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    Heart Inflammation Risk Higher From Moderna Vaccine Than COVID-19 for Those Under 40: Study


    Risks of myocarditis, pericarditis, and cardiac arrhythmias associated with COVID-19 vaccination or SARS-CoV-2 infection

    Risks of myocarditis, pericarditis, and cardiac arrhythmias associated with COVID-19 vaccination or SARS-CoV-2 infection - Nature Medicine
    A self-controlled case series using individual-patient-level data from over 38 million people aged 16 years and over, reveals an increased risk of myocarditis…
    www.nature.com


    Abstract

    Although myocarditis and pericarditis were not observed as adverse events in coronavirus disease 2019 (COVID-19) vaccine trials, there have been numerous reports of suspected cases following vaccination in the general population. We undertook a self-controlled case series study of people aged 16 or older vaccinated for COVID-19 in England between 1 December 2020 and 24 August 2021 to investigate hospital admission or death from myocarditis, pericarditis and cardiac arrhythmias in the 1–28 days following adenovirus (ChAdOx1, n = 20,615,911) or messenger RNA-based (BNT162b2, n = 16,993,389; mRNA-1273, n = 1,006,191) vaccines or a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive test (n = 3,028,867). We found increased risks of myocarditis associated with the first dose of ChAdOx1 and BNT162b2 vaccines and the first and second doses of the mRNA-1273 vaccine over the 1–28 days postvaccination period, and after a SARS-CoV-2 positive test. We estimated an extra two (95% confidence interval (CI) 0, 3), one (95% CI 0, 2) and six (95% CI 2, 8) myocarditis events per 1 million people vaccinated with ChAdOx1, BNT162b2 and mRNA-1273, respectively, in the 28 days following a first dose and an extra ten (95% CI 7, 11) myocarditis events per 1 million vaccinated in the 28 days after a second dose of mRNA-1273. This compares with an extra 40 (95% CI 38, 41) myocarditis events per 1 million patients in the 28 days following a SARS-CoV-2 positive test. We also observed increased risks of pericarditis and cardiac arrhythmias following a positive SARS-CoV-2 test. Similar associations were not observed with any of the COVID-19 vaccines, apart from an increased risk of arrhythmia following a second dose of mRNA-1273. Subgroup analyses by age showed the increased risk of myocarditis associated with the two mRNA vaccines was present only in those younger than 40.


    And now this

    Small Myocarditis Risk Now Seen for Adenovirus-based COVID-19 Vaccine

    Small Myocarditis Risk Now Seen for Adenovirus COVID Vaccine
    The large-scale analysis suggests the risk is low with the adenovirus vaccine and pales in comparison to that following a positive SARS-CoV-2 test.
    www.medscape.com

    Shark antibody-like proteins neutralize COVID-19 virus, help prepare for future coronaviruses


    Shark antibody-like proteins neutralize COVID-19 virus, help prepare for future coronaviruses
    Small, unique antibody-like proteins known as VNARs—derived from the immune systems of sharks—can prevent the virus that causes COVID-19, its variants, and…
    medicalxpress.com


    Small, unique antibody-like proteins known as VNARs—derived from the immune systems of sharks—can prevent the virus that causes COVID-19, its variants, and related coronaviruses from infecting human cells, according to a new study published Dec. 16.



    The new VNARs will not be immediately available as a treatment in people, but they can help prepare for future coronavirus outbreaks. The shark VNARs were able to neutralize WIV1-CoV, a coronavirus that is capable of infecting human cells but currently circulates only in bats, where SARS-CoV-2, the virus that causes COVID-19, likely originated.


    Developing treatments for such animal-borne viruses ahead of time can prove useful if those viruses make the jump to people.


    "The big issue is there are a number of coronaviruses that are poised for emergence in humans," says Aaron LeBeau, a University of Wisconsin-Madison professor of pathology who helped lead the study. "What we're doing is preparing an arsenal of shark VNAR therapeutics that could be used down the road for future SARS outbreaks. It's a kind of insurance against the future."


    LeBeau and his lab in the School of Medicine and Public Health collaborated with researchers at the University of Minnesota and Elasmogen, a biomedical company in Scotland that is developing therapeutic VNARs. The team published its findings in Nature Communications.


    The anti-SARS-CoV-2 VNARs were isolated from Elasmogen's large synthetic VNAR libraries. One-tenth the size of human antibodies, the shark VNARs can bind to infectious proteins in unique ways that bolster their ability to halt infection.


    "These small antibody-like proteins can get into nooks and crannies that human antibodies cannot access," says LeBeau. "They can form these very unique geometries. This allows them to recognize structures in proteins that our human antibodies cannot."


    The researchers tested the shark VNARs against both infectious SARS-CoV-2 and a "pseudotype," a version of the virus that can't replicate in cells. They identified three candidate VNARs from a pool of billions that effectively stopped the virus from infecting human cells. The three shark VNARs were also effective against SARS-CoV-1, which caused the first SARS outbreak in 2003

    One VNAR, named 3B4, attached strongly to a groove on the viral spike protein near where the virus binds to human cells and appears to block this attachment process. This groove is very similar among genetically diverse coronaviruses, which even allows 3B4 to effectively neutralize the MERS virus, a distant cousin of the SARS viruses.


    The ability to bind such conserved regions across diverse coronaviruses makes 3B4 an attractive candidate to fight viruses that have yet to infect people.


    The 3B4 binding site is also not changed in prominent variations of SARS-CoV-2, such as the delta variant. This research was conducted before the omicron variant was discovered, but initial models suggest the VNAR would remain effective against this new version, LeBeau says.


    The second-most-powerful shark VNAR, 2C02, seems to lock the spike protein into an inactive form. However, this VNAR's binding site is altered in some SARS-CoV-2 variants, which likely decreases its potency.


    "What is exciting is that these new potential drug molecules against SARS-CoV-2 differ in their mechanism of action compared to other biologics and antibodies targeting this virus," says Caroline Barelle, CEO of Elasmogen. "It is another great example of how Elasmogen can effectively deliver potent therapeutic molecules."


    Future therapies would likely include a cocktail of multiple shark VNARs to maximize their effectiveness against diverse and mutating viruses. This new class of drug is cheaper and easier to manufacture than human antibodies, and can be delivered into the body through various routes, but has yet to be tested in humans. LeBeau is also studying the ability of shark VNARs to help in the treatment and diagnosis of cancers.


    Vaccines form the bedrock of protection against SARS-CoV-2 and future coronaviruses. But some people, such as those with compromised immune systems, do not respond as well to vaccination and may benefit from other treatments like antibodies—which makes developing these treatments an ongoing priority.


    Explore further


    Scientists identify new antibody for COVID-19 and variants

    More information: Obinna C. Ubah et al, Mechanisms of SARS-CoV-2 neutralization by shark variable new antigen receptors elucidated through X-ray crystallography, Nature Communications (2021). DOI: 10.1038/s41467-021-27611-y

    Journal information: Nature Communications

    That led them to niclosamide. It's an anti-viral drug used around the world for 50 years to treat tapeworm and was planned for use during the 2003 SARS outbreak. Research suggests it could also slow down COVID-19.


    Niclosamide, an old drug being put to new use in COVID-19 patients


    https://www.wcvb.com/article/niclosamide-drug-being-used-in-covid-19-patients/36366791


    While there is currently a significant focus on vaccination, the search for effective COVID-19 treatments continues. It's a question New England researchers are working on.


    Dr. Harry Selker and his team at the Institute for Clinical Research and Health Policy Studies at Tufts Medical Center are taking a unique approach.


    "When COVID first came here, we realized we had to repurpose drugs that were already known to be safe," Selker said.


    That led them to niclosamide. It's an anti-viral drug used around the world for 50 years to treat tapeworm and was planned for use during the 2003 SARS outbreak. Research suggests it could also slow down COVID-19.


    "It turns out the way the virus attacks cells, it gets brought into the cell in these little vacuoles and then it starts to reproduce. It turns out that niclosamide makes that acidic and they can't really reproduce," Selker said.


    Now, Selker's team at Tufts Medical Center and teams at five other New England hospitals are testing how well it works.


    They're enrolling in a clinical trial looking for people newly diagnosed with COVID-19. It's all done from home. The research team uses telehealth to connect with participants after they receive a kit to enable them to take their temperature, pulse and oxygen saturation.


    Researchers are also asking for stool samples because the gut may have more to do with COVID-19 than we realize.


    "There's a lot of reservoir of the infection in your gut. We're optimistic that we'll be able to clear the gut with this drug, as well as treating the overall disease," Selker said.


    The trial is about half-enrolled. The ultimate goal is finding another treatment option for COVID-19 patients.


    "If you have a drug like niclosamide, which by the way costs 24 cents as a tablet, you can treat the disease when it comes here. So as soon as someone is symptomatic or tests positive, you can treat them and that will always be necessary no matter how many people are vaccinated," Selker said.


    Previous research suggests niclosamide could be 25-30% more effective than remdesivir, one of the few treatments available for COVID-19 patients. He hopes to have results from this study in the next few months.

    Quote from Fm1

    8.8 billion doses of vaccine administered to 4.6 billion people, 56% of the world's population and Covid still rages and mutates. Very telling!

    Would you happen to describe todays world assuming there were no vaccines at all since the virus outbreak in Nov 2019? (pls try to find a different solution than arguing IVM is the holy gral and would have ended this shortly after the wolrd became aware...).

    Quote from zorud

    Would you happen to describe todays world assuming there were no vaccines at all since the virus outbreak in Nov 2019? (pls try to find a different solution than arguing IVM is the holy gral and would have ended this shortly after the wolrd became aware...).

    I don't have to we all live in the present and vaccines are a reality. You can ponder what ifs.

    There were strong indications right from the very start of the COVID pandemic that any vaccine would have a very short shelf life against such a rapidly mutating pathogen. Whilst I was finishing several other papers on visual retinal neuroscience, we noticed that when rod photo receptors were exposed to cholera toxin which is a highly complex ADP-ribosylating toxin, flash responses were blocked which was accompanied by depolarization of the rod membrane potential. This action could be blocked by the Vitamin B component nicotinamide which is a reaction product of ADP-ribosylation. Further studies showed a positive effect both blocking and reversing (by the law of mass action) the effects of botulinum toxin (mammalian neuromuscular junction), pertussis toxin and cholera toxin in mammalian ileal sacs. This was such a clear effect so in 1989 we patented the use of ADP-ribosyltransferase inhibitors to treat cholera, whooping cough (pertussis), and other mainly third world diseases including diphtheria. Their cellular targets are a class of signal-transducing proteins, the GTP-binding or G-proteins. Whilst there is no direct evidence that viral toxins act in the same way, the question arises whether inhibitors of ADP-ribosylation including adenine and hypoxanthine its metabolite could be effective in blocking the intracellular actions of their toxins. Simply elevating adenine levels in the diet, or indeed raising dietary nicotinamide could well be effective as a simple anti-viral treatment. This patent has expired now and all the data is now PD, as usual Pfizer were not interested saying at the time 'its a third world problem etc etc no money in it.' Sildenafil came out at the same time giving them the Viagra windfall. Still, a Canadian professor now has a research team investigating the tertiary structure of both endogenous G-protein targeting mono ADP-ribosyltranferases and also poly-ADPR's involved in DNA repair mechanisms expressed in the cell nucleus.

    Quote from THHuxleynew

    That surge will go way up - 500K/day as minimum.

    Dilettante again. Just reproducing FM/R/B/H FUD. RSA is already near or over the peak! Hospitalizations this week will be lower than lasts weeks or just about the same level.


    A virus always enters a new reservoir. If it has been filled then its end of game. UK with 50% recovered and now facing a virus that only will affect 1/10 of the rest (9 out of 10 cases nobody will notice) has about 2.9 million vulnerable. So a maximum will be below 200'000 for sure. May be UK will see more ADE due to the Oxford crap vaccine as we now see with Delta already. So this is the real danger.

    Quote from Wyttenbach

    Dilettante again. Just reproducing FM/R/B/H FUD. RSA is already near or over the peak! Hospitalizations this week will be lower than lasts weeks or just about the same level.

    It takes 1 week for hospitlisation from infection.


    Omicron is currently (whole country) only 30% of infections. I never said there would be a country-wide increase immediately.


    That is why I stated a peak in deaths some time in the future (no sooner than 3 weeks - probably 4 or more weeks).


    However you can clearly now see the "omicron effect" on London hospitalisations, where omicron is now the dominant infection, one week or more ahead of the rest of the country (but not Scotland - where it is also now dominant).


    https://coronavirus.data.gov.uk/details/healthcare?areaType=nhsregion&areaName=London


    Hospitalisations have been clearly going up clearly since 3rd December.

    Quote from Wyttenbach

    UK with 50% recovered and now facing a virus that only will affect 1/10 of the rest (9 out of 10 cases nobody will notice) has about 2.9 million vulnerable. So a maximum will be below 200'000 for sure.

    Unfortunately it may be difficult to resolve this directly. We are likely to run out of tests: I'm not sure whether that will be before or after 200K.


    Today's count was 93,000. We will watch and see what happens.


    We can however extrapolate numbers from the ONS survey. The latest week, ending 9 December, has 1 in 60 infections (no change from previous week). That will change. If numbers get very high it will be much more reliable. But it will be larger than case numbers since many people with omicron will not test.


    The figure of interest - in any case - is hospital admissions.


    You think it will stay the same or go down. I think it will go up - a lot.

    Is it hospital admissions or ICU patients that's really a signal. Just my opinion but the UK should peak around Christmas and then a large drop by first week in January about the time the us will be peaking and a sudden drop by the end of month. The surges seem to peak around 20% saturation of the population and drops suddenly. I have no explanation for that. I think we have seen the worst Covid can throw at us and that was delta.

    Quote from Wyttenbach

    Latest UK report for week 50:: https://assets.publishing.serv…llance-report-week-50.pdf


    I compared week 45 and 50. The booster deliver about 30% added protection so far. But more - still just a few - younger people die. Also we see no change at all in some age groups e.g. 50..60 and 60..70. Here boosters show zero effect at all.

    Rather than correct you: let me ask you to make transparent your calculations:


    what would be an effect of boosters in a given age group?


    You need to combine:


    • When did (how many of) that age group get vaccinated
    • what was the covid rate in that age group, how much did it change.
    • Don't for get 7 days from date of jab to infection, and 14 days from infection to death.


    Lay it all out carefully with all the numbers. I will be interested (and a bit surprised) if you manage to do this.


    THH

    Quote from Fm1

    Is it hospital admissions or ICU patients that's really a signal. Just my opinion but the UK should peak around Christmas and then a large drop by first week in January about the time the us will be peaking and a sudden drop by the end of month. The surges seem to peak around 20% saturation of the population and drops suddenly. I have no explanation for that. I think we have seen the worst Covid can throw at us and that was delta.

    I have little idea how bad omicron will be, except that given known infection rate any peak will be fairly fast.


    • It will be better than delta in terms of total death - we hope and mostly expect - because of much higher overall vaccination levels and more prior infection.
    • It will be probably be worse than delta in terms of hospital demand due to faster and larger peak.
    Quote from Fm1

    8.8 billion doses of vaccine administered to 4.6 billion people, 56% of the world's population and Covid still rages and mutates. Very telling!

    AGAIN you post this nonsense. Nearly every person hospitalized with COVID is not vaccinated. Breakthrough cases are rare, less contagious, seldom serious enough to be hospitalized, and they almost never result in death. If 100% of the world's population were vaccinated, the virus would be extinct in the human race. The pandemic would be over.


    You are complaining that the vaccine does not work on people who do not get it. Yes, we know that. The polio vaccine does not prevent polio when people do not get it. No medicine or medical treatment works on people who do not get it. If your house catches on fire, and we spray water on another house five blocks away, it does not put out the fire. Do you have some difficulty understanding that?


    Seriously, are you out of your mind?!? Or, are you trying to fool stupid readers here? Why on earth are you saying that COVID rages and mutates despite the vaccine when you know perfectly well it only rages and mutates in people who are not vaccinated!!! You win the prize for the most ridiculous claim in this discussion.


    This figure shows fully vaccinated people had less risk of COVID-19 infection, hospitalization, and death.

    Quote from Dr Richard*

    There were strong indications right from the very start of the COVID pandemic that any vaccine would have a very short shelf life against such a rapidly mutating pathogen.

    There is no such indication. The original formula works almost as well against delta and omicron as it did against the first variant. It needs only a booster. At present Pfizer has no plans to change the formula, because there is no need to.


    In short, you made that up.

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