8 July 2020
The [NZ] Government has formally confirmed that it will not use any of the current or future serology tests to assess how widespread the Covid19 disease has been in New Zealand.
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https://youtu.be/QU0b-En3pCI
I do not normally address the issue of coronavirus genesis, but according to the last statement in this interview perhaps we all should have.
BEFORE YOU READ THIS REPORT (below) PLEASE BE AWARE OF THIS EARLIER REPORT: “SOUTH AFRICA BANS IVERMECTIN” (CLICK HERE)
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CAPE TOWN — South Africa was already one of the countries worst hit by the coronavirus, but in the six weeks since a new, more transmissible variant was first publicly announced here, an enormous spike of new cases and deaths has far surpassed previous waves of the pandemic.
The variant is thought to have emerged in South Africa’s Eastern Cape province but has now been found in at least 31 countries, sparking fears its unmitigated spread to new parts of the world could usher in new waves of contagion just as the long slog of global vaccine rollout gets underway.
The variant identified in South Africa is not yet proved to be more lethal than others, including similarly highly transmissible variants recently detected in Britain and Brazil, but mutations that make it around 50 percent easier to catch have allowed it to stage a takeover of what was already out-of-control community transmission in South Africa:
“Of the cases we’ve [DNA-]sequenced in South Africa, more than 90 percent are the new variant,” said Richard Lessells, a lead researcher at the KwaZulu-Natal Research and Innovation Sequencing Platform, or KRISP, which has played a pathbreaking role in identifying coronavirus variants in South Africa and elsewhere. “It’s amazing and terrifying how quickly it came to dominate, and it does feel like we’re in the beginning stages of watching this variant, and the other new ones, become more dominant around the world.”
Its rise has led to dozens of countries imposing bans on travelers who recently have been in South Africa, including the United States.
That move closely followed an announcement by the American vaccine producer Moderna that said the antibodies its vaccine creates were less effective at neutralizing it than previously dominant coronavirus variants. The company said it was developing a new booster shot and testing out a three-shot regimen as ways to boost the vaccine’s efficacy against the variant.
On Thursday, Pfizer and its research partner BioNTech released a yet-to-be-peer-reviewed study showing its vaccine was only slightly less effective against the variant from South Africa, though the findings were limited because it only looked at the vaccine’s effect on two of the 23 total mutations in the variant.
South African studies have also documented dozens of instances of people who contracted earlier strains of the coronavirus being infected with the new variant, suggesting that those who had contracted mild cases or otherwise had low antibody counts might be prone to reinfection.
In South Africa, despite a return to a stricter lockdown and curfew, many hospitals are overwhelmed, especially in Eastern Cape, which has become the epicenter of the new variant’s spread. Harrowing statistics released this week by the South African Medical Research Council show excess mortality numbers shooting nearly straight up in all of the country’s nine provinces.
“Ambulances and family members have said they would drive from hospital to hospital for up to six hours looking for a spot to get some oxygen,” said Imtiaz Sooliman, founder of one of South Africa’s biggest charity organizations, Gift of the Givers, which has been helping distribute oxygen machines.
“Doctors will tell you that people died in cars while waiting to be admitted to the casualty ward, or they died in casualty before they could be seen.”
Phumla Mnyanda, who runs a 260-bed hospital in Eastern Cape’s capital, Bhisho, said social media posts had spread misinformation on ways to avoid hospitals where people were dying, keeping an even greater number of people from coming in when they first felt symptoms. But as patients neared death, families would rush them to the hospital only to find that little could be done to save their relatives.
“They were coming too late and by then their oxygen levels are very low, and you saw it dropping and dropping, and there is nothing we could do,” she said in a telephone interview. “People are so scared because there are so many that have died.”
The SAMRC’s excess mortality figures indicate that more than 110,000 have likely died of covid-19 in South Africa since May, even though the official toll is just above 41,000. More than 30,000 excess deaths have been recorded in January alone.
If most of these excess deaths can be attributed to covid-19, which most South African experts believe they can, then the country’s death toll would be the highest as a proportion of its population in the world.
Debbie Bradshaw, a researcher at SAMRC, said that although South Africa generally had a good reputation of registering most deaths, those that took place outside hospitals often went undiagnosed and thus escaped the official toll.
“We think that most of the confirmed covid deaths are really only being reported from hospitals, whereas there are many who leave hospitals before death or never make it to the hospitals in the first place,” she said.
Despite potentially being the cause of tens of thousands of deaths, the South African variant has been sequenced by researchers fewer than 700 times. The British variant, on the other hand, has been sequenced almost 30,000 times. Nearly 80 percent of the South African variant sequences have been found in South Africa and another 10 percent in Britain.
Twenty-nine other countries make up the remainder, but Lessells at KRISP said it was likely the variant was circulating much more widely, especially in African countries with closer economic ties to South Africa but where sequencing capacity is limited or nonexistent.
South Africa’s land borders have been closed to nonessential travel, but a long list of exceptions means thousands of people still cross them every week. They also remained open through the December holidays, when many migrant workers returned to their home countries on leave.
Some of those neighboring or nearby southern African countries, such as Zimbabwe, Zambia, Mozambique and Malawi, have seen soaring case numbers after months of relative calm.
Lessells said his lab was expecting to release sequences from samples taken from neighboring Mozambique this week.
“We’re engaged in a huge amount of collaborative science with partners around the world trying to understand what caused their rise,” he said.
The consensus, he said, is that it’s no coincidence that new variants emerged in South Africa, Britain and Brazil, which suffered some of the world’s biggest initial waves of the virus. It was likely that in places where the virus was running into large numbers of people who already had antibodies that it mutated to more easily find new hosts.
“Our failures to clamp down on community spread, wherever they may be, will almost certainly lead to even more new variants,” Lessells said.
Sebastion Rushworth, MD
Jan 26, 2021
https://sebastianrushworth.com/2021/01/25/heres-a-graph-they-dont-want-you-to-see/
Here’s a graph that doesn’t get shown in the mass media, and that I’m sure all those who want you to stay fearful of covid don’t want you to see. It shows the share of the tested population with antibodies to covid in Sweden week by week, beginning in the 28th week of 2020 [is increasing].
[…]
No-one is discussing the obvious explanation – that so many people have now had covid, and have developed immunity, that the virus is having difficulty finding new hosts. In other words, Sweden’s oddly controversial “herd immunity” strategy worked.
Sebastian Rushworth
Dec 9, 2020
https://sebastianrushworth.com/2020/12/09/how-long-does-immunity-to-covid-last/
more important to look at what’s happening with memory B-cells than with antibodies, if you want to know how long your body maintains the ability to mount an antibody response to an infection.
[…]
it is clear from this study that there is significant immune memory at the six to eight month time point after infection. At six to eight months after infection, 90% of measured samples still had antibodies and T-helper cells specific for covid-19, and 50% still had measurable T-killer cells. If the decline continues linearly over time from what was seen in this study, then it is reasonable to assume that most people continue to be immune to covid after infection for at least a couple of years.
(Don’t quit early, second half of video best part.)
https://youtu.be/3mPIomjWwd4
TUCSON, Ariz., Sept. 21, 2020 /PRNewswire/ — For decades, physicians have been taught—and have told patients—that antimicrobials do not help viral diseases. But when studying the response of COVID-19 to the antimicrobial agents chloroquine (CQ) and hydroxychloroquine (HCQ), Lee Merritt, M.D., writes, in the fall issue of the Journal of American Physicians and Surgeons: “Like Rip Van Winkle, I suddenly awoke, after decades, to a completely new medical reality.”
In a quick internet search, she found more than 20 scientific papers, written in the last 40 years, on the use of lysosomotropic agents to treat viruses. These agents—which affect the cellular organelle involved in viral penetration and replication, include CQ, HCQ, and the common antibiotic azithromycin.
Several antibiotics, including doxycycline, metronidazole, and ciprofloxacin, have been shown to have activity against many viruses, she writes.
Instead of pursuing research on treatment, the pharmaceutical industry has focused solely on vaccination to respond to viral diseases, she observes. But vaccines have drawbacks. Dr. Merritt lists incomplete immunity and “immune enhancement,” which can worsen disease outcomes.
“Vaccination is not a panacea. It was once the last resort to the treatment of disease. In the age of huge vaccine profit it has become the first choice for every disease,” she states.
Dr. Merritt discusses the “war against hydroxychloroquine.” Politicians and media falsely claimed that HCQ is “experimental”—it has been approved and widely used for more than 65 years—or that “off label” prescribing is illegal—it is common for many drugs.
“Never have I seen such political brawling over a legal pharmaceutical.”
Dr. Merritt states that the pharmaceutical truth about the treatment of viral diseases has been suppressed for 40 years by methods including censorship, regulatory capture, and control of research funding. But with COVID, she writes that physicians and patients who have awakened to the “biggest lie” are beginning to say, “Yes, Virginia, antibiotics and other antimicrobials do treat viruses.”
The Journal of American Physicians and Surgeons is published by the Association of American Physicians and Surgeons (AAPS), a national organization representing physicians in all specialties since 1943.
SOURCE Association of American Physicians and Surgeons (AAPS)
To read Dr Merritt’s recent publication in the Journal of American Physicians and Surgeons go to the fall issue.
Milwaukee Journal Sentinel Jan 26, 2021
From a rare marine sea squirt found only in the waters around the Spanish island of Ibiza comes a potential COVID-19 treatment called Aplidin that researchers say has proven 27.5 times more effective than the well-known remdesivir in human cells in the lab.
The finding, reported Monday by an international team in the journal Science, comes at a time when potential treatments have been overshadowed by the U.S. vaccination campaign, now trying to recover from a slower-than-expected start.
A related preprint that has yet to be peer-reviewed says that tests have shown the drug is equally effective against the highly infectious new variant of the virus discovered recently in the United Kingdom.
Aplidin, already approved in Australia for treating multiple myeloma, has been developed as a potential COVID-19 treatment by the Spanish drug company PharmaMar.
So far, Aplidin, also known as Plitidepsin, has gone through a Phase II clinical trial against COVID-19 and is now awaiting the start of Phase III testing. It comes from sea squirts, marine creatures that look like plants and have tubular openings allowing them to draw in and expel water.
The drug was identified as a potential coronavirus treatment back in March after scientists at the University of California, San Francisco and elsewhere tried an unconventional approach.
Instead of randomly testing vast libraries of existing drugs or targeting key proteins in the virus, as other research groups were doing, the San Francisco team focused on the human proteins needed by the virus. The scientists then looked for existing drugs that would prevent the coronavirus from hijacking those human proteins.
“This was data driven instead of just randomly screening drugs,” stressed Nevan Krogan, one of three co-leaders of the new study in Science and director of the Quantitative Biosciences Institute at the University of California, San Francisco.
Krogan said focusing on human, rather the viral, proteins, offered a powerful advantage in the fight against the new coronavirus.
“If you target a human protein that the virus needs,” he said, “the virus will never mutate away from being reliant on that human protein.”
Fear that the virus could thwart vaccines and treatments by mutating has taken on greater urgency since the discovery of a new, significantly more infectious variant of SARS-CoV-2 identified in the United Kingdom.
However, work finalized this weekend by Greg Towers and colleagues at University College London show that Aplidin was effective when used against two different human lung and epithelial cells infected with the newly discovered variant.
Krogan’s co-leaders in the study published in Science were Kris M. White and Adolfo García-Sastre, both of whom work at the Icahn School of Medicine at Mount Sinai.
Researchers who did not participate in the Science study, or in the unpublished preprint, said the results are encouraging. They added that Aplidin will require further testing in people to better pin down its effectiveness and possible side effects.
“The drug performs quite well in mice and the authors hint at it having potential against other viruses too,” said David H. O’Connor, a professor of pathology and laboratory medicine at the University of Wisconsin-Madison. “It is premature to say if it will have clinical benefit, but it definitely merits clinical trials.”
At the University of Minnesota Medical School, Susan Kline said, “It’s not typical that we think of drugs that treat cancer being used also to treat viruses.” She said that even though “a drug is effective in cells in the laboratory, we don’t know what effect it will have on cells in the human body.”
Kline, who serves as interim director of infectious disease in the university’s Department of Medicine, also expressed concern that a drug used to kill cancer cells might harm human cells.
Krogan, however, said the dose of Aplidin used against the new coronavirus was far smaller than the dose used to treat multiple myeloma. Also, the drug would only be used for a matter of days against COVID-19; it is used for weeks or months against multiple myeloma.
The Science study found that the drug was effective treating infected human kidney cells and primary lung cells in the lab. In another experiment described in the paper, the drug was used to treat mice infected with a version of the new coronavirus, and reduced the infection 100-fold.
Early in the institute’s work on COVID-19, it formed an international team with scientists from the Icahn School of Medicine at Mount Sinai in New York, the Institut Pasteur in Paris, and the J. David Gladstone Institutes in San Francisco, among others.
Known as the QBI Coronavirus Research Group, the team now includes scientists from the European Bioinformatics Institute in Cambridge, England, and University of Freiburg in Germany.
“The institute’s mission are these collaborations,” said Jacqueline M. Fabius, one of the paper’s authors and the institute’s chief operating officer. “That’s why it was so easy to hit the ground running (when the new coronavirus was discovered).”
In previous papers published in Cell, Science and Nature, the QBI Coronavirus Research Group mapped out the molecular interactions shared by coronaviruses that cause COVID-19, Severe Acute Respiratory Syndrome and Middle East Respiratory Syndrome.
Early on, the group honed in on 332 proteins found in human lung cells and also in blood vessel cells that help the virus when it invades the body.
Using cutting edge technology, they investigated how the virus was affected when they eliminated each protein one by one, and then when they lowered the levels of each protein.
Krogan has said that he hopes knowledge of these interactions will help researchers find treatments that address the new coronavirus but also the next one that appears.
Research on potential COVID-19 treatments is important, not only because it will take months to vaccinate the majority of Americans, but also because it’s unclear whether the vaccines in use can prevent transmission of the virus.
“Work on treatments has been ongoing since the outbreak began and we have seen the benefits,” said Chris Beyrer, professor of public health and human rights at Johns Hopkins Bloomberg School of Public Health. “Survival is actually better than it was in March, April, May.”
Merck said Monday it will stop developing both of the current formulations of the Covid-19 vaccines the company was working on, citing inadequate immune responses to the shots.
The four following posts indicate the Covid-19 vaccine does not prevent transmission, even asymptomatic transmission.