Covid-19 News

  • Please stop repeating this falsehood. The FDA has not and cannot block the use of ivermectin for COVID or any other purpose. Off-label uses are allowed. The FDA made that quite clear in the web page I pointed to. And pointed to. And pointed to. Ivermectin is being used in the U.S. to treat COVID-19.

    Only in clinical trials no out patient treatment

  • Pfizer CEO says third Covid vaccine dose likely needed within 12 months


    KEY POINTS

    Pfizer CEO Albert Bourla said people will "likely" need a third dose of a Covid-19 vaccine within 12 months of getting fully vaccinated.

    He also said it's possible people will need to get vaccinated against the coronavirus annually.


    https://www.cnbc.com/amp/2021/…ded-within-12-months.html


    Pfizer CEO Albert Bourla said people will "likely" need a booster dose of a Covid-19 vaccine within 12 months of getting fully vaccinated. His comments were made public Thursday but were taped April 1.


    Bourla said it's possible people will need to get vaccinated against the coronavirus annually

  • Pfizer CEO says third Covid vaccine dose likely needed within 12 months

    The EU ordered > 1'000'000'000 dose after Pfizer cheated the press with J&J & Astra. This will give them 20'000'000'000$ extra profit for next year.


    This is how the mafia woman do contracts. Lets see how obidient the Europeans are.

    Pfizer CEO says third Covid vaccine dose likely needed within 12 months

    And the fourth, fifth and they will cancel your freedom passort in 12 months....May be you can deal in a kidney?!

  • Covid-19 Disease Triggers More Ultra-Rare Blood Clots Than Vaccines, Study Finds


    https://www.barrons.com/amp/ar…s-study-finds-51618488102


    The risk of contracting blood clots is much higher for Covid-19 patients than from vaccines, according to a study released on Thursday.


    The rare blood clotting known as cerebral venous thrombosis, or CVT, occurred at a rate of 39 per million Covid 19 patients, according to researchers at the University of Oxford, the same university that helped develop the AstraZeneca vaccine. That compares to five in a million people after the first dose of the AstraZeneca-Oxford vaccine, they said.


    “We’ve reached two important conclusions. Firstly, Covid-19 markedly increases the risk of CVT, adding to the list of blood clotting problems this infection causes. Secondly, the Covid-19 risk is higher than we see with the current vaccines, even for those under 30; something that should be taken into account when considering the balances between risks and benefits for vaccination,” said Paul Harrison, professor of psychiatry and head of the translational neurobiology group at the University of Oxford.


    Using a U.S. health records network, the study compared more than 500,000 patients with Covid-19 to nearly 200,000 with influenza and another roughly 500,000 who received the mRNA vaccine. They also drew on European Medicines Agency data of those who took the AstraZeneca vaccine. “…all comparisons must be interpreted cautiously since data are still accruing,” according to the study.


    The researchers claimed they found the rare blood clotting at a rate of four out of a million people receiving the vaccines from drug company Pfizer and biotech Moderna, but Pfizer disputed that claim. In a statement, Pfizer said its own review of safety data after over 200 million doses have been administered has found no evidence to conclude that arterial or venous thromboembolic events being investigated in the Johnson & Johnson vaccine are a risk associated with its Covid-19 vaccine.

  • GeNeuro's experimental multiple sclerosis drug shows hints it may help treat COVID-19


    https://www.fiercebiotech.com/…might-help-treat-covid-19


    The clinical manifestations of COVID-19 are believed to be caused by an abnormal immune response to the novel coronavirus, SARS-CoV-2. Targeting that rogue immune response is one of the approaches under investigation for treating COVID-19. Now, a team led by scientists at the University of Rome Tor Vergata has found a possible way to do just that via an otherwise silent genetic phenomenon in humans.

    In a new study published by the Lancet’s EBioMedicine, the team explained the discovery of a strong correlation between the expression of the envelope protein of the human endogenous retrovirus W (HERV-W ENV) in white blood cells and markers of inflammation in COVID-19 patients.


    Because HERV-W ENV has been linked to other inflammatory diseases, the researchers suggested the protein could help predict clinical progression of COVID-19 and might be targeted by drugs designed to treat the disease.


    Scientists from Swiss biotech GeNeuro also participated in the study. The company is developing an anti-HERV-W antibody, temelimab, to treat multiple sclerosis. It's in phase 2 clinical testing for MS, and now the company hopes to move it into COVID-19 trials as early as this summer.


    The HERV family of genes is a relic of the human genome, left from ancestral infection by retroviruses. The activation of these genes has been linked to other autoimmune diseases, including type 1 diabetes and rheumatoid arthritis. The protein HERV-W ENV can be activated by new viral infections and induces proinflammatory responses. So the University of Rome team wanted to see if it’s involved in COVID-19.

    Blood cells from 30 hospitalized COVID-19 patients were compared with those from 17 healthy donors who had been matched for age and sex.


    The researchers recorded significantly higher levels of HERV-W ENV mRNA and protein in lymphocytes of COVID patients. T cells with high HERV expression showed strong differentiation activity and exhaustion, which is typical of continuous immune stimulation during chronic infections.


    “This pro-inflammatory protein is usually found in specific disease situations, mostly in the brain, but has never before been observed circulating in the body at high levels and, in particular, was never seen expressed in T-lymphocytes,” Claudia Matteucci, Ph.D., the corresponding author of the study, pointed out in a statement.


    Further analysis showed HERV-W ENV mRNA correlated with the expression of pro-inflammatory molecules such as IL-6, IL-10 and IL-17RA. And the percentage of HERV-W ENV in lymphocytes was related to COVID-19 disease severity, as patients with high expression suffered more severe pneumonia.

    In lab dishes, the researchers found that stimulating immune cells from healthy donors with the SARS-CoV-2 spike protein prompted a significant increase in early expression of HERV-W ENV. But only about 30% of healthy donor cells responded that way, scientists from GeNeuro explained in a separate study published on the preprint site Research Square. That could explain individual susceptibility to COVID-19, they suggested.


    Before this study, HERVs had been observed mainly in neurologic disorders such as MS. Given the discovery of HERVs in lymphocytes, HERV-W ENV may have a double effect in COVID-19 patients, said GeNeuro Chief Scientific Officer Hervé Perron, Ph.D., a co-author of the study.


    “In the short-term, when activated in genetically susceptible individuals, HERV-W ENV can act as an accelerant to the innate immune response, fueling complications and leading to the need for ventilation,” he explained in a statement. “But even after the primary infection is over, if HERV-W ENV has reached a self-fueling expression level, it may cause persistent damage to endothelial cells in blood vessels and also to cells from the peripheral and central nervous system, which could explain many of the long-term neurological symptoms experienced by patients long after SARS-CoV-2 infection.”


    Based on the findings, GeNeuro is now working with medical centers in Europe and the U.S. to evaluate temelimab as a treatment both to prevent immune overreaction in acute patients and to tackle toxic neurological effects of the virus.

  • India Confirms More Than 200,000 Coronavirus Cases In A Day


    https://www.npr.org/2021/04/15…oronavirus-cases-in-a-day


    India surpassed a somber COVID milestone Thursday, confirming more than 200,000 new cases in a single day as patients and doctors grapple with a shortage of beds and cities announce curfews.


    Coronavirus cases had been declining in India for months after reaching a peak last September. But new cases started ticking up last month. Now, they're doubling every ten days or so. Thursday's tally was India's highest since the pandemic began – more than double the previous 2020 peak.


    "There are newer variants of concern that are emerging in India which are probably the biggest reason why the speed at which the cases are rising is almost exponential," said epidemiologist Giridhara Babu of the Public Health Foundation of India.


    Babu says the characteristic feature of India's second wave is that most people are asymptomatic. "But when the surge occurs, even 5 to 10% will be a large number requiring hospitalization," he said.


    India's health infrastructure has started to crack under the strain. Hospitals in many cities are running out of beds and oxygen. In the western Indian city of Ahmedabad, there was a queue of more than 100 ambulances waiting to bring COVID patients into one hospital. Patients have died while waiting to get a bed, and crematoriums and burial grounds are reportedly overloaded.

  • How the coronavirus origin story is being rewritten by a guerrilla Twitter group

    The group, known as Drastic, has investigated, corrected, uncovered and agitated in a quest to uncover the pandemic's starting point.


    https://www.cnet.com/google-am…-guerrilla-twitter-group/


    Coronavirus, SARS, horseshoe bat, Yunnan.


    It was May 18, 2020. At the time, the novel coronavirus, SARS-CoV-2, had infected fewer than 5 million people worldwide. Scientists were still attempting to unravel many of its mysteries. Chief among them was where, exactly, the virus had come from. The Seeker, too, was hooked on that mystery.


    After a lot of trial and error, the Seeker stumbled upon exactly what he was looking for: a master's thesis written by a Chinese doctor. The document contained an account of six cases of "severe pneumonia caused by unknown viruses" in workers who had been cleaning an abandoned copper mine in Yunnan, China, in 2012. The patients' symptoms seemed eerily similar to those of COVID-19. Three of the patients, it said, died from the mystery illness.


    The Yunnan mine and its resident bats, the Seeker knew, had been sampled by researchers at the Wuhan Institute of Virology. He'd uncovered a missing puzzle piece: an association between the closest known relative of the coronavirus and research conducted at the institute in Wuhan, China.


    "Finding it, at that moment, felt big," the Seeker, says, "like a homicide detective solving a cold case."


    Minutes after reading the abstract, he posted his find to Twitter, in a long tweet thread tagging members of a loosely defined group known as Drastic, a "Decentralized Radical Autonomous Search Team Investigating COVID-19." The master's thesis had the potential to rewrite the origin story of the pandemic.


    A majority of scientists and experts agree that the coronavirus emerged after jumping from a wild animal to humans somewhere in or around Wuhan, where the first cases appeared in 2019. The pathogen is believed to have lived most of its life inside a bat, before acquiring genetic mutations, potentially through another species, and infecting humans.

    But an alternative theory posits that the pandemic began after SARS-CoV-2 leaked from a laboratory in Wuhan, potentially the Wuhan Institute of Virology. A joint study by the World Health Organization and Chinese scientists in January and February 2021 considered this scenario "extremely unlikely." From the earliest days in the pandemic, it was represented as a conspiracy theory built on misinformation and fear.


    But Drastic, and an increasing number of scientists, are convinced it requires further investigation.


    In searching for the complete and naked truth surrounding the origins of COVID-19, this motley group of strangers has challenged the prevailing theories of the virus' beginnings by picking apart inconsistencies and trading data in the highly polarized theater of Twitter. This unorthodox approach has seen them branded by scientists and researchers as maniacs, thugs and conspiracy theorists. They've also been accused of racism, and their scientific credentials have been questioned.

    On Twitter, where access to world-renowned scientists is just a click away, they've been abrasive, too. Virologists and epidemiologists who refuse to engage with the lab leak theory have been targeted, and some have been accused of working for the Chinese Communist Party. As a result, Drastic's findings and investigation have often been dismissed out of hand.


    But over the past year the group's discoveries have proven too important to ignore.


    A loose thread

    Two months before the Seeker's discovery, Rossana Segreto stumbled upon her own revelation. Segreto, a microbiologist at the University of Innsbruck in Austria, had been growing skeptical about the coronavirus origin story from "very early on" in the pandemic. She'd quickly come around to the idea the virus may have leaked from a lab.


    In March 2020, Segreto noticed an inconsistency in one of the papers on SARS-CoV-2's potential origins, published in Nature on Feb. 3, 2020. The research was led by Zhengli Shi, a researcher at the Wuhan Institute of Virology. Shi has a long history working with bat coronaviruses, earning her the infamous title of China's "Bat woman."


    Her Nature paper was big news because it described, for the first time, the closest relative of SARS-CoV-2: RaTG13, a bat coronavirus collected by her team. The research showed RaTG13's genetic fingerprint was 96.2% similar to that of SARS-CoV-2. It didn't show where RaTG13 was discovered.


    The trouble with investigating the origins of COVID-19 is often not what is said, but what is unsaid.

    Just two days later, another paper described an even closer match for SARS-CoV-2. It was dubbed "BtCov/4991." The paper showed 4991 had been discovered by Shi's group in an abandoned mineshaft in Yunnan, in 2013, and brought back to the virology institute in Wuhan.


    However, unlike RaTG13, 4991 wasn't a whole genetic fingerprint, it was just a leftover fragment of one. Segreto wondered if it matched any other viruses known to science.


    She turned to an online tool called BLAST, which functions like a search engine to match genetic fingerprints of discovered viruses. When she ran 4991 through the tool in March 2020, it returned a 100% match with RaTG13.


    The 4991 fragment was actually just a small piece of RaTG13. They were the same virus.


    The WIV had not documented the name change, which obscured where RaTG13 was originally discovered (an addendum was added to the paper by Shi's team on Nov. 17, 2020, nine months after it was published).


    "I was so surprised," Segreto says.


    It was a critical moment, made all the more startling when the Seeker discovered the master's thesis (a translation was later provided by Independent Science News). Taking the two pieces together, Drastic was able to link RaTG13 to the mineshaft in Yunnan, 1,000 miles southeast of Wuhan, where workers fell ill in 2012 from a COVID-like disease.

    The lack of transparency from the Wuhan Institute of Virology prompted another Drastic member, Monali Rahalkar from India's Agharkar Research Institute, to publish a list of questions surrounding the miners' illnesses in October 2020. Many remain unanswered.


    Edward Holmes, a virologist at the University of Sydney, says "the miners' story tells us nothing about the emergence of SARS-CoV-2," and, according to Shi, experts at the Wuhan Institute of Virology retested blood samples from the sick miners, finding there was no evidence they were infected by a coronavirus. Instead, those experts suggest the miners may have suffered from a fungal infection. According to the Seeker's thesis find, this is simply untrue.


    Whether the miners' story can reveal more about the origins of SARS-CoV-2 is still to be explored, but the issues around transparency from researchers at the WIV has left a dangling thread Drastic continues to tug.


    Old threads

    When Yuri Deigin first heard the lab leak hypothesis in January 2020, he thought it was all "bullshit conspiracy theory." He wanted to smash those conspiracy theories with "cold, hard scientific facts." So he started doing a little digging on some of the laboratories in Wuhan.


    "Once I actually started reading up on what kind of research they were doing, I was worried that, you know, this could have been a lab leak," he says.


    Deigin, a Russian-born scientist working on developing drugs to combat aging, published an article on Russian blog site Habr and on Facebook about a month before the Seeker found the master's thesis. In it, he questioned whether SARS-CoV-2 could have escaped from a lab. Prominent Russian biologists immediately discredited the work, suggesting he was pushing forward "crazy narratives."


    When he posted a version in English on Medium, vocal virologists working on the coronavirus in the West mostly ignored it or disparaged it. One compared it to a racist manifesto. But Drastic took notice.


    Deigin began convening with the group via Twitter. It was one of the few platforms where discussions on lab leaks were occurring. Facebook had flagged such pieces as "false information" in February and "it was impossible to post anything on Reddit and not have it taken down," Deigin says. (The COVID-19 subreddit is still removing lab leak content from Drastic members because "the authors are not scientists outright, or not in relevant fields.")


    Part of the problem is that the origins story has become entangled in geopolitics and conspiracy. Bad actors have seized upon the lab leak theory for political gain, sometimes attempting to shift the blame for catastrophic failures in managing the pandemic. Instead of remaining a scientific debate, the origin story morphed into a political one. For instance, in March 2020, US President Donald Trump and Secretary of State Mike Pompeo began propagating the idea that SARS-CoV-2 may have leaked from a Wuhan lab. The lab leak became intertwined with Trump, foreign policy and the right. Deigin says Trump weighing in "poisoned" the discussion.

    But Segreto says she's motivated by trying to prevent the next pandemic. "I hope my daughter will understand me one day," she says.


    Anonymous threads

    Spend long enough in the Twitterverse looking into the lab origins debate, and you'll start to see a few familiar profiles. The most prolific appears to be helmed by a one-eyed, cartoon lab monkey: Twitter user @BillyBostickson.


    Bostickson, whose profile picture shows the aforementioned monocular primate, says they have been using a pseudonym for 10 years for professional reasons in "a country with vicious state subversion laws." Since February, they've been working 15-hour days, spending a majority of their time neck-deep in SARS-CoV-2 research. "I feel burnt out," they recently tweeted.


    Bostickson conceived and named Drastic, was one of the first people to bring members together in early 2020, and often collates the team's findings and outstanding questions in extensive Twitter threads. Before 2020, Bostickson says they hardly knew how to even compose a thread on the site, but the social media network has become invaluable. "Twitter serves as a very intuitive searchable database," they say.


    Since early 2020, Drastic has swelled to 28 members. While Bostickson and others have organized the group and built a website, there's no overarching, obvious hierarchy. Members work in subgroups on specific questions related to the origins of SARS-CoV-2 but there are "very few rules," according to Gilles Demaneuf, a New Zealand-based data scientist who is part of the group. "I think the only rule we have is to respect people, and we're not pressing people to tell us who they are," he notes.


    About half of the members prefer to remain anonymous, citing safety concerns, fear of losing their jobs and a constant stream of hacking attempts, according to Demaneuf. Drastic is only interested in telling the public enough about themselves to convince people they're "not a bunch of wackos hiding behind the internet," he says.


    Even as Drastic has rattled cages and unearthed a trail of obfuscation, their heavy-handed approach hasn't always been received positively.

    But working under pseudonyms has allowed for mudslinging and vitriol to fly. "It's nasty because people hide behind anonymity," says Mary-Louise McLaws, an epidemiologist from the University of New South Wales and WHO adviser. You don't have to search for very long to run into Drastic members clashing with prominent virologists. Many members have been blocked by those who have vocally supported a natural origin of SARS-CoV-2.


    There have been ugly incidents on Twitter, further complicating genuine debate around the origins question.


    Segreto, for instance, was falsely accused of attacking Angela Rasmussen, a virologist at the Georgetown Center for Global Health Science and Security, though this was denied by her former head of department. Rasmussen has stated Segreto has participated in attacks against her online, calling the conduct hurtful and upsetting.


    Holmes, the virologist at the University of Sydney, has collaborated closely with researchers in China and co-authored a highly cited Nature Medicine paper supporting the natural origin theory in March 2020. Bostickson has dubbed him a "Chinese puppet," and others have suggested that Holmes, with researchers working at the Wuhan Institute of Virology including Shi Zhengli, conspired to keep the origins of the pandemic a secret. Holmes has blocked many of the Drastic members on Twitter because member's tweets have descended into personal attacks.

    Members of a WHO-China mission to study the origins of SARS-CoV-2 in Wuhan earlier this year have also come under fire. Much of the venom has been aimed at Peter Daszak, president of nonprofit EcoHealth Alliance, a New York nonprofit that has helped fund research into coronaviruses in China. Daszak's close association with the WIV and its staff was perceived as a conflict of interest during the WHO-China study, and he has been a lightning rod for criticism. "Daszak needs to be charged with crimes against humanity," one Drastic member wrote.


    The abrasive attacks have, at times, overshadowed the team's work.

    While I admire their tenacity, they are very much on the edge from a scientific perspective," says Nikolai Petrovsky, a vaccine developer at Flinders University in Australia. "They definitely have a role, but more as detectives sifting through the evidence than as scientific commentators."


    New threads

    The trouble with investigating the origins of COVID-19 is often not what is said, but what is unsaid.


    Drastic's discoveries don't provide definitive evidence of a lab leak and don't prove any deliberate malfeasance on behalf of the Wuhan Institute of Virology or its collaborators, but they do highlight important holes in the story. At the very least, those holes reveal a problematic lack of transparency, but at worst they're indicative of a coverup, potentially implicating researchers in China and abroad.


    On the other hand, many virologists point to Wuhan's wet markets as a starting point in the pandemic, but definitive evidence implicating the markets is lacking, too. Especially when it comes to the Huanan Wholesale Seafood Market, once thought to be pandemic Ground Zero. Eyewitness testimony from Chinese citizens and market authorities state that no live animals were sold there, and the data gathered so far has not located SARS-CoV-2 in any animal samples. The implication here, then, is that citizens and market officials must be obscuring the truth.


    The only way to resolve these issues is to gather more evidence. Drastic has been doing what they can with online tools and databases for over a year. But there is now a chorus of voices asking for an independent investigation to occur.


    On March 5, a group of scientists and researchers, in collaboration with some Drastic members including Demaneuf and Segreto, published an open letter in The Wall Street Journal and French publication Le Monde calling for a "full and unrestricted investigation" into the origins of the coronavirus. They reason that such an investigation can only be carried out by a team independent of the WHO, which did not have the capability to adequately scrutinize a leak when it visited Wuhan in early 2021.

    Some signatories of the open letter have pointed out how important Drastic has been in finding clues and gathering data, including the link between RaTG13, the master's thesis and the miners. Yet even as Drastic has rattled the cages and unearthed a trail of obfuscation, their heavy-handed approach hasn't always been received positively by virologists, other researchers or the WHO.


    A recent 120-page report, released by the joint WHO-China team in Wuhan, found a laboratory origin of the pandemic to be "extremely unlikely." The highly anticipated study offered a number of recommendations for continued work in tracing the origin of the coronavirus, but none describes ongoing investigation of a lab leak.


    It made no reference to the sick miners, except in an annexed section detailing a visit to the WIV, and didn't provide raw data from the missing databases Drastic has called for. Some members expressed their disappointment in the report, others suggested it was "doctored." They weren't alone. On the day of the report's release, 14 countries, including the US, the UK and Australia, published a statement voicing concerns about a lack of access to complete, original data and samples in Wuhan.


    The highly politicized debate and lack of definitive evidence surrounding the origins of SARS-CoV-2 suggests we're still far from solving the puzzle. But in just over a year, a motley group of strangers have come together and helped shift the narrative -- if only slightly. "Working together we have been able to change the idea of a lab leak from conspiracy to a real possibility," says Segreto.


    It was once taboo to even mention an accidental leak. In March, once the WHO-China mission was complete, Tedros Adhanom Ghebreyesus, the WHO's director general, said that "all hypotheses remain on the table."

    Do we ever get an answer?" Deigin asks. "I hope, eventually, we do

    • Official Post

    Good story. In the old days, a journalists job was to root out the truth. They kept the corporations, organizations, and governments somewhat honest. Nowadays, more often than not, they play a role in protecting, and covering for whatever the official narrative is.


    That leaves it up to the new seekers of the truth, such as this internet sleuthing group, to fill the void. Unfortunately, big tech does not always make their job easy when their mission does not align with BT's agenda.

  • The researchers claimed they found the rare blood clotting at a rate of four out of a million people receiving the vaccines from drug company Pfizer and biotech Moderna, but Pfizer disputed that claim. In a statement, Pfizer said its own review of safety data after over 200 million doses have been administered has found no evidence to conclude that arterial or venous thromboembolic events being investigated in the Johnson & Johnson vaccine are a risk associated with its Covid-19 vaccine.

    The role Pfizer plays is the ugliest so far we know. between 20-50 people /Million jabs die directly from their vaccines. The larger part from CoV-19 induced by the jab weakened immune system. For classic vaccines this is 1-2 at most.

    There are two realities: The one Pfizer buys and the one Pfizer pays for (J&J, Astra)

    Holmes, the virologist at the University of Sydney, has collaborated closely with researchers in China and co-authored a highly cited Nature Medicine paper supporting the natural origin theory in March 2020.

    Such papers are the most ugly misconduct of a researcher. It is more than obvious that with 4% genetic difference = 1200 mutations that CoV-19 no way can be natural as some mutation steps would be stopping proliferation. Thus there is not even the slightest chance for a natural origin. Accepting money to spread professional lies is what discredits the whole science.


    Fact is: The miners virus has provided the base for further genetic engineering: And finally, may be, we will get a vaccine for AIDS thanks too the AIDS add-ons for the ACE-2 receptor...

    Did anybody getting the Pfizer jab afterwards do an ADIS test? Could be a surprise....

  • Only in clinical trials no out patient treatment

    Again, and again, and again, let me point out that it is use, and the use of it is entirely at the doctor's discretion. That is what the FDA website says. I do not know where you are getting your information but I am 100% certain that what the FDA says on its own website about its own policies is correct.

  • Good story. In the old days, a journalists job was to root out the truth. They kept the corporations, organizations, and governments somewhat honest. Nowadays, more often than not, they play a role in protecting, and covering for whatever the official narrative is.

    Why do you think journalists rooted out the truth in the good old days? I know why. I knew many journalists in the good old days and in the present day. They did it for money. It was their job, and it was lucrative. Scandal sells. Stories about governments and big corporations abusing power sells. Bad news sells. Anger and controversy sell. As one reporter put it, "news is what makes someone, somewhere, very angry." That is true now. It was true in the 19th century, and 2000 years ago, and for all of history. Newspapers are no more the lapdogs of the powerful today than they ever were. Because the ones that are lapdogs don't sell. No one wants to read anodyne support for the establishment. The establishment publishes any amount of that itself, in press releases that no one reads.


    Your assertion is a romanticized view of things.

    • Official Post

    Again, and again, and again, let me point out that it is use, and the use of it is entirely at the doctor's discretion. That is what the FDA website says. I do not know where you are getting your information but I am 100% certain that what the FDA says on its own website about its own policies is correct.

    Yes, it is at their discretion to administer drugs "off-label", but if they choose to do so, it comes with great risk to their livelihood. Especially so in this, the most politcized pandemic in history, where harmless drugs that show promise are demonized. Most doctors simply are not willing to take the chance.


    In most cases, the decision is not even theirs -as you naively suggest, and I have explained to you before. They have their Hospital Medical Staffs, Hospital Administrators, malpractice insurer, and health insurers they have to get approval from first.That is a hurdle too high for even the most stubborn to overcome.

  • odd stiff

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  • save Bill Gates next mega-plans nothing out of place here



    --- the odd lot are the sheep

    - the sheep who dont' want to look at facts, a year into lockdowns -- baaing baaing -- afraid but resolute they are not afraid

    - afraid of God, but treat the abusive govt like a God

    - the sheep who consider themselves scientists but self-edit

    - and worst go around and play policeman on what is allowed or not allowed to be discussed -- we know some of the designated assignments on this board

  • Again, and again, and again, let me point out that it is use, and the use of it is entirely at the doctor's discretion. That is what the FDA website says. I do not know where you are getting your information but I am 100% certain that what the FDA says on its own website about its own policies is correct.

    From the FDA website


    Why You Should Not Use Ivermectin to Treat or Prevent COVID-19

    https://www.fda.gov/consumers/…treat-or-prevent-covid-19


    COVID-19. We’ve been living with it for what sometimes seems like forever. Given the number of deaths that have occurred from the disease, it’s perhaps not surprising that some consumers are looking at unconventional treatments, not approved or authorized by the Food and Drug Administration (FDA).


    Though this is understandable, please beware. The FDA’s job is to carefully evaluate the scientific data on a drug to be sure that it is both safe and effective for a particular use, and then to decide whether or not to approve it. Using any treatment for COVID-19 that’s not approved or authorized by the FDA, unless part of a clinical trial, can cause serious harm.


    There seems to be a growing interest in a drug called ivermectin to treat humans with COVID-19. Ivermectin is often used in the U.S. to treat or prevent parasites in animals. The FDA has received multiple reports of patients who have required medical support and been hospitalized after self-medicating with ivermectin intended for horses.


    Here’s What You Need to Know about Ivermectin

    FDA has not approved ivermectin for use in treating or preventing COVID-19 in humans. Ivermectin tablets are approved at very specific doses for some parasitic worms, and there are topical (on the skin) formulations for head lice and skin conditions like rosacea. Ivermectin is not an anti-viral (a drug for treating viruses).

    Taking large doses of this drug is dangerous and can cause serious harm.

    If you have a prescription for ivermectin for an FDA-approved use, get it from a legitimate source and take it exactly as prescribed.

    Never use medications intended for animals on yourself. Ivermectin preparations for animals are very different from those approved for humans.

    What is Ivermectin and How is it Used?

    Ivermectin tablets are approved by the FDA to treat people with intestinal strongyloidiasis and onchocerciasis, two conditions caused by parasitic worms. In addition, some topical (on the skin) forms of ivermectin are approved to treat external parasites like head lice and for skin conditions such as rosacea.


    Some forms of ivermectin are used in animals to prevent heartworm disease and certain internal and external parasites. It’s important to note that these products are different from the ones for people, and safe when used as prescribed for animals, only.


    When Can Taking Ivermectin Be Unsafe?

    The FDA has not reviewed data to support use of ivermectin in COVID-19 patients to treat or to prevent COVID-19; however, some initial research is underway. Taking a drug for an unapproved use can be very dangerous. This is true of ivermectin, too.


    There’s a lot of misinformation around, and you may have heard that it’s okay to take large doses of ivermectin. That is wrong.


    Even the levels of ivermectin for approved uses can interact with other medications, like blood-thinners. You can also overdose on ivermectin, which can cause nausea, vomiting, diarrhea, hypotension (low blood pressure), allergic reactions (itching and hives), dizziness, ataxia (problems with balance), seizures, coma and even death.


    Ivermectin Products for Animals Are Different from Ivermectin Products for People

    For one thing, animal drugs are often highly concentrated because they are used for large animals like horses and cows, which can weigh a lot more than we do—a ton or more. Such high doses can be highly toxic in humans.


    Moreover, FDA reviews drugs not just for safety and effectiveness of the active ingredients, but also for the inactive ingredients. Many inactive ingredients found in animal products aren’t evaluated for use in people. Or they are included in much greater quantity than those used in people. In some cases, we don’t know how those inactive ingredients will affect how ivermectin is absorbed in the human body.


    Meanwhile, effective ways to limit the spread of COVID-19 continue to be to wear your mask, stay at least 6 feet from others who don’t live with you, wash hands frequently, and avoid crowds.



    This statement effectively blocks doctors from prescribing ivermectin opening a direct route for civil matters and loss of license.

  • Ivermectin or Fluvoxamine for Outpatient Treatment of COVID-19


    Hello. I'm Chuck Vega, a clinical professor of family medicine from the University of California, Irvine, School of Medicine. Today I'll be speaking about some recent trials among outpatients with drugs repurposed for COVID-19 therapy.


    We've all been looking for better therapeutic options for COVID-19, particularly in the outpatient realm, where most of our patients with the infection are being treated. So I was intrigued by the use of a couple of particular agents: ivermectin and fluvoxamine. These agents have captured our consciousness and our imaginations, and they have been used fairly frequently in both the inpatient and outpatient settings for the treatment of COVID-19. But what's the evidence for the use of these agents?


    Ivermectin

    Ivermectin is an antiparasitic agent, typically used for Strongyloides infections, but it also has in vitro antiviral actions. The question is whether we can get the levels of ivermectin in vivo up to the point where they can reduce viral replication. There's some research that supports the use of ivermectin in COVID-19 that says yes, this may be the case. We can actually make this drug effective.


    A retrospective review of 280 patients hospitalized with COVID-19 at four Florida facilities looked at patients who had received ivermectin. This study was done earlier in the pandemic; most of the patients received hydroxychloroquine, which we wouldn't use now. But it was a fairly sick group of patients with a median age of 56 years, and 55% of the cohort was Black. One fourth had severe pulmonary disease.


    Comparing patients who received ivermectin with those who received usual care, there was no difference in terms of length of hospital stay or rates of extubation, but they found a significant and profound difference in mortality risk — the odds ratio was 0.27 in the ivermectin group. Moreover, folks with more severe illness were more likely to benefit from ivermectin therapy.


    In addition, there is an unpublished, randomized controlled trial in 180 hospitalized patients that similarly found not only a reduced risk for mortality associated with ivermectin, but also shorter length of hospital stay. So, there's some smoke there suggesting that ivermectin might be effective, particularly for inpatients with COVID-19

    The only randomized controlled trial of ivermectin treatment for COVID-19 was done at a single site in Colombia, including 400 patients with mild symptoms of COVID-19 of less than 7 days' duration. They were randomized to receive ivermectin, 300 µg/kg for 5 days, or placebo. They had trouble matching placebo at the outset of study because ivermectin has a certain smell and taste. But they overcame that to a certain degree because only one person per household was allowed to participate in the study until they received placebo. So patients sharing a household couldn't compare the taste or feel of the treatment they were taking, giving clues as to who was receiving ivermectin and who was receiving placebo.


    In this randomized study, the median age of the cohort was 37 years, 58% were women, 79% had a comorbidity, and 58% were treated at home. Overall, they found no difference comparing ivermectin and placebo. The average time to resolution of symptoms was 10 days in the ivermectin group and 12 days in the placebo group. The findings were similar when looking at clinical deterioration and care escalation (including hospital admission); these were fairly rare, less than 5% overall, with no difference between the ivermectin and placebo groups.

    To summarize the evidence for ivermectin, there is a negative randomized controlled trial of ivermectin in patients with mild to moderate COVID-19 infection, and some weak observational data suggesting that ivermectin may be effective for patients who are hospitalized with COVID-19. Overall, however, there is no indication that we should be routinely using ivermectin for COVID-19 at this point. And it's worth noting that the US Food and Drug Administration (FDA), the World Health Organization (WHO), and even the drug manufacturer have all recommended against the use of ivermectin in COVID-19.


    Fluvoxamine

    The other agent I want to mention is fluvoxamine. This is a selective serotonin reuptake inhibitor that is used for depression. It's cheap and well tolerated, so it could have broad application. It does have some cytochrome p450 interaction, which is always something to be concerned about, but it doesn't appear to prolong the QT interval. Also, it has some effects in endoplasmic reticulum in terms of reducing cytokine production. The question is whether this drug could potentially help with the pathology of COVID-19, which involves an excess of inflammation.


    A cohort study was completed at a California worksite where there was an outbreak of COVID-19. A broad group of workers were tested for SARS-CoV-2. Those who were positive were offered fluvoxamine (either a 50-mg or 100-mg loading dose, followed by 50 mg twice daily for 14 days) or usual care (observation group).


    There were 113 positive tests, and half of these positive cases were asymptomatic. Only 65 participants opted to receive fluvoxamine, and 48 declined. Those who got fluvoxamine tended to be more symptomatic. They also had higher rates of diabetes. Fluvoxamine was associated with better outcomes in this study in terms of rates of hospitalization (0% in the fluvoxamine group and 12.5% in the observation group) and persistence of symptoms (none of the fluvoxamine group and 60% of the observation group). This wasn't a methodologically rigorous trial, but it still demonstrates some positive results for fluvoxamine.


    A randomized controlled trial of fluvoxamine, conducted exclusively in telehealth patients, has been published as well. It's interesting because it reflects how we take care of patients with COVID-19. Most of the study patients had mild COVID-19, with symptoms less than 7 days' duration. All had an oxygen saturation above 91%. They were randomized either to fluvoxamine (100 mg three times daily) or placebo for 15 days. The outcomes they were looking at were hospitalization rates, shortness of breath, a need for supplemental oxygen, or falling oxygen saturations (< 92%).


    Among the 152 adults who were randomized, the median age was 46 years, 76% were women, 25% were Black, and 76% completed the trial, with 24% dropping out. But there was a significant improvement in the fluvoxamine vs the placebo group in the broad outcome of clinical deterioration (0% in the fluvoxamine group and 8.3% in the placebo group). There was no difference in the rate of emergency department visits, but fluvoxamine was associated with a lower rate of side effects vs placebo. This study had some limitations. It was done at one geographic location, and it looked at a small number of outcomes. One in 5 patients dropped out by day 15.


    Here are my takeaways from the clinical data on these two drugs for the treatment of COVID-19. There's some weak evidence that ivermectin reduces mortality in patients hospitalized with COVID-19, but among outpatients, the trial with ivermectin failed to demonstrate that it was effective for improving symptoms or preventing clinical deterioration.


    Fluvoxamine has some support from a randomized, controlled trial among outpatients with COVID-19. But the authors of that study concluded that their results were more hypothesis-generating than a clear call that this is an effective treatment. More studies need to be done with fluvoxamine. But it is intriguing, and I look forward to seeing those studies and hopefully sharing the findings. Thanks for your attention, and be well.


    Charles Vega is a clinical professor of family medicine at UC Irvine and also serves as the UCI School of Medicine assistant dean for culture and community education. He focuses on medical education with an intent to resolve health disparities.

  • COVID-19 variants FAQ: How did the U.K., South Africa and Brazil variants emerge? Are they more contagious? How does a virus mutate? Could there be a super-variant that evades vaccines?


    https://theconversation.com/am…at-evades-vaccines-159032


    More and more countries around the world are struggling with a new wave of infections, with an alarming increase in COVID-19 cases. Mostly these new surges are attributed to variants of SARS-CoV-2.


    In lay terms, a variant refers to a virus genetically distinct from its original strain. The emergence of variants in the microbial world is nothing new, just think of “superbugs” such as MRSA (methicillin-resistant Staphylococcus aureus), which is resistant to almost all the existing antibiotics.


    How did the U.K., South Africa and Brazil variants emerge?

    Genetic transformation of a virus occurs by mutation. Mutations emerge naturally in the microbial world. They are mistakes in the genetic code caused by copying processes in the cell. These mistakes are exploited by the virus to survive and establish itself, especially under adverse conditions.


    Curiously, viruses mutate at a much higher rate than other micro-organisms. Often mistakes in the genetic code come and go without leaving any traces, but in a few instances, they are selected when they offer the microbe a growth (or infection) advantage.


    In the case of SARS-CoV-2, several mutations have been selected, meaning they are propagated to the next generation of viruses. They are selected for efficient access to host cells — fewer viruses are needed to infect the host — and effective evasion of the neutralizing antibodies of the immune system, meaning they are able to dodge immune response so they can circulate longer in the host, providing more opportunity to infect other cells.


    However, human intervention — such as the use of certain treatments like convalescent plasma or monoclonal treatment — can drive virus evolution in much the same way that antibiotic use drives the evolution of bacterial superbugs.


    How seriously should we take SARS-CoV-2 variants?


    The World Health Organization (WHO) categorizes virus variants into two different groups: variant of concern (VOC) and variant of interest (VOI). VOCs represent those variants that are linked to the rise of new infection waves in many countries, including the recent surges in Canada and United States.


    Here in Canada, the B.1.1.7 variant, which emerged in the United Kingdom in September 2020, is becoming the dominant variant.


    The other VOCs — such as B.1.351, first identified in South Africa, and P.1, first identified in Brazil — are being identified more often and have been responsible for several outbreaks in Canada.


    There is evidence, some of which has not yet been peer reviewed, that VOCs are associated with higher virulence than the coronavirus that originated in Wuhan, China: higher transmissibility, possible higher disease severity and, in the case of B.1.351, an increased ability to evade neutralizing antibodies.


    These attributes of VOCs have translated into higher hospitalizations of younger people and an increase in deaths across all age groups in Canada.


    VOIs are on the radars of public health agencies for their impact on virus transmission, the severity of disease and vaccine effectiveness.


    How does mutation change how a virus works?

    The genetic code of a virus provides instructions to make its proteins: strings of amino acids in defined sequences. Mutation can lead to amino acid substitution or deletion in the protein. The attention of the scientific community is focused on the amino acid substitutions that affect the SARS-CoV-2 spike protein, the protein that gives the virus its crown-like shape.

    The spike protein is the key that provides access to human cells via the human ACE-2 protein (the lock), and as such is the target of the currently approved COVID-19 vaccines. Research that has yet to be peer reviewed shows two ways in which changes to the amino acid sequence of the spike protein may affect its interaction with human cells:


    They can enhance the spike protein’s interaction with ACE-2, providing efficient access to host cells.

    They can decrease the spike protein’s interaction with neutralizing antibodies, helping it evade an immune system response long enough to infect other cells.

    Proteins can be thought of as microscopic Lego structures, with amino acids behaving as Lego pieces and held together by a single thread. However, protein structures are much more flexible than Lego structures (think of Lego pieces made of Jell-O), with the amino acids able to form transient bonds with other amino acids close to them as needed for structural stability and recognizing other structures.


    The spike protein’s structural flexibility allows it to sample the space inside the lock (ACE-2) to enable recognition of the key, but also to find the optimum key-shape for that lock. It is the latter function that is optimized through mutation: the best key-shape will open the lock faster and more easily.


    Could mutation lead to a super-variant that can evade all vaccines?

    Many VOCs and VOIs have been identified around the world, and more variants get reported daily (about one million variants have been recorded to date). Should we be afraid of the emergence of a super-variant, which is highly virulent and can overpower all current vaccines and any others in the future?


    The three current VOCs that have taken hold in many countries carry several amino acid substitutions in their spike proteins. Because of the spike protein’s crucial role in entering cells, all of the COVID-19 vaccines currently available work by targeting the spike protein.


    Peculiarly, a few of the amino acid substitutions in the spike protein are common to the three current VOCs and are considered to drive their dominance over other variants. Research that has yet to be peer reviewed shows the substitutions N501Y (asparagine to tyrosine) and D614G (aspartate to glycine) are common to all three, while E484K (glutamate to lysine) is common to B.1.351 and P.1.


    The E484K substitution is believed to be responsible for antibody evasion, and N501Y and D614G are thought to drive the higher transmissibility of these variants. (The CDC website offers more information on the attributes of the variants.)

    It is curious that the common amino acid substitutions identified among VOCs emerged independently and in different parts of the globe. There are, in fact, 20 different amino acids provided by the host cell, all of which have an equal opportunity to substitute an amino acid in the protein through mutation. Yet, remarkably, these three VOCs evolved to acquire some of the same amino acid substitutions!


    This phenomenon is referred to in biology as convergence evolution: when the same feature evolves independently. This means that the selected amino acids offer a unique property that makes the virus “fitter.”


    The spike protein has an important function: it has to unlock access to the host cell, but it is also the target of neutralizing antibodies, which the virus has to prevent from latching onto the protein in order to evade the immune system. Both these functions rely on the same part of the protein: the receptor binding domain (RBD).

    Enhancement of one of these two functions can diminish the other function. That means a compromise has to be reached. The fact that the same substitutions arose independently in different variants is an indication that the spike proteins in these variants have been optimized, and may not gain any further advantages.


    Based on this, emergence of a super-variant seems unlikely, because these two functions — unlocking the host cell and evading the immune system — will always be in competition with each other, so neither will be able to achieve perfect efficiency.


    However, never underestimate the force of evolution when there is a fertile playing field. We must adhere to public health measures, such as social distancing and masks, to mitigate the spread of the virus and limit the number of hosts that the virus can infect, for as long as most of the population remains unvaccinated.

  • Bad news sells. Anger and controversy sell.

    No longer. All journals/news channels are controlled by the FM/R/J mafia and certainly do not report about something what damages their grand masters... Pharma is owned & controlled the FM/R/J mafia.

    There’s a lot of misinformation around, and you may have heard that it’s okay to take large doses of ivermectin. That is wrong.

    The FM/R/J mafia bribed FDA plays a very ugly role see below

    Ivermectin Products for Animals Are Different from Ivermectin Products for People

    For one thing, animal drugs are often highly concentrated because they are used for large animals like horses and cows, which can weigh a lot more than we do—a ton or more. Such high doses can be highly toxic in humans.

    Most animal Ivermectin products are 100% human compatible. Just read the package leaflet.

    Here are my takeaways from the clinical data on these two drugs for the treatment of COVID-19. There's some weak evidence that ivermectin reduces mortality in patients hospitalized with COVID-19, but among outpatients, the trial with ivermectin failed to demonstrate that it was effective for improving symptoms or preventing clinical deterioration.

    This is an old study reported again and again with a fairly dilettante setup. 2 Days is to days shorter and not no effect. This is the same as seen in other early ivermectin studies.

    It all depends whether you give it to people just tested positive or to people with real symptoms. In the first case the study is nonsense.

    I tell everybody to take ivermectin only after real CoV-19 symptoms, where you need to have 2 at least! 99% of the people can handle CoV-19 without problems and drugs! So a 2 days shorter effect is huge! It was 1 day for Tamiflu and only given on first day of symptoms...Or to say it clear Tamiflu is useless. Just sold as a pharma porono.

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