Get Vaccinated Against the Covid Delta Variant

[atyy]

All of the studies so far, including the data from Israel, suggest that the vaccine is very effective (>90%) at preventing severe disease, hospitalization and death. The figure I presented above (>99% of COVID deaths in the US are in unvaccinated individuals) is consistent with this idea.

The US data isn't for Delta. The Israel data is for Delta (>90%), but I think it's not yet released in detail.

The UK has Delta data (<90%), but I think only for first and second dose risk reduction in hospitalization.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01358-1/fulltext
"Sequencing data from Scotland has found that for April 1 to May 28, 2021, the latest date until which data were available, 97% of S gene positive cases sequenced in Scotland were the Delta variant and that 99% of Delta variants were S gene positive. ...

Among S gene-negative cases, the effect of vaccination (at least 28 days after first or second dose) was to reduce the risk of hospital admission (HR 0·28, 95% CI 0·18–0·43) compared to unvaccinated. The corresponding hazard ratio for risk of hospital admission for S gene-positive cases was 0·38 (95% CI 0·24–0·58) ..."

 

[pinball1970]

I think that the science is definitely expected to follow the politics now!

The UK Government has based its strategy on the vaccinations being effective and the Delta variant being rendered largely harmless. We are now up to 32,500 cases today and the government's own projection is that we will be at 50,000 per day by July 19th when we open up and peak at 100,000 cases per day in August. Although, these may be optimistic figures.

It's a critical question for us is whether vaccination prevents hospitalisation and death. We'll soon find out.

What a gamble!

The September back to school wave is similar to the current wave

The only difference is September was pre DELTA and pre vaccine

We are at 32,000 per day now, similar numbers and curve to November 12th

Gradient is steeper now for this period but Delta is more infectious so that is expected?

The case rise through November led to 500-600 deaths per day whereas we are still at 35 per day.

Variant factories aside, this looks ok?

 

[Fra]

View attachment 285641

Variant factories aside, this looks ok?

Looking decent to me, but as a precaution there may an issue in the choice of measure.
Using only #death as a measure, lost QALY seems like a more relevant measure. It would be interesting to see that as well. For long-COVID or other unknowns there may be long term QALY loss which does not even involved death, and this are escaping the "death toll measure" altogether.

A model framework for projecting the prevalence and impact of Long-COVID in the UK
"The objective of this paper is to model lost Quality Adjusted Life Years (QALYs) from symptoms arising from COVID-19 in the UK population, including symptoms of ‘long-COVID’. The scope includes QALYs lost to symptoms, but not deaths, due to acute COVID-19 and long COVID...
...
we modeled 299,719 QALYs lost within 1 year of infection (90% due to symptomatic COVID-19 and 10% permanent injury) and 557,754 QALYs lost within 10 years of infection (49% due to symptomatic COVID-19 and 51% due to permanent injury)."
-- https://www.medrxiv.org/content/10.1101/2021.05.18.21252341v1.full

But another QALY paper, advocating ease of restructions (I apologize if this is posted elsewhere already)

"Stay at Home, Protect the National Health Service, Save Lives": A cost benefit analysis of the lockdown in the United Kingdom​

"This suggests that the costs of continuing severe restrictions are so great relative to likely benefits in lives saved that a rapid easing in restrictions is now warranted."
"- https://pubmed.ncbi.nlm.nih.gov/32790942/

So the antagonistic cynical statement may be?
"Go shopping, Protect the National Economy, Save Money"

/Fredrik

 

[pinball1970]

Yes I agree it is a lot more complicated than just cases/deaths.
I just noticed we have similar figures from September to Nov 2020 to the period we are in now.

Looking your references
If the vaccine reduces the ability of the virus to reproduce and do damage resulting in hospitalization and death could the vaccine reduce the risk of long Covid for instance?

In terms of a visit to A&E or an overnight stay not necessarily resulting in death, the below indicates the vaccine has had a huge impact.

We would expect those numbers to keep improving as the study starts from February when a lot less people were vaccinated or at least two doses plus 14 days.

https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_15.pdf

 

[Astronuc]

Here's a nice piece from the New York Times discussing various studies on the effectiveness of the Pfizer vaccine against the delta variant and the disagreement between the studies:

My wife was wondering about the effectiveness of Moderna against the Delta variant given a lot of news concerns the effectiveness of Pfizer vaccine.

LA Times has an article looking at the effectiveness of vaccines against Delta, but it seems to fall short without quantification.

Moderna said this week that its vaccine — which is very similar to the Pfizer shot — is also highly effective against the Delta variant.

Not much to go on.
https://www.latimes.com/science/sto...-do-covid-19-vaccines-cover-the-delta-variant

I still wear a mask going into public despite the rescinding of the 'mask mandate' for vaccinated people. The majority of the population do not wear masks, but I notice many elderly still do.

 

[atyy]

https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_15.pdf

Since I don't live in the UK, and think vaccinations should allow opening up - but don't know for sure - I'm very happy you are doing the experiment! OK, that's my bias. The one thing in the data you posted that makes me worried is that in Table 6 on p15, deaths as a proportion of cases is higher for the fully vaccinated (12/1785) than for the unvaccinated (23/19573) Perhaps not horrifying since the vaccinated were mostly old folks with a much higher risk of severe disease whereas the unvaccinated were young people not at risk, so one would need to know the age distribution ... I think

 

[Fra]

Looking your references
If the vaccine reduces the ability of the virus to reproduce and do damage resulting in hospitalization and death could the vaccine reduce the risk of long Covid for instance?

That seems like a logical expectation to me, and indeed even in Sweden we see reduced hospitalizations as well. So all looks promising. But so did it, last summer. Most was aware of a possible second wave, but NO experty I am aware of thought the second wave was going to be BIGGER than the first wave. Counterintuitive.

The major risk with the vaccine, seems to be it becomes a perfect excuse to opening up sooner. I totally understand the economical arguments though. Even early on in the pandemi, som ballpark estimates was that the cost supporting restrictions are massive, even compare to lost QALY. But that is a sensitive topic. If it wasnt for the cost of restrictions, it would seem reasonable to enjoy the effects of BOTH vaccines and some extended restrictions. But it's possible that with such strategy, we would have to keep up restrictions for years still, which may get unreasonable at some point.

I think a big nightmare outcome is that, motivated by the success of vaccines, a new mutation that perhaps makes an ADE exploit that Yggdrasil mentioned, so that those with antobodies are even MORE susceptible to a new mutation. But perhaps such an outcome is unlikely, who knows? But as per my poor understanding the risk for that would be higher if we vaccine everbody and then increase the spread of the virus because it's less harmful.

Personally I think thinks are looking decent, but I will hold my breath at least until christmas.

/Fredrik

 

[pinball1970]

I think that the science is definitely expected to follow the politics now!

Since I don't live in the UK, and think vaccinations should allow opening up - but don't know for sure - I'm very happy you are doing the experiment! OK, that's my bias. The one thing in the data you posted that makes me worried is that in Table 6 on p15, deaths as a proportion of cases is higher for the fully vaccinated (12/1785) than for the unvaccinated (23/19573) Perhaps not horrifying since the vaccinated were mostly old folks with a much higher risk of severe disease whereas the unvaccinated were young people not at risk, so one would need to know the age distribution ... I think

Yes I noticed that.
There was another report with over and under 50s vaccinated verses non vaccinated I will try and find that.

The numbers of those vaccinated who died roughly match those unvaccinated (20 and 23 resp) between 1/2/21 and 7/6/21The % of the unvaccinated for the 50+ group by June should have been very low (5% ish). They were vaccinating 50-60 years end of March.

@PeroK explained this better on another post (which I cannot find). 95% of that group (vaccinated 50+) yielded less deaths than the remaining 5% meaning being unvaccinated is 20 times more dangerous than being vaccinated.

I think we can apply that to these numbers?
Even if I have got the wrong end of the stick on that it is certain you are much more likely to end up in hospital if you are unvaccinated which means something potentially serious is going on.

Perhaps lead to some of the possible long term injuries/long Covid numbers discussed on pf.

 

[atyy]

LA Times has an article looking at the effectiveness of vaccines against Delta, but it seems to fall short without quantification.

The LA Times article is behind a paywall. I agree there aren't numbers yet for Moderna. However, Moderna used 2 tricks that Pfizer also used: (i) Kariko, Weissman and colleagues' tweak of the chemical composition of the mRNA so that the mRNA itself doesn't provoke the immune system so much (it's the protein product of the mRNA that we want to stimulate immune responses) (ii) McLellan and colleague's trick of holding the protein protein in correct pre-fusion shape, that we want the immune system to recognize and attack. So one would expect it performs very similarly to the Pfizer vaccine.

 

[atyy]

https://www.bbc.com/news/uk-england-london-57732002
Covid-19: Euro 2020 tickets offered as part of vaccine push

Mayor Sadiq Khan is offering two tickets to Sunday's final as well as 50 pairs of tickets to the Trafalgar Square Fan Zone.

 

[pinball1970]

I think a big nightmare outcome is that, motivated by the success of vaccines, a new mutation that perhaps makes an ADE exploit that Yggdrasil mentioned

/Fredrik

ADE? That is a new one to me.
I will keep my eye out for information on this relating to COVID as the paper is pre vaccine (September 2020)
With 79 million vaccinated an opportunity to see if ADE is a thing or not with COVIDThis one is post vaccine, a little harder to read (for me)
Note the mast cell reference also ( a worry for me during all this being asthmatic )
https://www.frontiersin.org/articles/10.3389/fimmu.2021.640093/full

Another search found this
https://www.news-medical.net/news/2...underlie-inflammation-in-severe-COVID-19.aspx

 

[Fra]

This is really interesting and fascinating indeed, but it seems also very complex. A broad nice T-cell immunity seems nice, but at the same time a broader immunity must be ensured not to overreat or borderling to autoimmunity. It seems evolution has taken well care of this to keep it balanced most of the time. Many papes report that severeity of disease seems linked to either a poor T-cell response, or a too strong (or incorrectly regulated) T-cell response.

Severe COVID-19 infection linked to overactive immune cells​

"Sometimes, our immune system overreacts to invaders, for example during an allergic reaction, resulting in T cells killing normal, healthy cells and causing tissue damage. However, there is a ‘brake mechanism’ that should kick in, causing T cells to reduce their activity and calming inflammation.
...
On closer inspection of the mechanism, the researchers found that the protein ‘Foxp3’, which usually induced the brake mechanism, is inhibited in lungs of severe COVID-19 patients. They are unsure why Foxp3 is inhibited, but further study could reveal this, and potentially lead to a way to put the brakes back on the T cell response, reducing the severity of the disease."
-- https://www.imperial.ac.uk/news/206173/severe-covid-19-infection-linked-overactive-immune/

I guess the more specific B-cell response seems is filling a gap here as well, in beeing "safer", with less risk of overdoing things? Marking a disarming a virus is one thing, but killing a "potentiall infected" cells is certainly more drastic unless the malign status is 100% certain.

/Fredrik

 

[Ygggdrasil]

That seems like a logical expectation to me, and indeed even in Sweden we see reduced hospitalizations as well. So all looks promising. But so did it, last summer. Most was aware of a possible second wave, but NO experty I am aware of thought the second wave was going to be BIGGER than the first wave. Counterintuitive.

It is perfectly reasonable to think that the second wave would be bigger than the first wave; that's what happened in the 1918 Influenza pandemic.

https://www.cdc.gov/flu/pandemic-resources/1918-commemoration/three-waves.htm

For example, here's an article for May 2020 of an expert with extremely prescient warnings of how the fall and winter of 2020/2021 would play out: https://www.ama-assn.org/delivering...emiologist-beware-covid-19-s-second-wave-fall

The major risk with the vaccine, seems to be it becomes a perfect excuse to opening up sooner. I totally understand the economical arguments though. Even early on in the pandemi, som ballpark estimates was that the cost supporting restrictions are massive, even compare to lost QALY. But that is a sensitive topic. If it wasnt for the cost of restrictions, it would seem reasonable to enjoy the effects of BOTH vaccines and some extended restrictions. But it's possible that with such strategy, we would have to keep up restrictions for years still, which may get unreasonable at some point.

I think a big nightmare outcome is that, motivated by the success of vaccines, a new mutation that perhaps makes an ADE exploit that Yggdrasil mentioned, so that those with antobodies are even MORE susceptible to a new mutation. But perhaps such an outcome is unlikely, who knows? But as per my poor understanding the risk for that would be higher if we vaccine everbody and then increase the spread of the virus because it's less harmful.

Many studies have looked for signs of ADE, but none have found any, even with the variants. To quote an article on the subject:

So here’s the short version: no sign of ADE during the preclinical animal studies. No sign during the human clinical trials. No sign during the initial vaccine rollouts into the population. And (so far) no sign of ADE even with the variant strains in different parts of the world. We have things to worry about in this pandemic, but as far as I can tell today, antibody-dependent enhancement does not seem to be one of them. I understand why people would worry about it, and want to avoid it. But if you’re coming across reports that say that it’s a real problem right now and that you should avoid getting vaccinated because of it, well, I just don’t see it. Some of that is well-intentioned caution, and some of it is probably flat-out anti-vaccine scaremongering.​

https://blogs.sciencemag.org/pipeli...dent-enhancement-and-the-coronavirus-vaccines (the full article is a good read if one is interested on the topic)

This is really interesting and fascinating indeed, but it seems also very complex. A broad nice T-cell immunity seems nice, but at the same time a broader immunity must be ensured not to overreat or borderling to autoimmunity. It seems evolution has taken well care of this to keep it balanced most of the time. Many papes report that severeity of disease seems linked to either a poor T-cell response, or a too strong (or incorrectly regulated) T-cell response.

Severe COVID-19 infection linked to overactive immune cells​

"Sometimes, our immune system overreacts to invaders, for example during an allergic reaction, resulting in T cells killing normal, healthy cells and causing tissue damage. However, there is a ‘brake mechanism’ that should kick in, causing T cells to reduce their activity and calming inflammation.
...
On closer inspection of the mechanism, the researchers found that the protein ‘Foxp3’, which usually induced the brake mechanism, is inhibited in lungs of severe COVID-19 patients. They are unsure why Foxp3 is inhibited, but further study could reveal this, and potentially lead to a way to put the brakes back on the T cell response, reducing the severity of the disease."
-- https://www.imperial.ac.uk/news/206173/severe-covid-19-infection-linked-overactive-immune/

I guess the more specific B-cell response seems is filling a gap here as well, in beeing "safer", with less risk of overdoing things? Marking a disarming a virus is one thing, but killing a "potentiall infected" cells is certainly more drastic unless the malign status is 100% certain.

It is well documented that severe COVID-19 is associated with dysregulation of the immune system which can result in a "cytokine storm," where at late stages of the disease, most of the damaging symptoms come from the immune response to the infection rather than the infection itself (which is why immunosuppresants like dexamethosone have been identified as effective treatments in later stage disease). However, patients progress to later-stage severe disease because their adaptive immune systems were not able to control the infection at an earlier point (see this article for a review).

Given the wide variety of clinical and observational data suggesting that both vaccination and prior infection can protect against severe disease, hospitalization and death, I don't think that having T-cell immunity is a problem for SARS-CoV-2 infection. Rather the problem is lacking immunity, getting infected, and having the virus replicate to high levels before the adaptive immune system catches up. Once the virus is widespread throughout the body, it is at this point where the immune response to the virus can trigger cytokine storms and other severe symptoms of the disease.

 

[artis]

So speaking about pandemic waves , do all virus pandemics follows a trend where the first wave is somewhat smaller, then the second wave is a killer and by each next wave the severity and numbers fall down ?
I hope this is the case for Covid, but it also seems to have been the case for the infamous and deadly "Spanish flu" and back then we did not have any vaccines but it seems that the path still resembles that of the current Covid even with us now having tons more safety gear and drugs and vaccines.
I would love some clever opinions on this one.

 

[Jonathan Scott]

There are many situations in which delayed feedback can cause increasing oscillations.

 

[Ygggdrasil]

So speaking about pandemic waves , do all virus pandemics follows a trend where the first wave is somewhat smaller, then the second wave is a killer and by each next wave the severity and numbers fall down ?
I hope this is the case for Covid, but it also seems to have been the case for the infamous and deadly "Spanish flu" and back then we did not have any vaccines but it seems that the path still resembles that of the current Covid even with us now having tons more safety gear and drugs and vaccines.
I would love some clever opinions on this one.

I'm not sure if there is a consensus accepted explanation for the three waves of the 1918 inflenza pandemic. Here are two articles that present differing explanations (one suggests individuals' behavioral responses and the other suggests the emergence of new variants), both of which are relevant to the current pandemic:

Inferring the causes of the three waves of the 1918 influenza pandemic in England and Wales
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3730600/

Study suggests 1918 flu waves were caused by 'distinct' viruses
https://www.cidrap.umn.edu/news-per...s-1918-flu-waves-were-caused-distinct-viruses

IMO, the first article seems to reflect what may be going on now. Essentially, they model behavioral responses as populations instituting/following social distancing measures when deaths are high (lowering transmission) and relaxing these measures when deaths are low (increasing transmission), which is able to recapitulate the course of the pandemic quite well. The fact that each wave was associated with different variants does not necessarily mean that the variants were causal for the different waves (indeed, given that viruses mutate over time, one would expect different waves to have viruses carrying different set of mutations).

 

[Fra]

Many studies have looked for signs of ADE, but none have found any, even with the variants. To quote an article on the subject:

So here’s the short version: no sign of ADE during the preclinical animal studies. No sign during the human clinical trials. No sign during the initial vaccine rollouts into the population. And (so far) no sign of ADE even with the variant strains in different parts of the world. We have things to worry about in this pandemic, but as far as I can tell today, antibody-dependent enhancement does not seem to be one of them.​

Regarding lack of indications, found this, what is your interpretation of this?

A perspective on potential antibody-dependent enhancement of SARS-CoV-2​

"At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies—regardless of what virus is the causative agent—it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward."
-- https://www.nature.com/articles/s41586-020-2538-8

/Fredrik

 

[atyy]

Yes I noticed that.
There was another report with over and under 50s vaccinated verses non vaccinated I will try and find that.

The numbers of those vaccinated who died roughly match those unvaccinated (20 and 23 resp) between 1/2/21 and 7/6/21The % of the unvaccinated for the 50+ group by June should have been very low (5% ish). They were vaccinating 50-60 years end of March.

@PeroK explained this better on another post (which I cannot find). 95% of that group (vaccinated 50+) yielded less deaths than the remaining 5% meaning being unvaccinated is 20 times more dangerous than being vaccinated.

I think we can apply that to these numbers?
Even if I have got the wrong end of the stick on that it is certain you are much more likely to end up in hospital if you are unvaccinated which means something potentially serious is going on.

Perhaps lead to some of the possible long term injuries/long Covid numbers discussed on pf.

Here's data with divided by age (Table 5, p16-17)
https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_18.pdf

50+
Unvaccinated: 71 deaths / 1267 Delta cases = 5.6%
2 doses: 116 deaths / 5234 Delta cases = 2.2%
Vaccine effectivess for preventing deaths ~ 60% (Oh, so low? But doesn't say how many days after 2 doses)

50-
Unvaccinated: 21 deaths / 70664 Delta cases = 0.03%
2 doses: 2 deaths / 5600 Delta cases = 0.036% (OMG I hope I've made absolutely silly mistakes in calculating)

 

[Fra]

2 doses: 2 deaths / 5600 Delta cases = 0.036% (OMG I hope I've made absolutely silly mistakes in calculating)

Is there a selection bias? Doesn't the table say "Attendance to emergency care"? I didn't real the whole paper though.

Perhaps a larger % of most 50+ end up there vs 50-?
/Fredrik

 

[Ygggdrasil]

Here's data with divided by age (Table 5, p16-17)
https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_18.pdf

50+
Unvaccinated: 71 deaths / 1267 Delta cases = 5.6%
2 doses: 116 deaths / 5234 Delta cases = 2.2%
Vaccine effectivess for preventing deaths ~ 60% (Oh, so low? But doesn't say how many days after 2 doses)

50-
Unvaccinated: 21 deaths / 70664 Delta cases = 0.03%
2 doses: 2 deaths / 5600 Delta cases = 0.036% (OMG I hope I've made absolutely silly mistakes in calculating)

Here's a good article explaining some of the pitfalls of trying to analyze such data without trying to correct for confounding factors:

But once vaccines hit the real world, it becomes much harder to measure their effectiveness. Scientists can no longer control who receives a vaccine and who does not. If they compare a group of vaccinated people with a group of unvaccinated people, other differences between the groups could influence their risks of getting sick.

It’s possible, for example, that people who choose not to get vaccinated may be more likely to put themselves in situations where they could get exposed to the virus. On the other hand, older people may be more likely to be vaccinated but also have a harder time fending off an aggressive variant. Or an outbreak may hit part of a country where most people are vaccinated, leaving under-vaccinated regions unharmed.

One way to rule out these alternative explanations is to compare each vaccinated person in a study with a counterpart who did not get the vaccine. Researchers often go to great lengths to find an unvaccinated match, looking for people who are of a similar age and health. They can even match people within the same neighborhood.

https://www.nytimes.com/2021/07/06/science/Israel-Pfizer-covid-vaccine.html

Given that studies from Britain and Scotland show that the vaccine is effective against the delta variant and presumably use some of the same data, it's likely that the vaccinated and unvaccinated populations in your dataset are not well matched.

 

[PeroK]

The Delta variant appears to have taken off in Spain, Portugal and the Netherlands, as well as the UK. In any case, there are large numbers of new cases in those countries again.

 

[Ygggdrasil]

Regarding lack of indications, found this, what is your interpretation of this?

A perspective on potential antibody-dependent enhancement of SARS-CoV-2​

"At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies—regardless of what virus is the causative agent—it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward."
-- https://www.nature.com/articles/s41586-020-2538-8

/Fredrik

At the end of the section assessing the risk of ADE of disease with SARS-CoV-2, the authors write "In summary, current clinical experience is insufficient to implicate a role for ADE of disease, or immune enhancement by any other mechanism, in the severity of COVID-19 (Table 1)," which is consistent with the information I posted previously.

The research community is certainly aware of the possibility of ADE, which is why there are so many studies ongoing to assess the efficacy of vaccines and antibody-based treatments against the variants (as discussed above throughout the thread). Not only will these studies show whether the viruses can evade protection from the vaccines or treatments, but they can also show whether the vaccines or treatments lead to ADE and give worse outcomes for people given the vaccines or antibodies.

 

[atyy]

Here's data with divided by age (Table 5, p16-17)
https://assets.publishing.service.g...ants_of_Concern_VOC_Technical_Briefing_18.pdf

50+
Unvaccinated: 71 deaths / 1267 Delta cases = 5.6%
2 doses: 116 deaths / 5234 Delta cases = 2.2%
Vaccine effectivess for preventing deaths ~ 60% (Oh, so low? But doesn't say how many days after 2 doses)

50-
Unvaccinated: 21 deaths / 70664 Delta cases = 0.03%
2 doses: 2 deaths / 5600 Delta cases = 0.036% (OMG I hope I've made absolutely silly mistakes in calculating)

Tweet by David Speigelhalter: "Latest PHE data: https://gov.uk/government/publications/investigation-of-novel-sars-cov-2-variant-variant-of-concern-20201201 Out of 257 Delta deaths, 118 (46%) fully vaxxed, 92 (36%) unvaxxed. What we would expect with high coverage by very effective – but not perfect – vaccine."

@PeroK and @pinball1970 made similar points earlier.

If the vaccine reduces deaths by (1-r). In an unvaccinated population x fraction die. In a vaccinated population (1-r)x fraction die. If v of the total population is vaccinated, then the fraction of deaths due to vaccinated people is z = [v(1-r)x]/[v(1-r)x + (1-v)x].

Solving gives r = [v - z]/[v(1-z)]. Using z = 0.46 from the data, and NHS data (page 4) that v = 0.9 or greater, we get r ~ 0.90. So the vaccine is ~90% effective in reducing Delta deaths. Much more reassuring, assuming again I haven't made errors.

 

[Evo]

A woman in Belgium after simultaneously contracting two different Covid variants.

A 90-year-old Belgian woman who died from COVID-19 in March contracted both the UK and South African strain simultaneously, researchers said at a press conference on Sunday.

Her case, which was discussed at this year's European Congress on Clinical Microbiology & Infectious Diseases (ECCMID) as part of Belgian research, is believed to be the first of its kind.

The woman, who reportedly was not vaccinated, got sick in March and was treated at a hospital close to Brussels, according to Belgian broadcaster VRT.

https://www.yahoo.com/news/woman-died-covid-19-first-171023624.html

@Ygggdrasil or @atyy Are the variants so different that you can catch more than one at once, but the same vaccine works to prevent all? So, if you had the UK type, you could then apparently catch another variant because you would not have immunity, or is the difference that the woman caught both at the same time with no prior immunity to either?

 

[bhobba]

We must all get vaccinated. The Delta variant just makes it more urgent. But even before the variant really took off, at least in the UK (and because we use the same vaccines), likely Aus as well, achieving herd immunity was going to be difficult:
https://www.medrxiv.org/content/10.1101/2021.01.16.21249946v1

I think it may now be out of reach without second-generation vaccines targeting Delta and boosters:
https://www.news-medical.net/news/2...accine-based-on-SARS-CoV-2-Delta-variant.aspx

Thanks
Bill

 

[atyy]

Are the variants so different that you can catch more than one at once, but the same vaccine works to prevent all? So, if you had the UK type, you could then apparently catch another variant because you would not have immunity, or is the difference that the woman caught both at the same time with no prior immunity to either?

I'm not sure about natural infection, but for the vaccines (say Pfizer) they reduce infection (asymptomatic and symptomatic) by about 85-95% for the alpha variant, and by about 60-80% for the Delta variant.

Alpha (or earlier variants):
https://www.cdc.gov/coronavirus/2019-ncov/science/science-briefs/fully-vaccinated-people.html

Delta:
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01358-1/fulltext
https://www.reuters.com/world/middl...n-against-infections-still-strong-2021-07-05/

 

[pinball1970]

We must all get vaccinated. The Delta variant just makes it more urgent. But even before the variant really took off, at least in the UK (and because we use the same vaccines), likely Aus as well. achieving herd immunity was going to be difficult:
https://www.medrxiv.org/content/10.1101/2021.01.16.21249946v1

I think it may now be out of reach without second-generation vaccines targeting Delta and boosters:
https://www.news-medical.net/news/2...accine-based-on-SARS-CoV-2-Delta-variant.aspx

Thanks
Bill

"Delta variant has been shown to be much more harmful than the Alpha variant, causing twice as many hospitalizations."

I thought DELTA was more transmissible but not necessarily associated with more severe disease?

A quick search suggests you are more likely to end up in hospital
https://www.bhf.org.uk/informations...virus-and-your-health/covid-variant#INDdeadlyIs the fact you are more likely to end up in hospital because the majority of cases are DELTA?

Also if DELTA is that more dangerous does that not mean that because deaths are still low the vaccine is doing an even better job that was expected?

Lots of questions!

Also on the paper was this link

https://www.news-medical.net/news/20210628/Study-suggests-vitamin-B12-as-a-SARS-CoV-2-antiviral.aspx

“The researchers employed a Quadratic Unbounded Binary Optimization (QUBO) model that runs on a quantum-inspired device to search for compounds similar to remdesivir.”
Probably better on another Covid thread or may have been posted already but I thought that was interesting

Vit B less expensive and toxic that remdesivir.

 

[Fra]

Lets see if we see a first case of the UEFA-2020 mutation, resistant both to pfizer and alcohol.

/Fredrik

 

[bhobba]

Lots of questions!

Yes, there is. And researchers are working to answer them. But we must be careful in interpreting the data. I heard some commentators say Delta is less deadly because of data from the UK. A lot of people are vaccinated in the UK, so I am not sure that conclusion is warranted.

Time will be needed to sort it out.

Thanks
Bill

 

[Ygggdrasil]

A woman in Belgium after simultaneously contracting two different Covid variants.

https://www.yahoo.com/news/woman-died-covid-19-first-171023624.html

@Ygggdrasil or @atyy Are the variants so different that you can catch more than one at once, but the same vaccine works to prevent all? So, if you had the UK type, you could then apparently catch another variant because you would not have immunity, or is the difference that the woman caught both at the same time with no prior immunity to either?

It is likely that the woman got infected with both variants at the same time with no prior immunity to either.

As @atyy state, the Pfizer vaccine seems effective against the newer variants. Studies have also shown that prior infection can also protect from re-infection, with efficacy similar to that of vaccination (example). While I have not seen studies on whether prior infection can protect against the newer variants, based on these data above (vaccines can protect against the newer variants and prior infection protects similarly as vaccines), I would expect that prior infection can protect, at least partially, from infection with the new variants and should likely give effective protection against severe disease, hospitalization and death. Consistent with this idea, studies looking at T-cells for both vaccinated individuals and indiviudials with prior infections suggest that the T-cells from these individuals can recognize the newer variant viruses (https://pubmed.ncbi.nlm.nih.gov/33594378/).

Regarding individuals, infected with multiple strains of the same virus, this is a rare event, but one that has been seen before both with influenza (https://www.sciencedirect.com/science/article/pii/S1386653215007404) and COVID-19 (https://www.sciencedirect.com/science/article/abs/pii/S0168170221000526?via=ihub).

 

[artis]

Isn't this rare case of getting infected with say two strains of the same virus just similar to having one strain but a higher viral load?
Because as far as I understand the main difference between the strains is the adaptation of the newer strains to better infect (attach) to the human cells in the respiratory system, so could I simply say that having two strains with one of the strains being the delta would be somewhat similar to like having the beta strain in higher viral load?

I guess there were some other mutations within delta that made it's disease form somewhat different although I don't know what causes the higher hospitalization and death rate from it whether it's the different form of the disease or simply the fact that it can enter more people and given that there is always a percentage of sick and weak people if a virus has higher transmission rate it can therefore affect more of the vulnerable etc. Somewhat like if we were able to give every single human on Earth the regular flu we too would see large numbers of deaths in total. But don't take this as fact I am speculating here

 

[.Scott]

The COVID Delta variant is a big change.
According to this Nature article (N=62+63):

Viral load is roughly 1,000 times higher in people infected with the Delta variant than those infected with the original Coronavirus strain, according to a study in China.

It's accepted that this virus spreads through an aerosol - though the particle size is so small (smaller than tobacco smoke), I prefer to call it a "colloidal dispersion". There is every reason to expect that the density of that COVID "smoke" will track the viral load in the index patients respiratory track. And therefore, we should expect that the smoke is 1000 times the "viral load".
For the original COVID, virus trackers would look for an exposure time of about 15 minutes. If you divide that by 1000, you get an infection from a single breath!

There are some indications that it really is that potent.
From a recent MIT article:

During a June outbreak in Australia, where the virus had been previously well controlled despite an extremely low vaccination rate, New South Wales Health Minister Jeroen Weimar warned that transmission had occurred with only “fleeting contact” between individuals. For example, contact tracing and genomic sequencing showed that a woman in her 70s was infected while sitting outside a cafe visited by “Patient Zero,” an airport limo driver. In another instance, the virus seems to have been transmitted in the time it took for two unmasked strangers to pass each other in a shopping center, an encounter captured by mall security cameras.

But I don't think the claim that this virus spreads twice as fast (about R=4 vs. R=2), tells the whole story.

Here is a Boston News article reporting local Health Department statistics:

When analyzing the number of overall COVID-19 cases reported by the DPH between July 10 and July 16, the breakthrough cases account for 43.4 percent of all new COVID-19 cases.

Massachusetts doctors say the biggest cause is the arrival of the COVID-19 delta variant, which is twice as infectious than the original virus.

So we should also expect that this variant will be much hard to contain. If you know someone who is immune compromised, it could be very difficult to protect them from exposure.

It also means that anyone who was hoping to ride this out without getting either vaccinated or infected is likely playing a loosing game.

 

[atyy]

It's accepted that this virus spreads through an aerosol - though the particle size is so small (smaller than tobacco smoke), I prefer to call it a "colloidal dispersion". There is every reason to expect that the density of that COVID "smoke" will track the viral load in the index patients respiratory track. And therefore, we should expect that the smoke is 1000 times the "viral load".
For the original COVID, virus trackers would look for an exposure time of about 15 minutes. If you divide that by 1000, you get an infection from a single breath!

Delta is more transmissible, but I'm skeptical of some of these specific ideas, especially the claims of transmission with fleeting contact. We have known since April 2020 that COVID-19 can be spread through aerosols in some circumstances, especially when ventilation is poor (https://www.medrxiv.org/content/10.1101/2020.04.16.20067728v1). There is not any good evidence that one has to worry about aerosols much more with Delta than with the original strain - ie. all non-pharmaceutical precautions for the original strain (safe distancing, mask wearing, ventilation, hand washing) should still work with Delta, and if you got infected with Delta, it doesn't mean that if you did the same thing, you would not have had a good chance of getting infected with the original strain - take a look at this report: https://pubmed.ncbi.nlm.nih.gov/33732749/. Before believing in the fleeting contact claim, I'd like to see something like sequencing data with good contact tracing.

And yes, vaccination is important, but one doesn't need Delta to know that. The breakthrough infections are not so much related to the increased transmissibility of Delta, as its ability to evade the immune response. So Delta's advanatge is partly due to a greater decrease of Alpha's fitness in the presence of previous infections or a vaccine. If one factors that in, the increase in transmissibility over Alpha is estimated to be between 1.1 to 1.4. https://www.researchsquare.com/article/rs-637724/v1

 

[atyy]

For the original COVID, virus trackers would look for an exposure time of about 15 minutes. If you divide that by 1000, you get an infection from a single breath!

There are some indications that it really is that potent.
From a recent MIT article:

Here is another reason I'm skeptical of the "fleeting contact" claim, which comes mainly from Australia. They made the same hypothesis with B.1.617.1 (Kappa). In fact the link given in the MIT article for the "fleeting contact" hypothesis refers to the Kappa variant, not the Delta variant. However, data suggests that the Kappa variant is not much more transmissible than Alpha (about which one would not take "fleeting contact" claims seriously).

https://www.theguardian.com/austral...more-infectious-than-previous-covid-outbreaks
Experts dispute Victoria claim that Kappa variant is more infectious than previous Covid outbreaks

 

[PeroK]

Here is another reason I'm skeptical of the "fleeting contact" claim, which comes mainly from Australia.

Also, there's an estimate that currently 1% of the UK population has the Delta variant. If it could be passed on reliably with fleeting contact, then the numbers would be out of control. Whereas, the numbers appear to be settling down in the UK (to about 50,000 per day). In fact, if anything, the numbers are starting to fall.

We expect, however, that these numbers start going up again now that we have removed almost all the remaining restrictions.

PS only 40,000 new cases today, so definitely on the way down at the moment.