Covid-19 News

    Gout Medicine Could Also Battle COVID-19 – FDA Approved and Has Potent Antiviral Properties


    Gout Medicine Could Also Battle COVID-19 – FDA Approved and Has Potent Antiviral Properties
    As COVID-19 cases continue to skyrocket across the U.S. and the world, few options are available for treating patients infected with the SARS-CoV-2. But new…
    scitechdaily.com


    As COVID-19 cases continue to skyrocket across the U.S. and the world, few options are available for treating patients infected with the SARS-CoV-2.


    But new research from the University of Georgia offers hope for a viable therapeutic to combat the disease that has claimed more than 4 million lives worldwide.


    Published in Nature’s Scientific Reports, the study found that probenecid has broad antiviral properties, making it a prime candidate to combat not only SARS-CoV-2 infection but also other common and deadly respiratory viruses like RSV and flu.


    Probenecid is an FDA-approved medication that’s primarily used to treat gout, and it’s already widely available in the U.S. The drug has been on the market for over 40 years and has minimal side effects

    There’s really nothing out there to safely fight these viruses,” said Ralph Tripp, lead author of the study and GRA Eminent Scholar of Vaccine and Therapeutic Studies in UGA’s College of Veterinary Medicine. “This antiviral works for all RNA respiratory viruses we tested, including SARS-CoV-2. RSV, coronavirus and flu all circulate in the same season. Bottom line is you can potentially reduce infection and disease using this one oral drug.”


    Blocking viral reproduction

    Viruses work by coopting a person’s own cells to replicate and produce more of the virus. Probenecid blocks that replication process, keeping the virus from infecting the individual’s cells.


    In clinical development at the pharmaceutical company TrippBio, Tripp showed the drug works as a prophylactic prior to virus exposure and as a post-exposure treatment in animal models against SARS-CoV-2 and flu. The drug also has proven effective in fighting the RSV in vitro, and in vivo studies are in progress.


    Although the drug would primarily be used after a person is positive for the virus, the prophylactic findings mean people with known exposures could also potentially take the drug to prevent getting sick.


    COVID-19 treatment options limited

    The current go-to treatments for seriously ill COVID-19 patients, remdesivir and monoclonal antibodies, can only be given through an IV. And by the time a COVID patient needs them, it’s often too late.


    “These treatments have seen some effectiveness against SARS-CoV-2, but they’re very expensive and very hard to come by,” Tripp said. “In reality, there are only a handful of options that can actually be used because of the cost, restricted IV usage, and lack of access. That’s not very useful to the world.”


    Probenecid, on the other hand, is widely available. Primary care physicians could prescribe a pill to patients, and they could pick it up at their local drugstore.


    Repurposing drugs that are already approved to work against one problem is common. For example, remdesivir was originally intended to fight Ebola virus, but when it showed some promise in fighting the coronavirus, it was enlisted to battle COVID-19.


    In addition to preventing illness before it starts, probenecid may also potentially increase the efficacy of other treatments. Probenecid is already used to up the potency of some antibiotics, so it’s possible the medication could work in conjunction with other COVID-19 treatments as well.


    Now the researchers are investigating what dosage of probenecid could have the biggest impact fighting viruses in people. TrippBio is set to begin clinical trials of the medication within the year.


    “SARS-CoV-2, RSV and flu have a huge impact on health systems throughout the world,” Tripp said. “Probenecid has a potent antiviral effect against these viruses, and it works safely.”


    Probenecid is already FDA approved and has potent antiviral properties against SARS-CoV-2.


    Reference: 10 September 2021, Scientific Reports.

    DOI: 10.1038/s41598-021-97658-w

    Platelets amplify endotheliopathy in COVID-19


    AAAS


    Abstract

    Given the evidence for a hyperactive platelet phenotype in COVID-19, we investigated effector cell properties of COVID-19 platelets on endothelial cells (ECs). Integration of EC and platelet RNA sequencing revealed that platelet-released factors in COVID-19 promote an inflammatory hypercoagulable endotheliopathy. We identified S100A8 and S100A9 as transcripts enriched in COVID-19 platelets and were induced by megakaryocyte infection with SARS-CoV-2. Consistent with increased gene expression, the heterodimer protein product of S100A8/A9, myeloid-related protein (MRP) 8/14, was released to a greater extent by platelets from COVID-19 patients relative to controls. We demonstrate that platelet-derived MRP8/14 activates ECs, promotes an inflammatory hypercoagulable phenotype, and is a significant contributor to poor clinical outcomes in COVID-19 patients. Last, we present evidence that targeting platelet P2Y12 represents a promising candidate to reduce proinflammatory platelet-endothelial interactions. Together, these findings demonstrate a previously unappreciated role for platelets and their activation-induced endotheliopathy in COVID-19.


    DISCUSSION

    Severe COVID-19 is associated with a hypercoagulable state and robust inflammatory response that predisposes patients to macro- and microthrombotic events (34–38). The coordinated activation of the inflammatory and thrombotic response has been termed thromboinflammation. Levels of prothrombotic acute phase mediators, including fibrinogen, vWF, and D-dimer, are increased in COVID-19 patients, implicating the endothelium, platelets, and the coagulation system as likely mediators of thromboinflammation in COVID-19. The resulting endotheliopathy is thought to link inflammation, immune dysregulation, and thrombosis, and be a driver of poor clinical outcomes in COVID-19 patients (39, 40). Despite suggestions that SARS-CoV-2 triggers endotheliopathy (12, 13), recent experimental evidence supports indirect activating mechanisms driving EC injury in COVID-19 (14).

    Platelets are first responders to vascular injury and act to bridge the immune system and thrombosis via activation and release of hemostatic and inflammatory mediators. Activated platelets secrete a host of proinflammatory mediators in the local microenvironment, altering the endothelium’s inflammatory and adhesive properties (18, 19). Activated platelets isolated from patients with inflammatory disease, such as systemic lupus erythematosus (SLE), HIV, and psoriasis, induce a proinflammatory EC phenotype (16, 20, 21). We and others previously reported that COVID-19 is associated with a hyperactive platelet phenotype (23, 24), characterized by increased platelet activation markers and a proinflammatory, prothrombotic transcriptome. Given the interconnection between activated platelets and the microvasculature, we explored whether platelet-released factors contribute to COVID-19 endotheliopathy.

    Our study details how COVID-19 hyperactive platelets release factors that induce a proinflammatory and hypercoagulable endothelium (Fig. 7). The change in EC transcription directly correlated with alterations in the platelet transcriptome, connecting differences seen in these complementary cell types. Sequencing of the platelets used to incubate with ECs found a set of 523 platelet genes that are consistently associated with the proinflammatory EC transcriptomic pathway changes. This block of genes is potentially a unique COVID-19 platelet signature that merits future exploration and study.

    Unbiased screening of candidate platelet genes differentially expressed in COVID-19 led to the identification of S100A8 and S100A9, and their protein product MRP8/14, as a likely candidate of platelet-mediated endotheliopathy. Platelet S100A8/A9 mRNA and platelet-derived MRP8/14 were increased in patients with COVID, and their expression and translation positively correlate with changes seen in EC coagulation and inflammatory pathways and the production of IL6 and IL8, proinflammatory cytokines that regulate EC adhesion molecule expression (41). While circulating plasma MRP8/14 was once considered only to be leukocyte-derived (42), platelets and megakaryocytes serve as an additional source of MRP8/14 (31, 32, 43, 44). While circulating plasma levels of MRP8/14 alone correlated with EC coagulation and inflammatory pathways, platelet S100A8/A9 mRNA and releasate MRP8/14 levels were more tightly associated with EC dysfunction directly, suggesting the importance of platelet-derived MRP8/14 on EC dysfunction. Our present study does not rule out other cellular and noncellular contributors of COVID-19 endotheliopathy, which may act synergistically with MRP8/14. For example, serum antiphospholipid (aPL) antibodies in COVID-19 sera were recently reported to induce adhesion molecule expression on ECs (45). Previous studies have found that aPL antibodies promote platelet activation and their release of MRP8/14 into the microenvironment, providing evidence of additional mechanisms by which interaction of platelets with the local inflammatory environment in COVID-19 contributes to EC dysfunction (32, 46).

    We find that the direct interaction of SARS-CoV-2 with primary megakaryocytes induces S100A8/A9 expression, a finding that has clinical implications given our observation that megakaryocytes from COVID-19 patients contain SARS-CoV-2 virions (26), and single-cell sequencing data reporting up-regulation of S100A9 in circulating megakaryocytes in COVID-19 (27). Intriguingly, up-regulation of S100A8/A9 does not occur following exposure of megakaryocytes to a coronavirus responsible for the common cold (CoV-OC43), highlighting that, independent of indirect mechanisms (e.g., systemic inflammation), SARS-CoV-2 can mediate proinflammatory changes to megakaryocytes and platelets (47, 48). Our data indicate that increased platelet S100A8/A9 mRNA translates to increased platelet MRP8/14 release, thus indicating that direct interactions of megakaryocytes with SARS-CoV-2 enhance proinflammatory platelet-EC interactions. Consistently, MRP8/14 is increased in activated platelets and platelets isolated from patients with peripheral artery disease and ST-elevation myocardial infarction. In vitro, MRP8/14 induces platelet surface P-selectin (31), a major ligand in the platelet-EC interaction. In addition, MRP-14−/− knockout mice had reduced expression of P-selectin in response to collagen and arachidonic acid, which was independent of platelet aggregation (44).

    The prothrombotic and proinflammatory nature of platelet MRP8/14 is supported by studies finding platelet transcript expression of S100A8/A9, positively correlates with plasma MRP8/14 concentrations, and is predictive of future atherothrombotic events (31, 43). MRP8/14 levels are increased in patients with cardiovascular diseases, metabolic disease, and several inflammatory conditions, including rheumatoid arthritis, SLE, and psoriasis (31, 43, 49–51). Prior studies have found increased MRP8/14 in patients infected with SARS-CoV-2 (52, 53). In the current study, we find platelet S100A8 and S100A9 mRNA to be increased in COVID-19 patients and a corresponding increase in platelet-released MRP8/14, all of which correlate with circulating MRP8/14. Among 291 patients hospitalized with COVID-19, circulating MRP8/14 increased during hospitalization. When measured at baseline, MRP8/14 correlates with incident thrombotic events, severe disease, and length of stay. In contrast to a small increase in MRP8/14 among patients with nonsevere illness, levels increased up to eightfold in COVID-19 patients who subsequently died.

    Recently, the therapeutic potential of suppressing MRP8/14 signaling has been suggested as an approach to reduce COVID-19–associated thromboinflammation (54). To understand the clinical potential of our findings, we investigated the (i) effect of antiplatelet therapy on S100A8/A9 platelet mRNA and (ii) in vitro effect of antiplatelet treatment on platelet-induced EC activation. In contrast to aspirin, targeting of P2Y12 with ticagrelor reduced S100A8 and S100A9 platelet mRNA. In vitro experiments found that P2Y12 inhibition significantly attenuated the COVID-19 platelet–mediated EC activation. The ability of aspirin to attenuate the platelet-EC interaction was less pronounced. The benefit of reducing platelet MRP8/14 release via targeting of P2Y12 is supported by murine studies, which found that the antithrombotic effect of the S100A9 vaccination is equivalent to that with clopidogrel (55). Furthermore, given evidence that P2Y12 inhibitors reduce platelet release of proinflammatory α-granule contents (56) and the formation of platelet-leukocyte aggregates (57), the beneficial effect of this approach is hypothesized to be multifaceted. These data collectively suggest that P2Y12 inhibition will mitigate platelet activation, reduce platelet-released MRP8/14, and ultimately suppress platelet activity and EC activation and improve clinical outcomes linked to COVID-19 thromboinflammation. While observational data suggested a potential benefit of aspirin on outcomes in hospitalized COVID-19 patients (58, 59), a large randomized trial of nearly 15,000 participants found that aspirin did not improve its primary end point of 28-day mortality (60). The clinical effect of a P2Y12 inhibitor strategy is being investigated in ACTIV4a (NCT04505774).

    Our study describes how platelets isolated from hospitalized COVID-19 patients release significant quantities of MRP8/14 that can act in a paracrine fashion on nearby ECs promoting endotheliopathy. Several limitations exist with our current study: (i) the relatively small sample size used for sequencing; (ii) the cellular source of plasma MRP8/14 cannot definitively be attributed to platelets and may originate from other cells, including neutrophils; (iii) it is unknown whether the observed MRP8/14 induced endotheliopathy occurs in other viral settings; (iv) a clinical diagnosis of thrombosis during hospitalization may be underestimated because imaging studies were limited due to concerns of transmitting infection or competing risk of death; and (v) the effect of antiplatelet therapies on the COVID-19 platelet–induced EC activation was not explored. Future studies will aim to address these limitations to further our understanding of the interaction of platelets with SARS-CoV-2 and other viral illnesses and the endothelium. An ongoing multinational trial is underway exploring the effect of P2Y12 inhibition on clinical outcomes of hospitalized COVID-19 patients (NCT04505774).

    In conclusion, we define a novel role for platelet-induced endotheliopathy in COVID-19. The activated platelet phenotype observed in COVID-19 consistently induces a proinflammatory and dysfunctional endothelium. Platelet-derived MRP8/14 is increased in COVID-19 and induces endothelial injury. Circulating MRP8/14 has the potential to serve as a useful biomarker of thrombosis and severity of disease in patients infected with SARS-CoV-2. Platelet-directed therapy, specifically P2Y12 inhibitors, may represent a particularly attractive therapy because of its effect on platelet S100A8/A9 and platelet-induced endotheliopathy (Fig. 7).

    Wyttenfact Roundup - India Edition


    Quote from Wyttenbach

    DO also not forget their WHO buddy [Soumya Swaminathan] has been arrested for promoting mass murder by blocking Ivermectin.

    No, she hasn't been arrested.


    Quote from Wyttenbach

    In Uttar Pradesh, start of May 2021 every household got a number of Ivermectin kits

    No they didn't... And my source for that is a friend who lives in Noida, UP.

    Although like other Wyttenfacts, you are welcome to waste your time trying to find a source online that says otherwise.


    Quote from Wyttenbach

    WE are using [ivermectin] and it works. See Uttar Pradesh, the best example! 1000x better than vaccines.

    Unbelievably, this one is TRUE!!!


    ...According to official figures, that is.


    In fact, the goverment of Uttar Pradesh has excelled themselves - not only have they cured covid, they have cured death itself!!


    Indian states don't publish (or even count) their covid death toll - apparently due to the reason that only 20% of all deaths are certified by a doctor.


    But this hasn't stopped researchers from trying to calculate how many Indians have died from covid... By comparing the number of yearly deaths prior to the pandemic with the current number of yearly deaths.


    This involves making freedom of information requests from each state, as this paper discusses:


    Preliminary Analysis of Excess Mortality in India During the Covid-19 Pandemic (Update August 4, 2021)
    Background As both testing for SARS Cov-2 and death registrations are incomplete or not yet available in many countries, the full impact of the Covid-19…
    www.medrxiv.org


    There are several similar papers that can be found by searching for "excess mortality covid india". All of them ignore the numbers received from Uttar Pradesh.


    Why is that?


    "For Uttar Pradesh, the raw mortality data obtained from a Right-to-Information request contained anomalies, such as multiple districts with zero deaths for numerous months."


    :/


    So it would seem that not only did the ivermectin kits (that were not distributed to every house) manage to cure covid, but it is also proven beyond doubt that they were able to prevent all deaths across large swathes of Uttar Pradesh. Incredible.

    I fully understand the wish of our FM/R/X/B proponents here to discredit the successful Ivermectin countries (Like Uttar Pradesh, Delhi, Chhattisgarh, Rajasthanm Gujarat, or Slovakia, Zaire) on this planet for wiping out CoV-19.


    Fact is in Europe Slovakia see no more CoV-19 and deaths from CoV-19 since the regimen has changed to Ivermectin. Of course some children here will know somebody from Facebook that claims to live in Slovakia and say other wise than all available public news...


    Fact is: The Pfizer gen therapy does not work for CoV-19 delta. The protection for people age <50 is non existent and only the group age >50 gets some protection for about 4-5 months.

    Pfizer has good connections to the X-mafia. As we can see here too, as these folks deliver the most silly arguments against Ivermectin.


    Quote from Fm1

    POTUS’ Sweeping Vaccine Mandates Showcase Unprecedented Use of Federal Powers in Modern Era

    This day is more sad than 9/11 where an other (US internal) group attacked the country. Here, now the mafia top good father destroys the last freedom of the US slaves.

    USA is now a worse mind terror state than Russia or Iran. I hope the people will react appropriately and quit health service especially in locations where the mafia members get treated.


    Ordering people to have a damaging and soon useless gen therapy is making USA to the largest Dr. Mengele concentration camp on planet earth. This war against the own population will cause 100..1000x more US deaths than 9/11. And this is still an optimistic estimation.

    New record for the vaccine Terror state Kerala of India


    Today about 80% of all India CoV19 infection are among the vaccine terror victims in Kerala!


    26'200 of 34,973 infections!! Deaths still about 50% of all India CoV-19 deaths


    Kerala suffers the same mafia terror regime as USA. State official bribed by big pharma (Except in children facebook...) blcok Ivermectin.

    for the notes https://www.globalresearch.ca/…ntist-mass-murder/5753831


    This, on the face of it, looks very interesting


    Probenecid inhibits SARS-CoV-2 replication in vivo and in vitro - Scientific Reports
    www.nature.com


    The Pathophysiology of COVID-19 and SARS-CoV-2 Infection: Consideration of Pannexin 1 channels in COVID-19 pathology and treatment
    www.ncbi.nlm.nih.gov


    and somone else with a research project to do the same thing - seems like a popular idea https://covid19.research.ubc.c…t-drug-treatment-covid-19


    What I cannot find is any reference to its testing in double-blind high quality studies - I guess that will be blocked till ivermectin is fully evaluated. That is the opportunity cost of putting a lot of effort into evaluating not very promising drug candidates.


    Probenecid has several pharmacological targets including blocking pannexins that underlie transmembrane channel function24,25 and decreasing ACE2 expression26,27. The major advantages of probenecid are that it is an FDA-approved therapeutic drug that has been on the market for >50 years, it can be administered orally with favorable pharmacokinetics, it operates at the host cell level, is refractory to viral mutation, and has the potential to treat multiple other viruses. Further, our data suggest that initiation of posttreatment following infection in mammalian cells, hamsters, and humans results in infection remarkably reduced SARS-CoV-2 replication, particularly in the lung target organ.

    Probenecid treatment will likely have the benefit of inhibiting SARS-CoV-2 variants as we show that it is effective against the VOC, lineage B.1.1.7. This is not unexpected, as targeting host processes essential for viral replication such as OAT3 would be expected to be universal. Among the host targets that have been identified as potential targets for inhibiting virus replication, OAT3 blockade will not likely confer any mechanism-based untoward effects for humans since humans with reduced OAT3 function are healthy28, and pharmacologic blockade of OAT3 is safely tolerated in humans29. Other compounds that interact with OAT3 include the antiviral drugs oseltamivir phosphate (Tamiflu) and acyclovir10, as well as angiotensin II receptor blockers30, however, their interaction is weak and their pharmacological actions confer safety and tolerability limitations that preclude their use in drug repurposing.

    Quote from Wyttenbach

    Fact is in Europe Slovakia see no more CoV-19 and deaths from CoV-19 since the regimen has changed to Ivermectin.

    Wyttenfact alert!


    The link below is dated 8 September.


    Slovakia has one of the quickest caseload increases in the world
    Most districts will follow stricter pandemic measures from next Monday.
    spectator.sme.sk


    The impact of the third pandemic wave is already visible in Slovakia's Covid-19 statistics.


    Slovakia belongs to the countries with the quickest growth in new Covid cases in the world; it is also witnessing quite a big increase in the number of hospitalisations.

    The situation is worsening on the regional level as well, with only a few regions remaining in the best, green tier of the alert system, known as Covid automat.

    Čítajte viac: https://spectator.sme.sk/c/227…the-world.html?ref=njctse

    Hilarious! Wyttenbach relies on a holocaust-denying 9/11 “truther” site for his covid “news”.


    Globalresearch.ca has well-known ties to the Kremlim, and a curious editorial policy that just happens to parrot narratives found in other Russian propaganda.


    In the linked article they make the mistake of conflating the American Bar Association (200,000 members), with the Indian Bar Association (a recently-formed group of 12 misfits), who have a habit of filing whinging civil suits against people who annoy them. None of these have had any effect on their targets, based on a quick googling.

    Quote from Fm1

    POTUS’ Sweeping Vaccine Mandates Showcase Unprecedented Use of Federal Powers in Modern Era

    That is a peculiar thing to say. Every single public school system in the U.S., and all universities, mandate that students be vaccinated. It has been that way since the 19th century. The first mandated vaccines for schools were in 1850, in Boston.

    Quote from THHuxleynew

    Wyttenfact alert!


    The link below is dated 8 September.

    THH FUD alert. Yes they had a growth last week from 50 to 250 cases a day. May be the same Holiday effect as in Switzerland: we here have + 140% ICU cases imported from ex Yugoslavia...


    If you can't beat them send them to ill countries...


    To reach the 98% vaccinated UK level the must multiply the cases by 5.

    Quote from JedRothwell

    That is a peculiar thing to say. Every single public school system in the U.S., and all universities, mandate that students be vaccinated.

    Nothing against vaccines!


    But here we talk of an experimental gen therapy! A gene therapy that for 30% works in cancer therapy...


    The Pfizer gen therapy according sound research does not imply a useful immune memory = has no vaccine like action.

    The gen therapy just forces, mostly endothelian cells, to intake & replicate the spike protein, what in follow up presentation reaction stimulates the production of spike antibodies only.


    This " pseudo vaccine" never helps to stimulate/produce new antibodies after an infection with CoV-19. Only the surviving - but waning - anti bodies help to fight an illness.


    Only scared to death or mad people kill them selves with an experimental gen therapy.


    So good by America! Was nice to see how a free state changed into a mad house.

    Quote from Wyttenbach

    Nothing against vaccines!

    Oh give us a break. Who do you think you are kidding? Of course you are opposed to vaccines.


    Quote from Wyttenbach

    But here we talk of an experimental gen therapy! A gen therapy that for 30% works in cancer therapy...

    I believe you mean gene therapy. This is complete bullshit. There are no genes involved. RNA cannot affect DNA, except with a retrovirus, and this is not a retrovirus.


    HOWEVER, you are missing the point. If you are opposed to mRNA vaccines, you can get a J&J adenovirus-based vaccine instead. That is a traditional design. So, you have no reason to oppose vaccination, only one particular type of vaccine. Despite that, I am sure you are as opposed to the J&J as any other. All of your comments claiming that the pandemic is not as bad as the CDC says, or that people below age 50 are not at risk, and so on, are vile lies intended to frighten people, and control them. You are a devotee of the Death Cult.

    Quote from Zeus46

    https://timjwise.medium.com/co…se-than-that-16d74186e46b


    :*

    Yup - it is good - though I am not sure it is correct. It assumes these anti-science idiots are capable of connected logical thought.


    To them, COVID was a virus of the big city and those who live there, of old people, or persons with multiple pre-existing conditions (of which they didn’t believe cholesterol-lined arteries and COPD qualified as examples).

    It was only killing the weak.


    And they were strong — cowboy strong, to be precise, or at least Sturgis motorcycle ridin’ strong.


    High on a delusional mix of rugged individualism, toxic masculine bravado, pseudoscientific faith in vitamin supplements, and a belief that God would pull them through, they were convinced they were safe.


    Only others were at risk — the less good people.


    The ones who don’t do CrossFit, or go to a megachurch, or better still, a CrossFit in a megachurch.


    The ones who don’t settle for the “power of positive thinking,” like FOX host Jesse Watters, who insisted that’s all he would need should he become infected.


    The ones who place their faith in science rather than a Bible study group.


    And for people like that? Who cares? To the right, those people don’t count.


    Indifference to the suffering of others is why Trump’s minions wouldn’t mask. They didn’t care that they might infect people, despite being asymptomatic.


    When you would tell them repeatedly that wearing a mask was less for the wearer than for others, they shrugged. If other folks are at risk, they should stay home and let the rest of us get back to the gym, the hairdresser, concerts, movies, and tailgate parties before the big game. I mean, this giant foam finger isn’t gonna wave itself.


    Their freedom to do as they pleased was more important than other people’s lives.


    ...


    Most who refused to mask (and reject the vaccine now) are not full-blown virus deniers. Instead, they simply didn’t believe — and still don’t — that it can harm people like them.


    But if you know it can harm others who aren’t like you, and you still refuse to take the measures that reduce the risk of spreading the virus to them, you are a sociopath.


    If you refuse a vaccine when you have no valid health reason to do so (as almost no one does), thereby keeping the virus alive longer by increasing the risk of mutations, you are saying that other people’s lives don’t matter to you.


    And if you expected to be infected, hospitalized, and die, you would never take these risks.


    That’s what these ICU confessions signify — that they care about their own lives quite a bit, whatever they might think of others.


    Quote from THHuxleynew

    Yup - it is good - though I am not sure it is correct. It assumes these anti-science idiots are capable of connected logical thought.

    I do not think this article describes every antivaxxer. It describes a segment of the U.S. public. I have been mystified by these people for some time. I had not thought about them in these terms. I could not understand how they went from attacking masks and the vaccine, and saying "I'll never get COVID" one day, to pleading for their lives and praying the next day. If you are so afraid for your life, why not take sensible precautions? It is like wearing a seatbelt. You don't do that because you expect to get into an accident. Or because you hope to get into an accident, like a Heaven's Gate Death Cult fanatic. These people thought they were invulnerable, and I think this article describes the reason why.


    There are other groups of antivaxxers with different motivations. There are highly religious people who sincerely believe that God will protect them and it would be a sin to doubt that. They are frightened, but they feel their best chance of survival is to put their faith in God and not betray God by doubting Him. I understand that. It is a traditional view. There are others who are simply ignorant, or innumerate, who honestly think the vaccine is more dangerous than the disease. I understand them, too. But the group described by the author baffled me. Not frightened, not willing to do anything to save themselves, yet it turns out they want to live. I think this analysis explains why.


    I think most of the Death Cult member here, such as Wyttenbach, are ignorant innumerates. They are not the kind of preening he-man cowboys who are sure they have natural immunity and COVID will never touch them. Whereas most of the people described in this web site are in the first category; the he-men who died much to their own surprise:


    Home | sorryantivaxxer.com
    www.sorryantivaxxer.com

    Quote from JedRothwell

    All of your comments claiming that the pandemic is not as bad as the CDC says, or that people below age 50 are not at risk, and so on, are vile lies intended to frighten people, and control them.

    CDC is a rotten bunch of free masons adepts. But an obese country deserves no better!


    What I linked is that the UK CoV-19 mortality among age group <50 is below 0.03% this is from real actual = factual data not from faked studies. Here in Switzerland it is even lower.


    The mortality from flu is 0.1% (mild flu) to 0.5% strong flu.


    The only vaccine I could recommend for the united states is one to fight military automatic guns...or even better (it will never be made) for taming greedy free masons.


    I clearly do not recommend the RNA gene therapy to anybody younger than 50 that is healthy.


    For JED: Genes ( coded in DNA) are always translated to RNA = the active version of genes. The RNA gene therapy just avoids to permanently store the information. But this is only half way true if you know how the RNA inference works!

Subscribe to our newsletter

It's sent once a month, you can unsubscribe at anytime!

View archive of previous newsletters

* indicates required

Your email address will be used to send you email newsletters only. See our Privacy Policy for more information.

Our Partners

Supporting researchers for over 20 years
Want to Advertise or Sponsor LENR Forum?
CLICK HERE to contact us.