TLS Guy

TLS Guy

Audioholic Slumlord
He stood silently while Trump spewed rhetoric that cost thousands of lives. He had a job to to and failed. His time to speak truth to power was when he was surgeon general...

I was being as nice as I could by stopping at bootlicker. If I see him in person I would say something much worse.
To be fair, there was no data available to make that call until he was well on his way out. The UK did not make that decision until well into January. Germany only made that decision yesterday, after negligently interpreting data and enacting disastrous policies which is, and will, cost them dearly. Most of Europe is a disaster zone as far a the pandemic is concerned.
 
Old Onkyo

Old Onkyo

Audioholic Chief
To be fair, there was no data available to make that call until he was well on his way out. The UK did not make that decision until well into January. Germany only made that decision yesterday, after negligently interpreting data and enacting disastrous policies which is, and will, cost them dearly. Most of Europe is a disaster zone as far a the pandemic is concerned.
He is concerned that 2,000 people a day are dying, but he was strangely quiet when 4,000 people a day were dying....
 
panteragstk

panteragstk

Audioholic Spartan
To be fair, people here were doing what they're going to do regardless of mandate. Especially when there is the "no penalty" for not complying. I'm not going to change what I'm doing, I'm sure the folks that pretend masks are bad will continue to do their thing to.

"Here's a rule with exactly zero consequences for breaking it".
 
cpp

cpp

Audioholic Field Marshall
To be fair, people here were doing what they're going to do regardless of mandate. Especially when there is the "no penalty" for not complying. I'm not going to change what I'm doing, I'm sure the folks that pretend masks are bad will continue to do their thing to.

"Here's a rule with exactly zero consequences for breaking it".
So very true. People are not wearing mask all over the US. NO penalty means they will just keep on doing it. ITs almost like some people just don't freaking care about those around them. Let one of these non mask wearers catch covid and end up in the hospital and you will find one of the biggest believers of mask wearing if they leave the hospital..,
 
Swerd

Swerd

Audioholic Warlord
Gov. Abbot has ordered to end social distance restrictions in Texas – lifting the mask mandate and allowing businesses to open unrestricted.

Below, I'm paraphrasing from an op-ed column in today's (3 March 2021) Washington Post
Why are we ‘bailing out’ Texas’s reckless decisions on covid-19? by Jennifer Rubin

Republicans have complained about proposed federal Covid-19 pandemic aid to states and localities, suggesting that it would amount to a “bailout for blue states”. At the same time, they ignored the widespread economic damage in their own red states. And of course, they never mentioned that many of those states receive more federal aid from the US government than they contribute in federal tax revenue. In essence, they're moochers.

Why should a state whose government behaves in a wholly irresponsible manner, deliberately endangering its own people, be treated the same as responsible states when it comes to direct Covid-19 aid?

Is Abbott using this latest gambit to deflect attention from his responsibility for the recent energy grid disaster? Unfortunately, the rollback in mask and social distancing requirements could increase Texas’s death toll from covid-19, some 42,000 dead, already the third-highest in the country.

Texas also ranks a miserable 45th among states and territories in the percentage of the population that has been vaccinated.

Fauci, Walensky and virtually all other experts have told us that masking and social distancing remain essential both to prevent others from being infected and to tamp down on mutations, which occur when the virus is transmitted. Put simply, Abbott’s recklessness puts all Americans at risk. (This is the umpteeth example of “pro-life” Republican governors showing disdain for human life.)
 
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panteragstk

panteragstk

Audioholic Spartan
Is Abbott using this latest gambit to deflect attention from his responsibility for the recent energy grid disaster? Unfortunately, the rollback in mask and social distancing requirements could increase Texas’s death toll from covid-19, some 42,000 dead, already the third-highest in the country.
That was my first thought. Before anyone makes the connection to his NOT forcing plants to winterize to the fact that people died and lots of property damage occurred, better do something to make all the loud people happy.

Plus, we can't be the biggest if we don't have the biggest death toll.
 
Swerd

Swerd

Audioholic Warlord
Some of you may remember that I have complained about reports that Covid-19 vaccines may be less effective against the various new mutations (variants) of SARS-CoV-2 that have recently appeared. All these reports focused only on neutralizing antibodies (products of B cells) and said nothing about T cell immunity. Antibody studies are easy to do, but studies of T cell immunity are much more difficult and slower to do. Here is some good news on that subject!

Only the effects of the Moderna and Pfizer Covid-19 vaccines were studied in this paper, but it's known that the AstraZeneca (Oxford) and the Johnson & Johnson (Janssen) vaccines also develop potent T cell responses. It's reasonable to believe that they also might not be less effective against the new mutant strains of SARS-CoV-2. That research is probably in progress now.

Two of the authors, Shane Crotty and Alessandro Sette are at the U. of California San Diego and the La Jolla Institute for Immunology. They are well-known T cell experts.

I've pasted in the Summary and the Introduction sections from this article. And I've marked in bold the sentences I think are important for readers. If you don't understand the author's language, just ask. I'll try to answer.

Negligible impact of SARS-CoV-2 variants on CD4+ and CD8+ T cell reactivity in COVID-19 exposed donors and vaccinees
[people who were vaccinated].

AUTHORS
Alison Tarke1,2, John Sidney1, Nils Methot1, Yun Zhang4, Jennifer M. Dan1,3, Benjamin Goodwin1, Paul Rubiro1, Aaron Sutherland1, Ricardo da Silva Antunes1, April Frazier1, Stephen A. Rawlings3, Davey M. Smith3, Bjoern Peters,1,3, Richard H. Scheuermann1,4,5, Daniela Weiskopf1, Shane Crotty 1,3, Alba Grifoni1*, Alessandro Sette

Summary
The emergence of SARS-CoV-2 variants highlighted the need to better understand adaptive immune responses to this virus. It is important to address whether also CD4+ and CD8+ T cell responses are affected, because of the role they play in disease resolution and modulation of COVID-19 disease severity.

Here we performed a comprehensive analysis of SARS-CoV-2-specific CD4+ and CD8+ T cell responses from COVID-19 convalescent subjects recognizing the ancestral strain, compared to variant lineages B.1.1.7, B.1.351, P.1, and CAL.20C as well as recipients of the Moderna (mRNA-1273) or Pfizer/BioNTech (BNT162b2) COVID-19 vaccines. Similarly, we demonstrate that the sequences of the vast majority of SARS-CoV-2 T cell epitopes are not affected by the mutations found in the variants analyzed. Overall, the results demonstrate that CD4+ and CD8+ T cell responses in convalescent COVID-19 subjects or COVID-19 mRNA vaccinees are not substantially affected by mutations found in the SARS-CoV-2 variants.

INTRODUCTION

The emergence of several SARS-CoV-2 variants of concern (VOC) with multiple amino acid replacements has implications for the future control of the COVID-19 pandemic (Davies et al., 2020; Kirby, 2021; Tegally et al., 2020; Volz et al., 2021). Variants of concern include the UK (United Kingdom) variant 501Y.V1 lineage B.1.1.7 (Davies et al., 2020), the SA (South Africa) variant 501Y.V2 lineage B.1.351 (Tegally et al., 2020), the BR (Brazilian) variant 501Y.V3 lineage P.1 (Voloch et al., 2020), and the CA (California) variant CAL.20C lineage B.1.427 (Zhang et al., 2021). The B.1.1.7 variant is associated with increased transmissibility (Rambaut et al., 2020;Washington et al., 2021), and similar epidemiological observations have been reported for the SA and BR variants (Tegally et al., 2020; Voloch et al., 2020).

Mutations of greatest concern are present in the viral Spike (S) protein, and include notable mutations in the receptor binding domain (RBD), N-terminal domain (NTD), and furin cleavage site region. Several of these mutations directly affect ACE2 receptor binding affinity, which may impact infectivity, viral load, or transmissibility (Greaney et al., 2021; Starr et al., 2021; Wang et al., 2021a; Zahradník et al., 2021). Several of these mutations were also noted to be in regions bound by neutralizing antibodies, so it is crucial to address to what extent the mutations associated with the variants impact immunity induced by either SARS-CoV-2 infection or vaccination.

Several reports address the effect of these mutations on antibody binding and function, by either monoclonal or polyclonal antibody responses, and considering both natural infection or vaccination
(Edara et al., 2021; Greaney et al., 2021; Muik et al., 2021; Shen et al., 2021; Skelly et al., 2020; Stamatatos et al., 2021; Supasa et al., 2021; Wang et al., 2021a; Wang et al., 2021b; Wibmer et al., 2021; Wu et al., 2021). In general, the impact of the B.1.1.7 variant mutations on neutralizing antibody titers is moderate (Emary et al., 2021; Muik et al., 2021; Shen et al., 2021; Skelly et al., 2020; Supasa et al., 2021; Wu et al., 2021). In contrast, the mutations associated with the B.1.351 and P.1.variants are associated with more pronounced loss of neutralizing capacity (Cele et al., 2021; Skelly et al., 2020; Wang et al., 2021a; Wibmer et al., 2021; Wu et al., 2021). Concerning vaccination responses, the AstraZeneca ChAdOx1 vaccine has been associated with a partial loss of neutralizing antibody activity against B.1.1.7 (Skelly et al., 2020), and a large loss of neutralizing activity against B.1.351 (Voysey et al., 2021). Consistent with these reports, ChAdOx1 maintains efficacy against B.1.1.7 (Emary et al., 2021; Hall et al., 2021), but has a major loss in efficacy against mild COVID-19 with the B.1.351 variant (Voysey et al., 2021). Current epidemiological evidence is that the BNT162b2 Pfizer/ BioNTechCOVID-19 vaccine retains its efficacy against B.1.1.7 in the UK and in reports from Israel (Amit et al., 2021). Novavax (NVX-CoV2373) has reported differential protective immunity against the parental strain, B.1.1.7, and B.1.351in vaccine clinical trials (96%, 86%, and 60%) (Novavax Inc., 2021), whereas the Janssen Ad26.COV2.S1-dose COVID-19 vaccine, which elicits lower neutralizing antibody titers (Sadoff et al., 2021), has relatively similar protection for moderate COVID-19 against both the ancestral strain and B.1.351 (72% and 64%) (FDA, 2021a, b).

Several lines of evidence suggest that CD4+ and CD8+ T cell responses play important roles in resolution of SARS-CoV-2 infection and COVID-19 (Sette and Crotty, 2021), including modulating disease severity in humans (Rydyznski Moderbacher et al., 2020; Tan et al., 2021) and reducing viral loads in non-human primates (Munoz-Fontela et al., 2020). Further, persons with agammaglobulinemia or pharmaceutical depletion of B cells generally experience an uncomplicated COVID-19 disease course (Sette and Crotty, 2021; Soresina et al., 2020). Robust CD4+ and CD8+ T cell memory is induced after COVID-19 (Breton et al., 2021; Dan et al., 2021; Peng et al., 2020; Wang et al., 2021b), and multiple COVID-19 vaccines elicit CD4+ and CD8+ T cell responses (Baden et al., 2021; Dowd et al., 2020; Keech et al., 2020; Sadoff et al., 2021; Voysey et al., 2021). It is therefore key to address the potential impact of SARS-CoV-2 variants mutations on T cell reactivity; however, little data is currently available on this topic (Skelly et al., 2020).

Here, we take a combined experimental and bioinformatics approach to address how SARS-CoV-2 variants of concern impact T cell reactivity. We directly assess T cell responses from persons recovered from COVID-19 obtained before the emergence of the variants, and from persons who were recently vaccinated with either the Moderna mRNA-1273 or Pfizer/BioNTechBNT162b2 vaccines, for their capacity to recognize peptides derived from the ancestral reference sequence and the B.1.1.7, B1.351, P.1and the CAL.20C variants. Bioinformatic analyses were used to predict the impact of mutations in the various variants with sets of previously reported CD4+ and CD8+ T cell epitopes derived from the ancestral reference sequence (Tarke et al., 2021).
 
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M

Mr._Clark

Audioholic Chief
The previous surgeon general is probably right. The UK elected early on to space vaccine doses by 90 days, and not follow manufacturers recommendation. Germany has now adopted the same policy.

Models show this is the fastest way to reduce deaths and hospitalizations. The AstraZeneca trial tested 30, 60 and 90 day spacing intervals, and the best immunity was a 90 day spacing. So the UK took the risk of applying the data to the Pfizer vaccine as well.

Over 30% of the UK has received at least one dose of one or other of those vaccines, mostly the AstraZeneca vaccine. The results have been spectacular, with mortality in the over 80 group down 70%, and over 65 by 65%. The results are exceeding the models.

You can see deaths are falling faster then the models are predicting. Also the more infectious and virulent UK variant is dominant in the UK now by a big margin.
As of Monday 96% if the UK population over 70 have received one dose. Hospitalizations are down 80%.

56% of the over 80s have a good antibody titers now. 25% of the UK population over 16 years of age now show antibodies. This is a combination of passed infection and vaccination.

This is excellent news for us here in the US also. I strongly believe we should also go to a 90 day vaccine spacing. We should also go ahead and approve the Oxford AstraZeneca vaccine in the US and not delay approval to April or May. Clearly is is a highly effective and safe vaccine.
I've wondered if a hybrid approach might make sense. e.g. two jabs for those 65 and older, one for younger people.

Either way, the reduction in deaths is certainly good news.

The reports coming out of Israel are also very promising.

 
M

Mr._Clark

Audioholic Chief
Some of you may remember that I have complained about reports that Covid-19 vaccines may be less effective against the various new mutations (variants) of SARS-CoV-2 that have recently appeared. All these reports focused only on neutralizing antibodies (products of B cells) and said nothing about T cell immunity. Antibody studies are easy to do, but studies of T cell immunity are much more difficult and slower to do. Here is some good news on that subject!

Only the effects of the Moderna and Pfizer Covid-19 vaccines were studied in this paper, but it's known that the AstraZeneca (Oxford) and the Johnson & Johnson (Janssen) vaccines also develop potent T cell responses. It's reasonable to believe that they also might not be less effective against the new mutant strains of SARS-CoV-2. That research is probably in progress now.

Two of the authors, Shane Crotty and Alessandro Sette are at the U. of California San Diego and the La Jolla Institute for Immunology. They are well-known T cell experts.

I've pasted in the Summary and the Introduction sections from this article. And I've marked in bold the sentences I think are important for readers. If you don't understand the author's language, just ask. I'll try to answer.

Negligible impact of SARS-CoV-2 variants on CD4+ and CD8+ T cell reactivity in COVID-19 exposed donors and vaccinees [people who were vaccinated].

AUTHORS
Alison Tarke1,2, John Sidney1, Nils Methot1, Yun Zhang4, Jennifer M. Dan1,3, Benjamin Goodwin1, Paul Rubiro1, Aaron Sutherland1, Ricardo da Silva Antunes1, April Frazier1, Stephen A. Rawlings3, Davey M. Smith3, Bjoern Peters,1,3, Richard H. Scheuermann1,4,5, Daniela Weiskopf1, Shane Crotty 1,3, Alba Grifoni1*, Alessandro Sette

Summary
The emergence of SARS-CoV-2 variants highlighted the need to better understand adaptive immune responses to this virus. It is important to address whether also CD4+ and CD8+ T cell responses are affected, because of the role they play in disease resolution and modulation of COVID-19 disease severity.

Here we performed a comprehensive analysis of SARS-CoV-2-specific CD4+ and CD8+ T cell responses from COVID-19 convalescent subjects recognizing the ancestral strain, compared to variant lineages B.1.1.7, B.1.351, P.1, and CAL.20C as well as recipients of the Moderna (mRNA-1273) or Pfizer/BioNTech (BNT162b2) COVID-19 vaccines. Similarly, we demonstrate that the sequences of the vast majority of SARS-CoV-2 T cell epitopes are not affected by the mutations found in the variants analyzed. Overall, the results demonstrate that CD4+ and CD8+ T cell responses in convalescent COVID-19 subjects or COVID-19 mRNA vaccinees are not substantially affected by mutations found in the SARS-CoV-2 variants.

INTRODUCTION

The emergence of several SARS-CoV-2 variants of concern (VOC) with multiple amino acid replacements has implications for the future control of the COVID-19 pandemic (Davies et al., 2020; Kirby, 2021; Tegally et al., 2020; Volz et al., 2021). Variants of concern include the UK (United Kingdom) variant 501Y.V1 lineage B.1.1.7 (Davies et al., 2020), the SA (South Africa) variant 501Y.V2 lineage B.1.351 (Tegally et al., 2020), the BR (Brazilian) variant 501Y.V3 lineage P.1 (Voloch et al., 2020), and the CA (California) variant CAL.20C lineage B.1.427 (Zhang et al., 2021). The B.1.1.7 variant is associated with increased transmissibility (Rambaut et al., 2020;Washington et al., 2021), and similar epidemiological observations have been reported for the SA and BR variants (Tegally et al., 2020; Voloch et al., 2020).

Mutations of greatest concern are present in the viral Spike (S) protein, and include notable mutations in the receptor binding domain (RBD), N-terminal domain (NTD), and furin cleavage site region. Several of these mutations directly affect ACE2 receptor binding affinity, which may impact infectivity, viral load, or transmissibility (Greaney et al., 2021; Starr et al., 2021; Wang et al., 2021a; Zahradník et al., 2021). Several of these mutations were also noted to be in regions bound by neutralizing antibodies, so it is crucial to address to what extent the mutations associated with the variants impact immunity induced by either SARS-CoV-2 infection or vaccination.

Several reports address the effect of these mutations on antibody binding and function, by either monoclonal or polyclonal antibody responses, and considering both natural infection or vaccination
(Edara et al., 2021; Greaney et al., 2021; Muik et al., 2021; Shen et al., 2021; Skelly et al., 2020; Stamatatos et al., 2021; Supasa et al., 2021; Wang et al., 2021a; Wang et al., 2021b; Wibmer et al., 2021; Wu et al., 2021). In general, the impact of the B.1.1.7 variant mutations on neutralizing antibody titers is moderate (Emary et al., 2021; Muik et al., 2021; Shen et al., 2021; Skelly et al., 2020; Supasa et al., 2021; Wu et al., 2021). In contrast, the mutations associated with the B.1.351 and P.1.variants are associated with more pronounced loss of neutralizing capacity (Cele et al., 2021; Skelly et al., 2020; Wang et al., 2021a; Wibmer et al., 2021; Wu et al., 2021). Concerning vaccination responses, the AstraZeneca ChAdOx1 vaccine has been associated with a partial loss of neutralizing antibody activity against B.1.1.7 (Skelly et al., 2020), and a large loss of neutralizing activity against B.1.351 (Voysey et al., 2021). Consistent with these reports, ChAdOx1 maintains efficacy against B.1.1.7 (Emary et al., 2021; Hall et al., 2021), but has a major loss in efficacy against mild COVID-19 with the B.1.351 variant (Voysey et al., 2021). Current epidemiological evidence is that the BNT162b2 Pfizer/ BioNTechCOVID-19 vaccine retains its efficacy against B.1.1.7 in the UK and in reports from Israel (Amit et al., 2021). Novavax (NVX-CoV2373) has reported differential protective immunity against the parental strain, B.1.1.7, and B.1.351in vaccine clinical trials (96%, 86%, and 60%) (Novavax Inc., 2021), whereas the Janssen Ad26.COV2.S1-dose COVID-19 vaccine, which elicits lower neutralizing antibody titers (Sadoff et al., 2021), has relatively similar protection for moderate COVID-19 against both the ancestral strain and B.1.351 (72% and 64%) (FDA, 2021a, b).

Several lines of evidence suggest that CD4+ and CD8+ T cell responses play important roles in resolution of SARS-CoV-2 infection and COVID-19 (Sette and Crotty, 2021), including modulating disease severity in humans (Rydyznski Moderbacher et al., 2020; Tan et al., 2021) and reducing viral loads in non-human primates (Munoz-Fontela et al., 2020). Further, persons with agammaglobulinemia or pharmaceutical depletion of B cells generally experience an uncomplicated COVID-19 disease course (Sette and Crotty, 2021; Soresina et al., 2020). Robust CD4+ and CD8+ T cell memory is induced after COVID-19 (Breton et al., 2021; Dan et al., 2021; Peng et al., 2020; Wang et al., 2021b), and multiple COVID-19 vaccines elicit CD4+ and CD8+ T cell responses (Baden et al., 2021; Dowd et al., 2020; Keech et al., 2020; Sadoff et al., 2021; Voysey et al., 2021). It is therefore key to address the potential impact of SARS-CoV-2 variants mutations on T cell reactivity; however, little data is currently available on this topic (Skelly et al., 2020).

Here, we take a combined experimental and bioinformatics approach to address how SARS-CoV-2 variants of concern impact T cell reactivity. We directly assess T cell responses from persons recovered from COVID-19 obtained before the emergence of the variants, and from persons who were recently vaccinated with either the Moderna mRNA-1273 or Pfizer/BioNTechBNT162b2 vaccines, for their capacity to recognize peptides derived from the ancestral reference sequence and the B.1.1.7, B1.351, P.1and the CAL.20C variants. Bioinformatic analyses were used to predict the impact of mutations in the various variants with sets of previously reported CD4+ and CD8+ T cell epitopes derived from the ancestral reference sequence (Tarke et al., 2021).
This makes me wonder what is driving the spike in cases in Manaus Brazil. Perhaps it's not true that the Brazil variant "gained the ability to infect some people who had immunity from previous bouts of Covid-19" as reported by the NYT.

>>>Now three studies offer a sobering history of P.1’s meteoric rise in the Amazonian city of Manaus. It most likely arose there in November and then fueled a record-breaking spike of coronavirus cases. It came to dominate the city partly because of an increased contagiousness, the research found. But it also gained the ability to infect some people who had immunity from previous bouts of Covid-19. And laboratory experiments suggest that P.1 could weaken the protective effect of a Chinese vaccine now in use in Brazil.<<<


 
TLS Guy

TLS Guy

Audioholic Slumlord
I've wondered if a hybrid approach might make sense. e.g. two jabs for those 65 and older, one for younger people.

Either way, the reduction in deaths is certainly good news.

The reports coming out of Israel are also very promising.

The UK data shows that the immunity is barely altered by advancing age. Both Pfizer and especially the Oxford vaccine, are showing excellent results in the field. The Oxford vaccine is outperforming the data from the trial by a significant margin. It is in fact marginally, but not significantly better than the Pfizer in the field. The bottom line is that they are both equally effective. The dominant strain is the UK variant from Kent. The vaccines seem equally effective against that variant.
The UK is now doing genome decoding on 25% of positive tests.
To be honest, I very surprised at how effective the UK response has been from the basic science and medical communities.
If the Liverpool team come through with their universal Corona virus vaccine, I think we really would be home free. Corona viruses are currently the most worrisome for making the transition from animals to humans. So that vaccine would greatly reduce the risk of a another Corona virus pandemic.
 
S

Speedskater

Audioholic Chief
Wednesday morning Dr. Fauci had a simplified chart showing Pfizer not doing much at 21 days, but at 28 days it popped way up and then leveled off at 35 days.
 
cpp

cpp

Audioholic Field Marshall
I was speaking to my brother this morning on COVID since his wife had it back in Sept 2020 and stayed in bed 3 weeks, aches, alternating fever, but he never got it. He mentioned that our sister who works in a hospital area, where a co worker had covid ( caught it from a patient it the ER) and my sister never got it. My brother, said I wonder if its our blood type, I asked what is his BT, he said 0+. So I texted our sister and asked her BT< she said, 0+

So I did some checking : the infectious disease center Noted in Jan 2021

"The O- blood group had a 2.1% chance of getting SARS-CoV-2 infection (95% CI, 1.8-2.3%), the lowest unadjusted probability of all blood groups. The aRR for SARS-CoV-2 infection in the O blood group was 0.88 (95% CI, 0.84-0.92) vs all other blood groups, and the ARD was -3.9 per 1,000 (95% CI, -5.4 to -2.5).Jan 13, 2021 "

OF course this doesn't mean you will not catch it, as nothing is 100%. But interesting.
 
Swerd

Swerd

Audioholic Warlord
I was speaking to my brother this morning on COVID since his wife had it back in Sept 2020 and stayed in bed 3 weeks, aches, alternating fever, but he never got it. He mentioned that our sister who works in a hospital area, where a co worker had covid ( caught it from a patient it the ER) and my sister never got it. My brother, said I wonder if its our blood type, I asked what is his BT, he said 0+. So I texted our sister and asked her BT< she said, 0+

So I did some checking : the infectious disease center Noted in Jan 2021

"The O- blood group had a 2.1% chance of getting SARS-CoV-2 infection (95% CI, 1.8-2.3%), the lowest unadjusted probability of all blood groups. The aRR for SARS-CoV-2 infection in the O blood group was 0.88 (95% CI, 0.84-0.92) vs all other blood groups, and the ARD was -3.9 per 1,000 (95% CI, -5.4 to -2.5).Jan 13, 2021 "

OF course this doesn't mean you will not catch it, as nothing is 100%. But interesting.
Interesting… But I'd still get vaccinated.
 
Swerd

Swerd

Audioholic Warlord
Today, I got my first vaccine dose, a shot in the arm with the Moderna mRNA vaccine. I'm very glad as I write this, even if my arm is beginning to get sore. I'll be glad to take it easy tomorrow.

It took a road trip to get this. I easily got an appointment in a small town, Weldon, in North Carolina. I wondered if being from another state would be a problem. I live in Maryland, 211 miles away. Clearly, it was not a problem. There were also other people there, among the 25 people in my group, from Virginia, or who were noticeably younger than I am.

When asked about eligibility, the nurse there said that Halifax County, NC had already vaccinated all it's residents 65 and older, as well as those whose jobs or medical conditions required vaccination. Now they were open to all comers.

I'm very glad I took the 8½ hour, 420 mile, round trip, including the vaccination (less than an hour) and a side trip to Ralph's BBQ for some take-out pulled pork. This also a poor reflection on the chaos I've experienced trying to get vaccinated in my own state. I've been completely frustrated at getting an appointment for vaccination. So frustrated, that I took a road trip.

If any of you want details about where I got vaccinated, and how I signed up, send me a PM.
 
M

Mr._Clark

Audioholic Chief
This is annoying. Just what we need, more vaccine misinformation.

>>>The New York Times reported Monday that officials in the Phillippines have now balked at the safety and efficacy of the Chinese Sinovac vaccine because of lack of any real data. In response, Chinese state media has started a campaign against the American vaccines, questioning the safety of the Pfizer and Moderna shots and distributed online videos.<<<

 
Verdinut

Verdinut

Audioholic Ninja
This is annoying. Just what we need, more vaccine misinformation.

>>>The New York Times reported Monday that officials in the Phillippines have now balked at the safety and efficacy of the Chinese Sinovac vaccine because of lack of any real data. In response, Chinese state media has started a campaign against the American vaccines, questioning the safety of the Pfizer and Moderna shots and distributed online videos.<<<

People won't stop misinforming. It's even more stupid when human lives are involved with the World's worse pandemic.
 
M

Mr._Clark

Audioholic Chief
In addition to discussion of the E406W mutation, this article has an interesting discussion of mutations in a persistently infected immunocompromised person. Apparently there were numerous mutations circulating in the patient and the mutations swapped mutations (I believe that is what is meant by "hitchiking"?)(paging @Swerd or @TLS Guy)

>>>Structural analyses and viral-escape selections led Regeneron to posit that no single amino acid mutation could escape both antibodies in the cocktail (11, 12), but our complete maps identify E406W as a cocktail escape mutation. E406W affects the REGN-COV2 antibodies in a relatively specific way and does not grossly perturb the function of the RBD, given that it only mildly reduces neutralization by LY-CoV016 (Fig. 1C) and the titers of spike-pseudotyped lentiviral particles (fig. S3F). . . . Notably, E406W is not accessible by a single-nucleotide change, which may explain why it was not identified by the Regeneron cocktail selections despite being relatively well tolerated for RBD folding and ACE2 affinity. <<<


>>>Notably, the mutations did not all sweep to fixation after antibody treatment; instead, there were competing rises and falls (Fig. 2C). This pattern has been observed in the adaptive within-host evolution of other viruses (17, 18) and can arise from genetic hitchhiking and competition among viral lineages. Both these forces appear to be at play in the persistently infected patient (Fig. 2C and fig. S4C): E484A (not an escape mutation in our maps) hitchhikes with F486I (which escapes REGN10933) after treatment, and the viral lineage carrying N440D and Q493K (which escape REGN10987 and REGN10933, respectively) competes first with the REGN10933 escape-mutant Y489H and then with the lineage carrying E484A and F486I and the Q493K lineage.<<<

 
Swerd

Swerd

Audioholic Warlord
In addition to discussion of the E406W mutation, this article has an interesting discussion of mutations in a persistently infected immunocompromised person. Apparently there were numerous mutations circulating in the patient and the mutations swapped mutations (I believe that is what is meant by "hitchiking"?)(paging @Swerd or @TLS Guy)
I've heard 'hitchhiking' used in a variety of ways for viruses. I don't think there is one and only one definition. I take it to mean that viruses can use a wide variety of unexpected methods to propagate themselves. Viruses are opportunists who haven't read the standard biology textbooks. Example:
>>>Structural analyses and viral-escape selections led Regeneron to posit that no single amino acid mutation could escape both antibodies in the cocktail (11, 12), but our complete maps identify E406W as a cocktail escape mutation. E406W affects the REGN-COV2 antibodies in a relatively specific way and does not grossly perturb the function of the RBD, given that it only mildly reduces neutralization by LY-CoV016 (Fig. 1C) and the titers of spike-pseudotyped lentiviral particles (fig. S3F). . . . Notably, E406W is not accessible by a single-nucleotide change, which may explain why it was not identified by the Regeneron cocktail selections despite being relatively well tolerated for RBD folding and ACE2 affinity. <<<

>>>Notably, the mutations did not all sweep to fixation after antibody treatment; instead, there were competing rises and falls (Fig. 2C). This pattern has been observed in the adaptive within-host evolution of other viruses (17, 18) and can arise from genetic hitchhiking and competition among viral lineages. Both these forces appear to be at play in the persistently infected patient (Fig. 2C and fig. S4C): E484A (not an escape mutation in our maps) hitchhikes with F486I (which escapes REGN10933) after treatment, and the viral lineage carrying N440D and Q493K (which escape REGN10987 and REGN10933, respectively) competes first with the REGN10933 escape-mutant Y489H and then with the lineage carrying E484A and F486I and the Q493K lineage.<<<

This article shows the very limited usefulness of monoclonal antibody therapy to treat widespread pandemics of SARS-CoV-2, or other viruses. The rapid appearance of mutations quickly render the monoclonal antibodies useless. Vaccination is far better.
 
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