Covid-19 News

  • Half Of Los Angeles Covid-19 Samples Analyzed Show Mutant “West Coast Variant,” As Region Runs Out Of First-Dose Vaccine Appointments…coast-variant-1234689970/

    As for the South African variant, also more transmissible and possibly also vaccine resistant, “Assume it’s here,” said Ferrer. Then she dropped the real bombshell.

    “At least 50% of our samples have shown the West Coast variant,” said Ferrer, before hedging that “more research needs to be done.”

    Last week, California’s top health official revealed that over 1,000 cases of the West Coast variant had been discovered in the state. California Governor Gavin Newsom said on Monday that that number had risen to 1,200. That’s a 20% increase in less than a week.

    Such increases could make the effort to vaccinate Los Angeles residents even more critical. The region has ramped up its vaccination infrastructure considerably in the past few weeks, but a bottleneck of vaccine supplies is hampering the effort.

  • Coronavirus can mutate in every single person it infects, research into Kent strain indicates…every-single-19821983.amp

    Covid-19 can change and mutate in every single person it infects.

    The virus has the potential to become deadlier and more infectious - and even more resistant to the vaccines that are currently our best hope of getting out of the pandemic.

    Changes to Sars-CoV-2 happen slowly or fail to have any material impact in the vast majority of cases.

    But in some cases, the virus can "hit the jackpot" and change to the point where is is able to evolve into a new, more transmittable form, Wales Online reports.

    Scientists believe that this has happened with the Kent variant of the virus which they fear could well become the world's most dominant strain.

    And one theory is that a single person in the English county was infected with the Sars-CoV-2 virus for so long that it was able to develop "special features".

    The distinctiveness of this variant pointed to two likely origins: either the virus had mutated abroad and only been detected once it entered the UK; or it emerged through something called recombination where viruses swap parts of their genome with other viruses, or many of the changes had happened within a single person.

    In an article on Wired UK, Matt Reynolds reported that this theory that all the changes happened in one person is what many scientists believe is most likely. While most coronaviruses tend to pick up one or two mutations a month, this had 17 changes.

    He cited work by Ravi Gupta, a professor of clinical microbiology at the University of Cambridge, who studied the evolution of Sars-CoV-2 in a cancer patient who was infected with the virus for 102 days before dying.

    After the man was treated with blood plasma from a recovered patient, the genetic makeup of the virus began to change. By day 82, viruses with one specific mutation were dominant. The same mutation was found in other chronically infected patients. In Prof Gupta's patient, the Sars-Cov-2 virus kept changing and being overtaken by new mutations.

    Prof Gupta believes this is the most likely explanation for the Kent mutation. When the virus enters the body of someone whose immune system cannot fight it, it finds a way around other defences such as the blood plasma and evolves quickly.

  • A good optimistic Vacine interview

    with DR Paul Offit.

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  • The vaccination rate in the U.S. is improving. It is now ~1.6 million per day. See:…tates-distribution-doses/

    The distribution speed is also improving. That is, vaccines distributed are being administered more quickly; fewer are left in storage. See:…e-doses-distribution.html

    After a Sluggish Start, Vaccine Rollout Is Improving in Every State

    . . . [H]ealth officials say that while current vaccine supply levels still limit how many vaccines they can administer, states are becoming more efficient at immunizing people as shipments arrive.

    The on-line and telephone reservations systems in all 50 states are still a nightmare. This leaves many elderly people unable to reserve a vaccination. Two programmers independently wrote quick-and-dirty programs to cut through this mess and simplify the reservation process. One of the programmers did this in a week while taking care of a newborn baby! She must be an awesome programmer, but also, it couldn't be that difficult, could it? Uncle Sam supposedly paid a ton of money to a software consulting company to do this but it did not work out.…ine-appointments/35438098

    Here is her website, which only works for Massachusetts, alas:

  • China refuses to give WHO raw data on early COVID-19 cases -WSJ…9-cases-wsj-idUSFWN2KI17H

    WASHINGTON, Feb 12 (Reuters) - China has refused to give the World Health Organization raw data on its early COVID-19 cases, the Wall Street Journal reported on Friday, citing WHO investigators who it said described heated exchanges over lack of detail.

    The world health agency officials said raw, personalized data could help them determine how and when the coronavirus first spread in China, the newspaper said.

  • Could this kind of so far unexpected fast virus replications / mutations within ONE single "transmitter" a potential alternative answer to some interpretations this virus could be human-engineered only because naturally there is no possibilty at all this can happen in such a short time within humans?

    In utopia Bats have been treated with immune suppresiva for one year. The only question is : Who did eat the bat?

  • Covid-19: Patient in France critical after reinfection with S.African variant…=en-US&gl=US&ceid=US%3Aen

    The 58-year-old man had a history of asthma and initially tested positive for Covid-19 in September when he presented to medical staff with a fever and shortness of breath.

    The symptoms persisted only for a few days, and the man tested negative for Covid-19 twice in December 2020.

    However, he was admitted to hospital in January and diagnosed with the South African variant.

    The patient's condition worsened, and he is currently in a "critical condition" on a ventilator.

    "This is, to our knowledge, the first description of reinfection with the South African (variant) causing severe Covid-19, four months after a first mild infection," said authors of a study published this week in the journal Clinical Infectious Diseases.

    More infectious

    The 501Y.V2 coronavirus variant emerged late last year in South Africa and immediately provoked alarm among disease specialists.

    It has eight key mutations, one of which affects the virus' spike protein, making it more effective at binding to human cells and therefore more infectious.

    Vaccine manufacturers Pfizer/BioNTech and Moderna say their mRNA vaccines retain their effectiveness against the South African variants and another that emerged last year in Britain.

    However a study last week showed that AstraZeneca's vaccine failed to prevent mild and moderate cases of infection of the South African variant.

    "The impact of 501Y.V2 mutations on the effectiveness of vaccines developed based on earlier SARS-CoV-2 strains is still unknown," said the authors of the reinfection study.

  • Coronavirus variant cases have doubled in US since the end of January…=en-US&gl=US&ceid=US%3Aen

    The United States has seen cases of coronavirus variants from South Africa, the United Kingdom and Brazil double since the end of January.

    The Centers for Disease Control and Prevention updated the numbers on Thursday to show 997 reported U.S. cases of the variants. The number of cases reported at the end of January was 471, according to The Associated Press.

    The rise of new variants is a cause of concern given that they are more contagious.

    There are 981 reported cases of the U.K. variant across 37 states. The U.K. variant has been shown to spread more quickly and have higher mortality rates, but it is not clear if that is due to the virus itself or external factors.

  • ‘A very dangerous epoch’: historians try to make sense of Covid…=en-US&gl=US&ceid=US%3Aen

    It was in the first few weeks of 2020, when early reports began filtering through of a mystery virus threatening to spread across the world, that Rob Perks decided to begin collecting.

    As lead curator for oral history at the British Library, Perks’s team routinely gather testimony to be archived for future research. But a comment by a historian who advises the institution stopped him in his tracks.

    “I remember him saying: ‘History will be written Before Covid and After Covid.’ And I thought, he’s got something here. It began to sink in that this was different from anything I’ve ever encountered in my 30-year career at the British Library, and that we should do something about it.”

    For the past year, that has meant gathering interviews with thousands of NHS workers, archiving websites, recording TV and radio channels, and collecting poetry and audio diaries, sometimes with partner organisations. It will build, he hopes, into a national archive of Covid-19 reminiscences, and an “amazing resource” for future researchers.

    It is not just the Covid pandemic that can make these feel like unusually significant times. Populism, Trump’s rise and (perhaps) fall, Brexit, the Black Lives Matter and #MeToo protests, mass movement of refugees, the increased might of both China and India and many other issues have contributed to a sense of humanity having reached a historic moment, all while the climate crisis rages with ever more urgency.

    On the other hand, disease is not new, and societies have always faced crises. So is it really the case that in the future we will regard this as a pivotal moment?

    On the scale of things, this is not a terrible pandemic,” says the historian and author Tom Holland, arguing that Covid will be under control globally within a few years, “and that’s an amazing achievement”. But it may still signal a very important moment, he believes.

    “A lot of people are arguing that these kinds of zoonotic pandemics [originating in other species] are expressive of biodiversity ecosystems coming under uncontrollable stress.

    “And so the question is whether in 100 years, people will look back and see this as being the first of a number of epidemics [caused by] humanity crashing into ecosystems that previously humans were not part of.

    “I suspect that they will, and I feel quite pessimistic about that.”

    Holland – who has written widely about the ancient world, Rome and the influence of Christianity – believes social movements in the west such as BLM are part of a cultural and moral upheaval that began in the 1960s, and which he sees as being as significant as the Protestant Reformation.

    Important as individual movements are, however, Holland warns against taking too parochial a perspective on their global impact, arguing that BLM’s influence, for instance, has been limited to certain countries and that beyond the west “I don’t think it has had any impact at all”.

    It is a caution shared by Vinita Damodaran, a professor of south Asian history and director of the Centre for World Environmental History at the University of Sussex.

    Describing herself as “a global historian who thinks in big waves”, Damodaran says what we are living through is “clearly a period of heightened uncertainty where the old ideologies no longer work” – naming liberalism, colonialism and the free market economy.

    In specific local contexts around the world, she says, small- and large-scale tipping points are being reached, all of which add up to a global sense of crisis, the impact of which, particularly on the environment, is being felt even by those in more prosperous and comfortable societies.

    “No longer is this happening [only] in Haiti, where you could say, right I’ll send them some money. This is a globally interconnected world, and climate change knows no borders.”

    But the problem is not new, she says: “There’s this hubris which comes out of the Enlightenment of the 18th century, that humans in some senses can dominate nature” – and we should not claim to be surprised.

    “There is a price we are paying for intensive farming practices. Covid has not just suddenly sprung upon us. You just have to be a historian to understand this moment.”

    The historian and broadcaster Michael Wood, a professor of public history at the University of Manchester, says: “Everything that is going on at the moment, it seems to me, all links together.”

    History has seen great civilisations in China, India and across Eurasia, “but they’ve not caused these crises that we are living through now, and nor has the African world.

    “You know what happened? Roughly 500 years ago, these small, aggressive maritime powers on the shores of Europe went across the world with their technology and created their empires by sea.

    “And I think what we are seeing now can all be interpreted in the light of the post-imperial [age].”

    Other societies may now be enthusiastic participants, but it was not they who created western industrial capitalism, he argues.

    Wood has changed his mind on the long-term significance of Covid. Six months ago, cycling through a deserted city, “I thought, my God, if London can be emptied like this and everything stopped, this is going to have an amazing impact on our psychology.”

    Now, he is not so sure. The psychological toll on many people has been huge, he acknowledges, but in the main “people get over these things. The Black Death killed in some places half the population of Britain, and they had six more outbreaks between the 1350s and early 1400.”

    His most recent book is about China, and he argues that for all that country’s environmental problems, the scale of the climate crisis is well understood in Beijing given the risks to its society from food and water insecurity.

    “Everything comes back to the climate crisis, because everything is affected by it – the political order, social order, food, water, the migration of people. So we are in a very, very dangerous epoch.”

    And yet interventions can change history; many hope the UN climate change conference in Glasgow later this year, for instance, could offer such an opportunity.

    In that sense, is not history – and the significance or otherwise of this time – in our own hands? “It is totally in our hands,” says Wood.

    “And if you were going to be really hopeful, you’d say this is the moment when we are going to wake up and realise that our true interests on the planet are served by cooperating.

    “These are things that are self-evident, there’s no denying them. What we will do about it is the imponderable.”

  • How ‘killer’ T cells could boost COVID immunity in face of new variants

    In the race against emerging coronavirus variants, researchers are looking beyond antibodies for clues to lasting protection from COVID-19

    Concerns about coronavirus variants that might be partially resistant to antibody defences have spurred renewed interest in other immune responses that protect against viruses. In particular, scientists are hopeful that T cells — a group of immune cells that can target and destroy virus-infected cells — could provide some immunity to COVID-19, even if antibodies become less effective at fighting the disease.

    Researchers are now picking apart the available data, looking for signs that T cells could help to maintain lasting immunity.

    “We know the antibodies are likely less effective, but maybe the T cells can save us,” says Daina Graybosch, a biotechnology analyst at investment bank SVB Leerink in New York City. “It makes sense biologically. We don’t have the data, but we can hope.”.e.”.

    Coronavirus vaccine development has largely focused on antibodies, and for good reason, says immunologist Alessandro Sette at the La Jolla Institute for Immunology in California. Antibodies — particularly those that bind to crucial viral proteins and block infection — can hold the key to ‘sterilizing immunity’, which not only reduces the severity of an illness, but prevents infection altogether.

    That level of protection is considered the gold standard, but typically it requires large numbers of antibodies, says Sette. “That is great if that can be achieved, but it’s not necessarily always the case,” he says.

    Killer cells

    Alongside antibodies, the immune system produces a battalion of T cells that can target viruses. Some of these, known as killer T cells (or CD8+ T cells), seek out and destroy cells that are infected with the virus. Others, called helper T cells (or CD4+ T cells) are important for various immune functions, including stimulating the production of antibodies and killer T cells.

    T cells do not prevent infection, because they kick into action only after a virus has infiltrated the body. But they are important for clearing an infection that has already started. In the case of COVID-19, killer T cells could mean the difference between a mild infection and a severe one that requires hospital treatment, says Annika Karlsson, an immunologist at the Karolinska Institute in Stockholm. “If they are able to kill the virus-infected cells before they spread from the upper respiratory tract, it will influence how sick you feel,” she says. They could also reduce transmission by restricting the amount of virus circulating in an infected person, meaning that the person sheds fewer virus particles into the community.

    T cells could also be more resistant than antibodies to threats posed by emerging variants. Studies by Sette and his colleagues have shown that people who have been infected with SARS-CoV-2 typically generate T cells that target at least 15–20 different fragments of coronavirus proteins1. But which protein snippets are used as targets can vary widely from person to person, meaning that a population will generate a large variety of T cells that could snare a virus. “That makes it very hard for the virus to mutate to escape cell recognition,” says Sette, “unlike the situation for antibodies.”

    So when laboratory tests showed that the 501Y.V2 variant identified in South Africa (also called B.1.351) is partially resistant to antibodies raised against previous coronavirus variants, researchers wondered whether T cells could be less vulnerable to its mutations.

    Early results suggest that this might be the case. In a preprint published on 9 February, researchers found that most T-cell responses to coronavirus vaccination or previous infection do not target regions that were mutated in two recently discovered variants, including 501Y.V22. Sette says that his group also has preliminary evidence that the vast majority of T-cell responses are unlikely to be affected by the mutations.

    If T cells remain active against the 501Y.V2 variant, they might protect against severe disease, says immunologist John Wherry at the University of Pennsylvania in Philadelphia. But it is hard to know from the data available thus far, he cautions. “We’re trying to infer a lot of scientific and mechanistic information from data that doesn’t really have it to give,” he says. “We’re kind of putting things together and building a bridge across these big gaps.”

  • Rise of variants sparks push for all-in-one COVID-19 vaccines

    Dangerous coronavirus variants identified in Africa, Europe and South America…-vaccines-1.1613201716480

    Just weeks into the rollout of vaccines to combat COVID-19, researchers are shifting their focus to a new class of potential shots to take on the threat posed by fast-spreading mutations.

    Dangerous coronavirus variants identified in Africa, Europe and South America are carpeting the globe, pushing scientists in the U.K. and elsewhere to target multiple versions of the pathogen in a single shot and perhaps head off more lethal foes that may emerge.

    A variant that arose in South Africa has already shown itself capable of partially evading defenses raised by several vaccines. The country paused rolling out a shot from AstraZeneca Plc because it offered minimal protection against mild to moderate illness cause by the mutant, called B.1.351. With a spreading virus comes an increased risk of more alarming mutations.

    "We cannot be complacent that we've got the vaccines we need and it's just a matter of time to ending the pandemic - it's not," said Richard Hatchett, chief executive officer of the Coalition for Epidemic Preparedness Innovations, which has worked to accelerate development of COVID inoculations. "We're in a race with the virus and we've got to get ahead of it."

    Britain snapped up huge COVID vaccine supplies early and became the first Western country to approve a shot. Now it's seeking to catch up with the outbreak and sustain its momentum in the next phase of the crisis, a difficult task as the virus runs rampant.

    Blunted optimism

    The government last week announced a pact with CureVac NV to tackle variants, pairing artificial intelligence to predict future mutations with messenger RNA technology that can rapidly generate new vaccines. After a once-promising partnership with Sichuan Clover Biopharmaceuticals Inc. ended and separate trials with Sanofi ran into delays, London-based GlaxoSmithKline Plc is also working with CureVac on mutant-quelling vaccines.

    Meanwhile, countries across the European Union, which has lagged the U.S. and U.K. in immunizations, have raised questions about the bloc's strategy on mutants. At a meeting of ambassadors Wednesday, countries including Malta and Germany urged the European Commission to ensure contracts with manufacturers cover sufficient batches if booster shots are needed, according to a cable seen by Bloomberg.

    The new variants, including the B.1.1.7 lineage that surfaced in southern England, have blunted the optimism that greeted highly-effective mRNA shots from Pfizer Inc. and Moderna Inc. late last year. The companies should be able to quickly redesign their inoculations based on the distinctive spike protein that the coronavirus uses to invade human cells, according to Michael Kinch, a vaccine specialist at Washington University in St. Louis. While scientists have the tools to keep pace, further mutations call for alternative approaches, he said.

    "The bad news with these particular variants, and the reason many of us are nervous, isn't that the vaccines will suddenly not work," Kinch said, "but that they will slowly become obsolete."

    Pfizer, Moderna and Johnson & Johnson have said they're starting work on developing booster shots or other efforts to bolster their vaccines. AstraZeneca and partner Oxford aim to have a tweaked version tailored to new variants available by fall.

    Another strategy involves including a variety of antigens, the molecules in the vaccine that provoke an immune response, Kinch said. Although the spike protein has proven to be a good target, other surface proteins in the virus's envelope and membrane could turn out to be important, too.

    'Almost Job Done'

    "Vaccines based on the spike protein are the first out the door," said Julian Hiscox, a coronavirus specialist and chair of infection and global health at the University of Liverpool. The next round could add the N - or nucleocapsid - protein, whose job is to bind viral RNA, he said. With both S and N proteins, "that's almost job done," he said.

    Traditional methods that use the virus itself in a weakened or inactivated form and provide a broader choice of potential targets - like those used by some Chinese developers including Sinovac Biotech Ltd. - could also play a more significant role, Kinch said.

    CEPI, the Oslo-based group that has funded a number of COVID vaccine programs, has set a goal of developing "strain changes" within 100 days if needed, Hatchett said. Pfizer's partner BioNTech SE has said that if their vaccine turns out to be ineffective against a new strain, they could, in theory, produce an updated shot targeting that variant within six weeks.

    For years, multivalent flu vaccines targeting three or four versions of the pathogen have provided protection against multiple strains circling the globe. Glaxo and CureVac plan to rely on mRNA technology to develop a product that addresses multiple variants in one COVID vaccine. If the work is successful, a vaccine could be ready next year.

  • Did the coronavirus really come from frozen food, as the WHO suggests?…-as-the-who-suggests/amp/

    The idea that the coronavirus was carried inside or on the surface of frozen food, which has been advanced by Chinese state media, could place the source of the virus beyond China, from an animal imported from another country.

    Yet it is far from clear whether the virus could survive in an infectious form via frozen food. “I would say it’s extremely, extremely unlikely the virus would have spread through that type of route,” says Lawrence Young at the University of Warwick, UK, who specialises in human virology.

    The reason why, according to Young, is that SARS-CoV-2 is an enveloped virus, meaning it is covered with a fatty, lipid membrane that it uses to infect human cells. This membrane is very vulnerable to cycles of freezing and thawing, as can happen during the transit and sale of frozen food. Stripped of this envelope, such viruses cannot infect people.

    A review by Jie Han and Zue Zhang at Xi’an Jiaotong University and their colleagues of evidence on spreading the coronavirus via food concluded that “major knowledge gaps exist” on the role that frozen food plays. “Data are lacking on the long-term survival of SARS-CoV-2 under freezing temperatures (-10°C to -20°C) that are frequently encountered on the storage and transport of frozen foods,” the team wrote.

    Just one study, a preprint, has tried to obtain that data. Researchers put the virus into cubes of pork, chicken and salmon, finding no decline in the viral load after 21 days in a lab at refrigeration temperatures of 4°C or at a standard freezing temperature of -20°C. However, it isn’t clear whether the viral load was still infectious to humans, and the experimental parameters may not reflect real-world viral loads or conditions in supply chains.

    The WHO has lost all credibility!

  • Get a dog, treat early and save your life!

    Dogs Can Detect COVID-19 More Accurately Than Tests: Research…sts-research-4418777/amp/

    Dogs are human's best friends for ages. They never fail to put smiles on faces by doing cute little things, whether they are begging for food, or convincing you to take them out for a walk, dogs are always there for their human. Dogs cannot just sniff their treat but also COVID-19. As per new research, trained dogs can detect Coronavirus 94 % of the time. And interestingly they can do it more rapidly and accurately. Also Read - Dogs Can Detect COVID-19 More Accurately Than Tests: Research

    Tommy Dickey from the University of California, Santa Barbara in the US is also part of the research. He said, "The most striking result is that studies have already demonstrated that dogs can identify people who are Covid-19 positive. Not only that, they can do it non-intrusively, more rapidly, and with comparable or possibly better accuracy than our conventional detection tests.

    One dog twice indicated positive results that could not be confirmed. Two weeks later they found that both people who gave those samples had to be hospitalized with Covid," Dickey added. Also Read - As Revenue Losses Mount, Delhi Metro Urges Centre to Allow Trains to Run At Full Seating Capacity

    The magic lies in the canine sense of smell, which gives dogs the ability to detect molecules in tiny concentrations -- "one part in a quadrillion compared with one part in one billion for humans," according to the paper published in the Journal of Osteopathic Medicine.

  • Op-Ed: Don't Let COVID-19 Patients Die With Vitamin D Deficiency

    — We can't wait for perfect evidence

    The U.S. is breaking new records in the number of daily deaths from COVID-19. The breakneck speed with which several vaccines have been developed and deployed is nothing short of breathtaking. Yet we still have to confront the grim prediction that our national death toll will exceed 500,000 Americans before widespread vaccinations can dig us out of this crisis. The response to the pandemic, therefore, should include an effort to aggressively eliminate what is becoming apparent as a morbidity and mortality risk factor in COVID-19 -- vitamin D deficiency.

    For any COVID-19 risk factor, like obesity, hypertension, or diabetes, strong correlational data is sufficient to inform clinical care, as in Surgeon General Luther Terry's 1964 Report on Smoking and Health. This groundbreaking publication, which has saved tens of millions of lives from lung cancer, was based on a causation analysis by an advisory committee. The team reviewed existing data and drew on the work of Sir Austin Bradford Hill and Sir Richard Doll who had examined the increase in lung cancer cases in the U.K. Hill later outlined the standards that were the result of their inquiry, now known as Hill's criteria for causation. He surmised that correlational data can be used to infer causality by satisfying various criteria such as consistency, specificity, temporality, and dose-responsiveness. Vitamin D deficiency, associated with deleterious effects on innate and adaptive immunity, has many small but growing datasets that satisfy all of Hill's criteria as a risk factor for severe COVID-19. And unlike other risk factors, it can be acutely modified.

    Jain and colleagues studied 154 patients who presented to a medical center over 6 weeks. When deaths were evaluated on the basis of vitamin D deficiency (serum 25-OH-D <20 ng/mL), the fatality rate was 21%, compared to only 3% for those with higher levels. More striking was that vitamin D deficiency was found in 97% of severely ill patients who required ICU admission but in only 33% of asymptomatic cases, suggesting that low levels are a necessary component of severe COVID-19. This is one of numerous studies this year establishing the correlation of low vitamin D levels with an aggravated course of COVID-19, as a meta-analysis by Pereira and colleagues reveals.

    Yet to firm up Hill's criteria, some experimental evidence is not only recommended but necessary, and small randomized trials with aggressive vitamin D replenishment have shown positive results. Rastogi and colleagues treated 40 individuals with mild COVID-19 and vitamin D deficiency (25-OH-D <20 ng/mL) with either placebo or 420,000 IU of cholecalciferol (vitamin D3) in a fast-acting nano-emulsion divided over seven days, i.e., 60,000 IU (1,500 μg) per day. The results showed that supplementation helped clear the virus faster -- 63% of the treated patients tested negative for SARS-CoV-2 by the 14th day compared to only 21% of the placebo group. In addition, the treated group showed a decrease in levels of fibrinogen, which is thought to contribute to the higher risk of thrombotic events in COVID-19.

    Castillo's team in Cordoba, Spain, randomized 76 hospitalized COVID-19 patients in a 2:1 ratio to receive either open-label calcifediol or no supplementation, in addition to standard care. The intervention group received 1,064 μg of this fast-acting vitamin D analogue in the first week three times more potent than vitamin D3, followed by 266 μg weekly thereafter. Of the treated patients, only 2% (1 out of 50) needed ICU admission compared to 50% (13 of 26) of the untreated group. In addition, 8% of the untreated patients died, compared to none in the intervention group. Though vitamin D deficiency was not identified on admission, the researchers cite a report that the 25-OH-D levels in Cordoba in wintertime are deficient, averaging 16 ng/mL. Using a study population that skews towards vitamin D deficiency makes this a good study to examine the benefits of aggressively correcting this deficiency in COVID-19. To our knowledge, only one critical care program in the U.S. has adopted a replenishment protocol this aggressive in their treatment of COVID-19.

    There's more evidence pointing in this direction. Using a quasi-experimental approach, Annweiler and colleagues looked at frail, elderly patients hospitalized for COVID-19 in France. The researchers obtained records for those who regularly received bolus vitamin D3 supplementation -- 20,000 to 50,000 IU per month, a common practice in French nursing homes -- and those who did not. Only 10% of those who received regular supplementation progressed to severe COVID-19 compared to 31% of the non-supplemented group. In addition, 14-day mortality rates were only 7% in the supplemented group compared to the same 31% in the non-supplemented group. The researchers also identified a third group of patients -- those who were given a single dose of 80,000 IU of cholecalciferol at the time of their COVID-19 diagnosis. This group fared better than the group that got none, but the outcome did not reach statistical significance, suggesting that the dose might have been too low or came too late.

    We did discover one study awaiting peer-review which failed to show benefits of treating vitamin D deficiency in COVID-19. Researchers administered a single dose (200,000 IU of vitamin D3) to patients ten days after COVID-19 symptoms first appeared. Unlike calcifediol, it can take a week or longer for the body to convert vitamin D3 to its active form. In addition, being fat-soluble, the body competes against adipose tissue to procure the necessary amount, requiring higher doses in obesity (the average BMI in this study was 31.6). Compare the dose given here to the standard protocol to correct vitamin D deficiency in healthy outpatients, who are routinely given a total of 600,000 IU divided over twelve weeks, at 50,000 IU per week.

    Data like this are not new. A 2014 Austrian study of 475 patients showed that supplementation with 540,000 IU of vitamin D3 followed by 90,000 IU per month cut the hospital mortality rate in half for ICU patients with severe vitamin D deficiency (25-OH-D level <12 ng/ml). Patients with higher levels did not show benefit, bringing to light a possible shortcoming of many vitamin D trials -- should they focus on outcomes only for those who are deficient?

    It's not yet common practice to check serum 25-OH-D levels in COVID-19 inpatients, even though many practitioners are prescribing supplementation at typical (and possibly insufficient) doses. A Canadian study of 22,214 supplemented individuals found that 1,000 IU of daily cholecalciferol increased 25-OH-D levels by an average of only 4.8 ng/mL with diminishing returns for each additional increment of 1,000 IU per day. Toxicity was not seen in people who reported taking doses as high as 20,000 IU per day, an amount roughly equivalent to what's generated by an afternoon of summer sun on the skin. (Various medical societies state that doses only up to 4,000 IU of vitamin D per day are safe without medical supervision, and that up to 10,000 IU per day showed no observed adverse effects.)

    It is our responsibility as physicians not to wait for perfect evidence when making life-and-death decisions. Given the safety profile of vitamin D, the 40% prevalence of vitamin D deficiency in the U.S., and the fact that this season will likely be the deadliest phase of the pandemic to date, we need to act now. Identifying and eradicating vitamin D deficiency with early and aggressive supplementation in COVID-19 has the potential to save thousands of lives and should be one of our highest public health priorities.

  • DR Campbell talk on Vitamin D.

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  • Such BS answers don‘t really help to understand the topic better.

    I discussed pattern insert in one of the last response. That time it was not a pattern instead that patient certainly got reinfected many times.

    But 17 mutations is far less than >2000 needed to the closest known virus. You may remember that all old corona virus have been found in animals e.g. MERS in Camels.

    Key is that we know all existing 300'000 bat virus as bats are closely monitored since more than 10 years. No more bat virus have been found the last few years despite intense search.

    The biggest problem is that WHO goes to Wuhan despite we have 4 earlier findings in Italy that hosts some 10'000 Chinese slaves. Also the statement that all experts agree to the natural origin is 100% wrong. Only expert that say so are allowed to publish. Among them are no serious ones.