numbers and ICU occupation.

I would still opt not to get it, even if I have to drink beer at home for another year.

From one of the references ine the nice summary paper Yggdrasil recommended...

Multi-organ impairment in low-risk individuals with long COVID​

"Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection has disproportionately affected older individuals and those with underlying medical conditions. Research has focused on short-term outcomes in hospital, and single organ involvement. Consequently, impact of long COVID (persistent symptoms three months post-infection) across multiple organs in low-risk individuals is yet to be assessed.
...
In a young, low-risk population with ongoing symptoms, almost 70% of individuals have impairment in one or more organs four months after initial symptoms of SARS-CoV-2 infection. There are implications not only for burden of long COVID but also public health approaches which have assumed low risk in young people with no comorbidities."
-- https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1

/Fredrik

And more generally, COVID is not fully understood. There must be serious risks for any country that let's the Delta variant get out of control.

We still have over 20 million people unvaccinated (mostly under 18's) and 12 million people who have had only one jab. That's just over half the population. It's impossible to predict the numbers, but we could easily have 5 million cases of the Delta in the next couple of months.

That said, the number of cases in Spain and Portugal is rising quickly. Perhaps a pan-European surge of the Delta variant will be hard to avoid.

 

[Tom.G]

In a young, low-risk population with ongoing symptoms, almost 70% of individuals have impairment in one or more organs four months after initial symptoms of SARS-CoV-2 infection.

Questionable at this point. Read the comments to the study:
(https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1)

The trials registry protocol suggests n=507 symptomatic cases would be recruited and followed up, ... . Yet the preprint appears to focus on n=201 individuals still "symptomatic after recovery" and it is therefore not surprising that nearly 100% of them report symptoms, as this appears to be the eligibility criteria for the paper.

We'd all like to know the denominator, i.e. of all young low risk patients, what percent go on to have long Covid symptoms? This paper is confusing, with regard to this question.

 

[pinball1970]

Given the big grey area of long COVID, which is a much larger fraction of people than those that die there are still some concerns I think? We rarely see the nice graphs on this stuff. Media mainly focuses also on death numbers and ICU occupation.

I would still opt not to get it, even if I have to drink beer at home for another year.

From one of the references ine the nice summary paper Yggdrasil recommended...

Multi-organ impairment in low-risk individuals with long COVID​

"Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection has disproportionately affected older individuals and those with underlying medical conditions. Research has focused on short-term outcomes in hospital, and single organ involvement. Consequently, impact of long COVID (persistent symptoms three months post-infection) across multiple organs in low-risk individuals is yet to be assessed.
...
In a young, low-risk population with ongoing symptoms, almost 70% of individuals have impairment in one or more organs four months after initial symptoms of SARS-CoV-2 infection. There are implications not only for burden of long COVID but also public health approaches which have assumed low risk in young people with no comorbidities."
-- https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1

/Fredrik

Metro UK this morning
https://metro.co.uk/2021/07/01/hund...red-long-covid-for-more-than-a-year-14857070/

 

[artis]

Well I would be cautious about the study , from all the folks I know around my age almost no one has had prolonged symptoms except me and in my case they are mostly to do with CNS and somewhat lower physical endurance.

 

[pinball1970]

And more generally, COVID is not fully understood. There must be serious risks for any country that let's the Delta variant get out of control.

We still have over 20 million people unvaccinated (mostly under 18's) and 12 million people who have had only one jab. That's just over half the population. It's impossible to predict the numbers, but we could easily have 5 million cases of the Delta in the next couple of months.

That said, the number of cases in Spain and Portugal is rising quickly. Perhaps a pan-European surge of the Delta variant will be hard to avoid.

And more generally, COVID is not fully understood. There must be serious risks for any country that let's the Delta variant get out of control.

We still have over 20 million people unvaccinated (mostly under 18's) and 12 million people who have had only one jab. That's just over half the population. It's impossible to predict the numbers, but we could easily have 5 million cases of the Delta in the next couple of months.

That said, the number of cases in Spain and Portugal is rising quickly. Perhaps a pan-European surge of the Delta variant will be hard to avoid.

Hi Perok Has this been mentioned previously?
Lambda from Peru? On another thread? A search gave me a load of mathy stuff
Its in the UK now too.

https://www.medrxiv.org/content/10.1101/2021.06.21.21259241v1

Also what happened to Epsilon?

EDIT: https://www.healthline.com/health-n...new-covid-19-variants-have-scientists-worried

I am way behind actually

Page 5

https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_17.pdf

 

[Fra]

Questionable at this point. Read the comments to the study:
(https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1)

Yes, it looks a bit hard to see the selection criteria, but I there seems to be more discussions that this sole paper. Anyway, I think the main point is the lack of knowledge of secondary effects. Beeing floored for a couple of weeks and recover is one thing, but long terms effects that may or may not involve even mild forms of local tissue scarring in organs that may go unnoticed or even brain(smell/taste) etc is unpleasant and might be as bad. Without more knowledge perhaps what is this can have implications as predispositions for future problems that show up years later? Even things that long terms loss of smell and taste is IMO quite serious. It won't kill you but will will impact quality of life.

One in ten have long-term effects 8 months following mild COVID-19​

-- https://news.ki.se/one-in-ten-have-long-term-effects-8-months-following-mild-covid-19​

Edit: as this study is behind in time, it likely refers to the original Covid-19 strain, if things is different for delta or other variants is i supposed even more unsure, we have to wait another year for next study. UK is taking the lead with delta I think, in sweden we still have i think only around 50% delta.

/Fredrik

 

[nphysics]

Preliminary data from Public Health England suggests 88% effeciveness of the Pfizer vaccine against the delta variant (B.1.617.2) vs 93% effectiveness against the alpha variant (B.1.1.7), so despite initial worries, the vaccines do still work well against this variant -- more reason to get vaccinated if you have not already.

Effectiveness of COVID-19 vaccines against the B.1.617.2 variant
https://khub.net/documents/13593956...iant.pdf/204c11a4-e02e-11f2-db19-b3664107ac42

AbstractPopular press summary: https://www.bmj.com/content/373/bmj.n1346

It's just an puzzle of no. . we just need full protection against death.

 

[pinball1970]

It's just an puzzle of no. . we just need full protection against death.

By "full" you mean 100%? No such thing.

"greatly reduce" with the published numbers as per @Ygggdrasil post is is as good as it gets.

 

[Ygggdrasil]

@Fra brought up an interesting point here that I have also read elsewhere, maybe also @Ygggdrasil can comment.
I won't publish the source for this because it is in Russian and not from an authoritative source , nevertheless the guy saying these things is rather well known and not your typical anti vaxxer or conspirator.
So the point of argument is basically this. "It is far better to (not accounting for risk factors) develop natural immunity from the disease than to ramp up antibodies via vaccine"

Regarding immunity from infection vs immunity from vaccines, one theoretical reason to think that vaccines might be more effective at inducing immunity is that viruses have evolved measures try to hide themselves from the body's immune system while vaccines are designed to stimulate strong immune responses. Furthermore, the prime-boost strategy used by most of the vaccines might be more effective at inducing long term immunity (though we don't have a lot of data on long term immunity yet).

Empirically, an observational study in Denmark identified 11k people infected during the first wave of COVID-19 and tracked whether they were infected during the second wave of infection. They found previous infection conferred 80.5% protection from reinfection (and a 93% protection against symptomatic infection). This level of protection is similar to that reported for the more effective vaccines (e.g. Pfizer, Moderna, Novavax). However, the study did find that previous infection was not as effective at protecting older adults (age > 65) from subsequent infection (~50% protection) whereas the vaccines above showed no signs of reduced efficacy in older individuals.

So, for younger individuals, it seems like there is a similar amount of protection from previous infection vs vaccination, but in older individuals, vaccination likely provides stronger protection than prior infection.

The argument then goes like this. If the virus doesn't mutate or doesn't do it strongly enough then sure get a vaccine and have your antibodies and be happy , much like has been the case with tick-borne encephalitis.
But if the virus does mutate and that mutation is severe enough to transform the virus or it's function (the way it attaches and the success of it) considerably then a high antibody rate against a previous virus form like one would have from a vaccine might be detrimental in some cases as the large portion of antibodies present will tend to fight off the intruder but will be unsuccessful and spend energy in the process and slow down the capability of the naive T cells and the non-memory part of the immune system to fight off the virus. Also could a factor be the different level of antibody present for each individual after the vaccine as some develop a high level/large amount of them while others develop "just enough" to be considered "positive"What are your thoughts on this take , could it indeed be the case?

I do not think that an antibody response would slow down a T-cell response. Do you have any scientific references that would support such a hypothesis?

Also I am searching but find it hard to get any valid information about the immune response to newer variants like the Delta from those that have had the real virus and developed natural immunity , which is my case. I wonder what are the effectiveness ratio between a natural immunity versus the best of current vaccines aka the Pfizer , Moderna etc ?

I also have not seen much data on this issue. Based on the studies I cited earlier showing that T-cell responses developed against the original strain are also effective against the virus and evidence that prior infection provides similar effectiveness against re-infection as the vaccines, I would guess that prior infection should provide similar effectiveness against symptomatic disease and very good protection against severe disease, hospitalization and death. However, more data would be required to fully test this hypothesis.

 

[Ygggdrasil]

Hi Perok Has this been mentioned previously?

Lambda from Peru? On another thread? A search gave me a load of mathy stuff
Its in the UK now too.

https://www.medrxiv.org/content/10.1101/2021.06.21.21259241v1

Also what happened to Epsilon?

EDIT: https://www.healthline.com/health-n...new-covid-19-variants-have-scientists-worried

I am way behind actually

Page 5

https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_17.pdf

Here's a page from the WHO that lists the variants of concern (alpha, beta, gamma and delta) as well as the variants of interest (epsilon, zeta, eta, theta, iota, kappa, and lambda): https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/

Note that widespread transmission of a new variant does not always mean that the new variant is a more transmissible form of the virus. Often, certain variants could be spread more widely by chance (e.g. they happen to get spread at a superspreader event). Here's a good example of the 20E/EU1 variant that emerged in Spain early in the summer and became widespread across Europe, yet researchers subsequently found no evidence that the variant itself had showed increased transmissibility. Rather, the researchers attribute the success of the variant to it being present in the right place at the right time (emerging just as travel and quarantine restrictions were being lifted in Europe).

Spread of a SARS-CoV-2 variant through Europe in the summer of 2020
Hodcroft et al. Nature 2021
https://www.nature.com/articles/s41586-021-03677-y

Abstract:

Following its emergence in late 2019, the spread of SARS-CoV-21,2 has been tracked by phylogenetic analysis of viral genome sequences in unprecedented detail3,4,5. Although the virus spread globally in early 2020 before borders closed, intercontinental travel has since been greatly reduced. However, travel within Europe resumed in the summer of 2020. Here we report on a SARS-CoV-2 variant, 20E (EU1), that was identified in Spain in early summer 2020 and subsequently spread across Europe. We find no evidence that this variant has increased transmissibility, but instead demonstrate how rising incidence in Spain, resumption of travel, and lack of effective screening and containment may explain the variant’s success. Despite travel restrictions, we estimate that 20E (EU1) was introduced hundreds of times to European countries by summertime travellers, which is likely to have undermined local efforts to minimize infection with SARS-CoV-2. Our results illustrate how a variant can rapidly become dominant even in the absence of a substantial transmission advantage in favourable epidemiological settings. Genomic surveillance is critical for understanding how travel can affect transmission of SARS-CoV-2, and thus for informing future containment strategies as travel resumes.

 

[Ygggdrasil]

Here's a nice paper that estimates the transmissibility of various SARS-CoV-2 VOCs and VOIs:

Increased transmissibility and global spread of SARS-CoV-2 variants of concern as at June 2021
Campbell et al. Euro Surevill. 26: 2100509
https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2021.26.24.2100509

Abstract:

We present a global analysis of the spread of recently emerged SARS-CoV-2 variants and estimate changes in effective reproduction numbers at country-specific level using sequence data from GISAID. Nearly all investigated countries demonstrated rapid replacement of previously circulating lineages by the World Health Organization-designated variants of concern, with estimated transmissibility increases of 29% (95% CI: 24-33), 25% (95% CI: 20-30), 38% (95% CI: 29-48) and 97% (95% CI: 76-117), respectively, for B.1.1.7, B.1.351, P.1 and B.1.617.2.

 

[atyy]

Increased transmissibility and global spread of SARS-CoV-2 variants of concern as at June 2021
Campbell et al. Euro Surevill. 26: 2100509
https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2021.26.24.2100509

The estimate for delta by Campbell et al looks a lot higher than that given by Mlcochova et al. I guess it's partly because they use different definitions?

Mlcochova et al try to separate out transmissibility from immune evasion, whereas Campbell et al say "It is important to note that our analysis cannot distinguish between a genuine increase in transmissibility (i.e. the basic reproduction number) and immune evasion as explanations for higher effective reproduction numbers. For variants with relevant levels of immune evasion, as potentially observed for B.1.351 [7], the future nature of competitive growth with other variants will depend on the immune context, both infection- and vaccine-derived, of each country under consideration."

 

[atyy]

The estimate for delta by Campbell et al looks a lot higher than that given by Mlcochova et al. I guess it's partly because they use different definitions?

Mlcochova et al try to separate out transmissibility from immune evasion, whereas Campbell et al say "It is important to note that our analysis cannot distinguish between a genuine increase in transmissibility (i.e. the basic reproduction number) and immune evasion as explanations for higher effective reproduction numbers. For variants with relevant levels of immune evasion, as potentially observed for B.1.351 [7], the future nature of competitive growth with other variants will depend on the immune context, both infection- and vaccine-derived, of each country under consideration."

I guess after comparing the papers, transmissibility is defined differently in each. I'm not sure the terms in the models can be mapped exactly onto each other, but it looks like Campbell's relative reproduction number would seem be closer Mlcochova call the transmissibility increase, and if we compare those, the estimates are closer. Campbell (Fig. 3) gets about 1.5 while Mlocochova gets about 1.1 to 1.4. Campbell's number is still towards the upper end of Mlocochova's range, but that could be due to founder effects and not accounting for immune evasion, as Campbell discuss.

 

[Jonathan Scott]

Here in the UK, I'm seeing two types of numbers being used alarmingly inconsistently with one another:

a) When x% of the population is immune, due to vaccination or previous infection, the spread will finally be under control (where x% depends on the variant being discussed but is usually given as about 85%).

b) The fraction of the population who have been vaccinated is approaching x%, so we should be seeing the effects of this any day now.

This appears to completely ignore the fact that having been vaccinated is nowhere near the same as being immune due to vaccination, especially as the widely used Oxford/AstraZeneca vaccine (the one which my wife and I had) after both doses is still apparently only about 62% effective against symptomatic disease due to the delta variant, which is thought to still allow transmission, so even if everyone had been vaccinated, the immunity level would be nowhere near high enough to stop the spread. The Pfizer vaccine is better from that point of view, at around 95%, but even then the percentage of immunity is still somewhat less than the percentage vaccinated.

In the mean time, the rise in the UK over the last few weeks has been higher than exponential; the percentage increase per week has been steadily increasing, to 74.1% as of 28th June, according to the UK government web site: https://coronavirus.data.gov.uk/details/cases

Even if I'm unlikely to die of it, I really don't want to get it. Swine flu back in 2009 was horrible; fever gives me hallucinations like waking nightmares, and it took months to get back to my normal sleep patterns. I find the idea of simply letting the delta variant spread because "it is no longer expected to reach levels which could overwhelm the health service" really scary.

[Edited for typo in increase: 74.1% not 71.4%]

 

[PeroK]

Even if I'm unlikely to die of it, I really don't want to get it. Swine flu back in 2009 was horrible; fever gives me hallucinations like waking nightmares, and it took months to get back to my normal sleep patterns. I find the idea of simply letting the delta variant spread because "it is no longer expected to reach levels which could overwhelm the health service" really scary.

You're not the only one frightened by the government's plans:

https://www.theguardian.com/world/2...tm_source=esp&utm_medium=Email&CMP=GTUK_email