Virus takes advantage of weak immune systems

U.K. variant puts spotlight on immunocompromised patients’ role in the COVID-19 pandemic

It’s simply too many mutations to have accumulated under normal evolutionary circumstances. It suggests an extended period of within-host evolution.

By Kai Kupferschmidt,  Dec. 23, 2020



Sciences COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation.

In June, Ravindra Gupta, a virologist at the University of Cambridge, heard about a cancer patient who had come into a local hospital the month before with COVID-19 and was still shedding virus. The patient was being treated for a lymphoma that had relapsed and had been given rituximab, a drug that depletes antibody-producing B cells. That made it hard for him to shake the infection with SARS-CoV-2.

Gupta, who studies how resistance to HIV drugs arises, became interested in the case and helped treat the patient, who died in August, 101 days after his COVID-19 diagnosis, despite being given the antiviral drug remdesivir and two rounds of plasma from recovered patients, which contained antibodies against the virus. When Gupta studied genome sequences from the coronavirus that infected the patient, he discovered that SARS-CoV-2 had acquired several mutations that might have allowed it to elude the antibodies.

Now, his analysis, reported in a preprint on medRxiv earlier this month, has become a crucial puzzle piece for researchers trying to understand the importance of B.1.1.7, the new SARS-CoV-2 variant first found in the United Kingdom. That strain, which appears to spread faster than others, contains one of the mutations that Gupta found, and researchers believe B.1.1.7, too, may have originated in an immunocompromised patient who had a long-running infection. “It’s a perfectly logical and rational hypothesis,” says infectious disease scientist Jeremy Farrar, director of the Wellcome Trust.

Scientists are still trying to figure out the effects of the mutations in B.1.1.7, whose emergence led the U.K. government to tighten coronavirus control measures and other countries in Europe to impose U.K. travel bans. But the new variant, along with research by Gupta and others, has also drawn attention to the potential role in COVID-19 of people with weakened immune systems. If they provide the virus with an opportunity to evolve lineages that spread faster, are more pathogenic, or elude vaccines, these chronic infections are not just dangerous for the patients, but might have the potential to alter the course of the pandemic.

It’s still very unclear whether that is the case, but Farrar believes it’s important to ensure doctors take extra precautions when caring for such people: “Until we know for sure, I think, treating those patients under pretty controlled conditions, as we would somebody who has drug resistant tuberculosis, actually makes sense.”

Researchers’ concern mostly focuses on cancer patients being treated for chemotherapy and similar situations. “We don’t yet know about people who are immunocompromised because of HIV, for instance,” Farrar says.

Foreshadowing the future

B.1.1.7 attracted scientists’ attention because it was linked to an outbreak in England’s Kent county that was growing faster than usual. Sequences showed that virus had accumulated a slew of mutations that together caused 17 amino acid changes in the virus’ proteins, eight of them in the crucial spike protein. Among them are at least three particularly concerning ones.

One is 69-70del, a deletion that Gupta also found in his Cambridge, U.K., patient whose virus seemed to evade the immune system. It leads to the loss of two amino acids in the spike protein. In lab experiments, Gupta found that lentivirus engineered to carry the SARS-CoV-2 spike protein with this deletion was twice as infectious.

The second is N501Y, a mutation that evolutionary biologist Jesse Bloom of the Fred Hutchinson Cancer Research Center has shown to increase how tightly the protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor, its entry point into human cells. The mutation is also present in 501Y.V2, a variant discovered by researchers in South Africa who investigated rapidly growing outbreaks in three coastal provinces. “We found that this lineage seems to be spreading much faster,” says Tulio de Oliveira, a virologist at the University of KwaZulu-Natal whose work first alerted U.K. scientists to the importance of N501Y. “Anytime you see the same mutation being independently selected multiple times, it increases the weight of evidence that that mutation is probably beneficial in some way for the virus,” Bloom says.

The third worrisome change is P681H, which alters the site where the spike protein has to be cleaved to enter human cells. It is one of the sites on spike where SARS-CoV-2 differs from SARS-CoV-1, the virus that caused the worldwide outbreak of severe acute respiratory syndrome in 2003, and the change there may allow it to spread more easily. “This one is probably as important as N501Y,” says Christian Drosten, a virologist at Charité University Hospital in Berlin.

So far, SARS-CoV-2 typically acquires only one to two mutations per month. And B.1.1.7 is back to this pace now, suggesting it doesn’t mutate faster normally than other lineages. That’s why scientists believe it may have gone through a lengthy bout of evolution in a chronically infected patient who then transmitted the virus late in their infection. “We know this is rare but it can happen,” says World Health Organization epidemiologist Maria Van Kerkhove. Stephen Goldstein, a virologist at the University of Utah, agrees. “It’s simply too many mutations to have accumulated under normal evolutionary circumstances. It suggests an extended period of within-host evolution,” he says.

People with a weakened immune system may give the virus this opportunity, as Gupta’s data show. More evidence comes from a paper published in The New England Journal of Medicine on 3 December that described an immunocompromised patient in Boston infected with SARS-CoV-2 for 154 days before he died. Again, the researchers found several mutations, including N501Y. “It suggests that you can get relatively large numbers of mutations happening over a relatively short period of time within an individual patient,” says William Hanage of the Harvard T.H. Chan School of Public Health, one of the authors. (In patients who are infected for a few days and then clear the virus, there simply is not enough time for this, he says.) When such patients are given antibody treatments for COVID-19 late in their disease course, there may already be so many variants present that one of them is resistant, Goldstein says.

It’s simply too many mutations to have accumulated under normal evolutionary circumstances. It suggests an extended period of within-host evolution.

The question is whether the mutations arising in such patients could also help the virus spread more rapidly. In research published a few years ago, Bloom showed some of the mutations that arose in influenza viruses in immunocompromised patients later spread globally. “It’s totally possible that what’s happening in immunocompromised patients could foreshadow what happens in the future” with the pandemic, Bloom says. But adaptations that help a virus outperform other viruses in a patient can also be very different from what a virus needs to better transmit from patient to patient, he says.

U.K. scientists and others were initially cautious about concluding that B.1.1.7’s mutations made the virus better at spreading from person to person. But the new variant is rapidly replacing others, says Müge Çevik, an infectious disease specialist at the University of St. Andrews. “We can’t really rule out the possibility that seasonality and human behavior explain some of the increase,” she says. “But it certainly seems like there is something to do with this variant.” Drosten says he was initially skeptical, but has become more convinced as well.

But exactly what impact each mutation has is much more difficult to assess than spotting them or showing they’re on the rise, says Seema Lakdawala, a biologist at the University of Pittsburgh. Animal experiments can help show an effect, but they have limitations. Hamsters already transmit SARS-CoV-2 virus rapidly, for instance, which could obscure any effect of the new variant. Ferrets transmit it less efficiently, so a difference may be more easily detectable, Lakdawala says. “But does that really translate to humans? I doubt it.” A definitive answer may be months off, she predicts.

One hypothesis that scientists are discussing is that the virus has increased how strongly it binds to the ACE2 receptor on human cells, and that this allows it to better infect children than before, expanding its playing field. But the evidence for that is very thin so far, Çevik says. Even if children turn out to make up a higher proportion of people infected with the new variant, that could be because the variant spread at a time when there was a lockdown but schools were open. Another hypothesis is that P681H helps the virus better infect cells higher up in the respiratory tract, from where it can spread more easily than from deep in the lungs, Drosten says.

No reason to freak out

One important question is whether the South African or U.K. lineage might lead to more severe disease or even evade vaccine-induced immunity. So far there is little reason to think so. Although some mutations have been shown to let the virus evade monoclonal antibodies, vaccines and natural infections both appear to lead to a broad immune response that targets many parts of the virus, says Shane Crotty of the La Jolla Institute for Immunology. “It would be a real challenge for a virus to escape from that.” The measles and polio viruses have never learned to escape the vaccines targeting them, he notes: “Those are historical examples suggesting not to freak out.”

At a press conference yesterday, BioNTech CEO Uğur Şahin pointed out that the U.K. variant differed in only nine out of more than 1270 amino acids of the spike protein encoded by the messenger RNA in the very effective COVID-19 vaccine his company developed together with Pfizer. “Scientifically it is highly likely that the immune response by this vaccine also can deal with the new virus,” he said. Experiments are underway that should confirm that in the first week of 2021, Şahin added.

Sébastien Calvignac-Spencer, an evolutionary virologist at the Robert Koch Institute, says this marks the first time countries have taken such drastic actions as the U.K. lockdown and the travel bans based on genomic surveillance in combination with epidemiological data. “It’s pretty unprecedented at this scale,” he says. But the question of how to react to disconcerting mutations in pathogens will crop up more often as genomic surveillance expands, he predicts. People are happy they prepared for a category 4 hurricane even if predictions turn out to be wrong and the storm is less severe, Calvignac-Spencer says. “This is a bit the same, except that we have much less experience with genomic surveillance than we have with the weather forecast.”

Although the rise of B.1.1.7 in the United Kingdom is troubling, Farrar says he is equally concerned about the other variant spreading quickly in South Africa and that has now been detected in two travelers in the United Kingdom as well. It includes two further mutations in the part of the spike protein that binds to its receptor on human cells, K417N and E484K. These could impact the binding of the virus to human cells and also its recognition by the immune system, Farrar says. “These South African mutations I think are more worrying than the constellation of the British variant.” South African hospitals are already struggling, he adds. “We’ve always asked, ‘Why has sub-Saharan Africa escaped the pandemic to date?” Answers have focused on the relative youth of the population and the climate. “Maybe if you just increase transmission a bit, that is enough to get over these factors,” Farrar says.

To Van Kerkhove, the arrival of B.1.1.7 shows how important it is to follow viral evolution closely. The United Kingdom has one of the most elaborate monitoring systems in the world, she says. “My worry is: How much of this is happening globally, where we don’t have sequencing capacity?” Other countries should beef up their efforts, she says. And all countries should do what they can to minimize transmission of SARS-CoV-2 in the months ahead, Van Kerkhove says. “The more of this virus circulates, the more opportunity it will have to change,” she says. “We’re playing a very dangerous game here.”

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Common drug reduces severity of COVID-19

Israeli study shows generic anti-lipid drug may squelch COVID-19 severity

The medicine, which is sold under a number of brand names, is America’s 73rd most prescribed drug. It is designed to reduce lipids known as triglycerides, the most common type of fat.

By Nathan Jeffay

Jerusalem researchers say they have shown that an existing drug used to lower lipid levels significantly downgrades the intensity of COVID-19, after conducting a comparative study of 1,500 medical records from hospitalized patients.

Fenofibrate, a generic fat-lowering medication that is among the most prescribed drugs in the US, appeared to give patients an “astounding” advantage in fighting the disease, Prof. Yaakov Nahmias of the Hebrew University of Jerusalem told The Times of Israel.

“This is a cheap and widely available drug with minimal side effects, and we were excited to find that all the main biomarkers indicate that it reduces the severity of COVID-19,” Nahmias said on Sunday.  

Nahmias has spent six months analyzing the impact of the numerous different medicines taken by 1,500 coronavirus patients treated at two Israeli hospitals.

The study included 13 subjects who regularly took fenofibrate, and had been doing so before they caught the coronavirus, to address their lipid levels. The result, quicker-than-expected recovery from virus-induced pneumonia, dovetailed with his earlier hypothesis that lipids play a role in the severity of the disease.

Had the 13 patients responded to COVID-19 with the same level of severity as others in the study, there would have been at least two deaths and six ICU admissions among the fenofibrate patients, but there were no deaths and there was only one ICU admission.

Prof. Yaakov Nahmias of the Hebrew University of Jerusalem (courtesy of the Hebrew University of Jerusalem)

Clinical trial results are still needed, but there is now a “very high” chance that fenofibrate will become a common treatment for the coronavirus within a few months, said Nahmias, director of Hebrew University’s Grass Center for Bioengineering.

Even before the patient study was completed, an international clinical trial by the University of Pennsylvania got underway, and he is now starting a clinical trial in the Israeli city of Ashkelon.

Vaccination programs don’t reduce the importance of fenofibrate; it will take a long time before the whole world is vaccinated so his drug research can still save many lives, Nahmias suggested. He noted that even after vaccination, some people will still get infected, so drugs will still be needed.

In June, Nahmias announced that experiments in his lab indicated that fenofibrate could help coronavirus patients.

The medicine, which is sold under a number of brand names, is America’s 73rd most prescribed drug. It is designed to reduce lipids known as triglycerides, the most common type of fat.

His team hypothesized at the time that the novel coronavirus is so vicious because it causes lipids to be deposited in the lungs, and that fenofibrate could break down the lipids and help patients.

“We suggested in June that lipid accumulation is harming COVID patients, and this study shows exactly that,” he said Sunday. “If you encourage lipid breakdown you resolve inflammation faster and you have less mortality.”

A radiograph image showing inflamed lungs (sompong_tom via iStock by Getty Images)

Putting this idea to the test, based on patient data from Tel Aviv Sourasky Medical Center and Hadassah Medical Center in Jerusalem, has not only paved the way for a possible new treatment option, but may also throw some light on why patients suffering from obesity and high levels of fat in their body are so badly hit by COVID-19.

Nahmias emphasized that his latest analysis, which must still be peer-reviewed, was carried out using a scientific system called propensity score matching, which means that background diseases, age, gender and other risk factors were identical.

“Our statistics were very strong,” he reported. “Based on the overall sample, the patients who were taking fenofibrate before and during their COVID-19 illness, there should have been two to three deaths, and it should have been about 14 days to resolve their pneumonia.

“But there were no deaths, fewer ICU admissions than expected, and while all [fenofibrate] patients had pneumonia, it took them three to five days to recover from pneumonia. This is astounding.”

The chemical composition of the fenofibrate lipid-lowering drug Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), chlorine (green) (iStock)

Oren Shibolet, a senior doctor at Tel Aviv Sourasky Medical Center who provided data on his institution’s coronavirus patients to Nahmias, said that while only 13 coronavirus patients taking fenofibrate were studied, the results are important.

“The differences seen between them and the other patients was highly statistically significant, meaning that it can’t be explained by chance,” he said. “There is some biological phenomenon in these patients.”

Nahmias said his team also found that patients taking fenofibrate showed indications of better lung function, respiratory functions and C-reactive protein levels, which are an indicator of lung inflammation, than other patients, including those taking statins.

Nahmias recently started a Phase 3a clinical study of the drug on coronavirus patients at Barzilai Hospital in Ashkelon. The study is partly funded by Abbott Laboratories, which sells the drug as Tricor and which has received some scrutiny in academic circles for its zealous marketing. However, Nahmias said that before then, he received no funding from any of the various firms that manufacture drugs based on the fenofibrate generic.

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Ivermectin should be used now for COVID-19

Doctors: Ivermectin Can Help Treat COVID: Will Anyone Listen?

Dec 14, 2020, TrialSite News
Introducing the Physicians for Civil Defense: Prominent Doctors Know #Ivermectin can Help Treat COVID-19: Will Anyone Listen? A group calling itself Physicians for Civil Defense as it turns out is a group of physicians TrialSite Knows very well. In fact, they include Dr. Jacques Rajter of Fort Lauderdale, Florida, co-principal investigator and author of the ICON study evidencing the efficacy and safety of ivermectin as a treatment for COVID-19. The group recently presented at the U.S. Senate Homeland Security and Government Affairs Committee discussing possible safe and economical treatment for both prophylaxis and treatment for COVID-19: namely ivermectin.

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Vitamin D prophylaxis for COVID-19

Vitamin D and COVID 19: The Evidence for Prevention and Treatment of Coronavirus (SARS CoV 2)

Premiered Dec 11, 2020, MedCram
Professor Roger Seheult, MD explains the important role Vitamin D may have in the prevention and treatment of COVID-19. Dr. Seheult illustrates how Vitamin D works, summarizes the best available data and clinical trials on vitamin D, and discusses vitamin D dosage recommendations. Roger Seheult, MD is the co-founder and lead professor at He is an Associate Professor at the University of California, Riverside School of Medicine and Assistant Prof. at Loma Linda University School of Medicine Dr. Seheult is Quadruple Board Certified: Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine Interviewer: Kyle Allred, Producer and Co-Founder of
REFERENCES: The National Human Activity Pattern Survey (NHAPS)… (J. of Exposure Analysis and Environmental Epidemiology) |… Aging decreases the capacity of human skin to produce vitamin D3 (The J. of Clinical Investigation) | Racial differences in the relationship between vitamin D… (Osteoporosis Int.) |… Decreased bioavailability of vitamin D in obesity (The American J of Clinical Nutrition) |… Vitamin D Insufficiency and Deficiency and Mortality from Respiratory Diseases … (Nutrients) | Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis… (BMJ) |… Randomized trial of vitamin D supplementation to prevent seasonal influenza A… (The American J.of Clinical Nutrition) |… Vitamin D and SARS-CoV-2 infection… (Irish J. of Medical Science) |…. Factors associated with COVID-19-related death… (Nature) |… Editorial: low population mortality from COVID-19 … (Alimentary Pharm. & Therap.) |… The role of vitamin D in the prevention of coronavirus … (Aging Clinical & Experimental Research) |… 25-Hydroxyvitamin D Concentrations Are Lower in Patients with … SARS-CoV-2 (Nutrients) | Vitamin D deficiency in COVID-19: Mixing up cause and consequence (Metabolism) |… Low plasma 25(OH) vitamin D level… increased risk of COVID-19… (The FEBS J.) |… The link between vitamin D deficiency and Covid-19… |… SARS-CoV-2 positivity rates… with circulating 25-hydroxyvitamin D levels (PLOS One) |… Vitamin D status and outcomes for… COVID-19 (Postgrad Medical J.) |… Vitamin D Deficiency and Outcome of COVID-19… (Nutrients) | “Effect of calcifediol treatment…” (The J. of Steroid Bio. and Molec. Bio.) |… Vitamin D and survival in COVID-19 patients… (The J. of Steroid Bio. and Molec. Bio.) |… Effect of Vitamin D3 … vs Placebo on Hospital Length of Stay…: A Multicenter, Double-blind, Randomized Controlled Trial |… Short term, high-dose vitamin D… for COVID-19 disease: a randomized, placebo-controlled, study [SHADE study] (Postgraduate Medical Journal) |… Association of Vitamin D Status… With COVID-19 Test Results (JAMA Network Open) |… Vitamin D Fortification of Fluid Milk … A Review (Nutrients) |… Analysis of vitamin D level among asymptomatic and critically ill COVID-19 patients… (Scientific Reports from the Journal Nature) |…

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Ivermectin prophylaxis for COVID-19

Ivermectin Placebo Controlled Trial And COVID-19: 4 Different Dosing Strategies

December 3, 2020

Youtube channel
In this video we will dive into a study that looked at variable dosing strategies of Ivermectin for COVID-19. This was a multicenter, double blinded, placebo controlled trial that looked at hospitalized patients with COVID-19. They had 6 different treatment arms (1) HCQ (standard care at the time), (2) Placebo, (3-6) Variable Doses of Ivermectin. We will discuss the study structure and setup and then dive into their results. They found that the Ivermectin groups had lower mortality and shorter hospital length of stay. What doses had the most efficacy? What may this mean? Check out the video for all the details!

In this video we will dive into a study that explored the incidence of COVID-19 in countries that have prophylaxis programs using Ivermectin. In many countries, Ivermectin is used as a prophylaxis agent for parasitic infections. This studied focused on these countries comparing them to other countries that have parasitic prophylactic programs that don’t use Ivermectin, as well as countries without prophylaxis programs at all. They did this on a global scale and then focused in on countries within the continent of Africa. They found a statistically significant decrease in COVID-19 incidence in countries that utilized Ivermectin prophylaxis programs. What does this mean though and what are the limitations? Check out the video for the details!

Link to study:…

In this video we will dive into a study published in the International Journal Of Infectious Disease that treated hospitalized patients with COVID-19 with either Ivermectin, Ivermectin and Doxycycline, or Placebo (with standard care). They looked specifically at the time to viral clearance, oxygen requirements, and mortality. The setup of the trial was interesting as they excluded anyone with comorbid conditions, which led to a fairly young and healthy population. The mortality in the study overall was zero and no one required oxygen. Nonetheless, they did find some significant results. Check out the video for all the details! Link to study:…

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Israeli doctors help Gaza fight virus

Israeli medical delegation enters Gaza to provide essential COVID-19 care

The delegation includes senior doctors, orthopedists, neurologists, heart surgeons, and mental health experts, according to PHRI. The doctors have also opened a mobile medical facility in the southern Gaza town of Khan Younis to accept patients.

By Aaron Boxerman

A delegation of Israeli doctors entered the Gaza Strip on Thursday morning to provide free treatment for hundreds of Gazans impacted by the coronavirus pandemic.

The medical delegation — organized by Physicians for Human Rights – Israel — is the first of its kind from Israel to the coastal enclave since the beginning of the pandemic nine months ago.

The twelve doctors, all of whom are Israeli Arabs, will conduct surgeries, medical training, and instruction for Palestinian medical teams, the rights group said.

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The delegation will bring some medical equipment and drugs with which to help combat the pandemic. But the doctors’ chief focus will be on other urgent cases that have been delayed as Gaza’s hospitals have filled with coronavirus patients.

The delegation includes senior doctors, orthopedists, neurologists, heart surgeons, and mental health experts, according to PHRI. The doctors have also opened a mobile medical facility in the southern Gaza town of Khan Younis to accept patients.

“The treatments will not deal with coronavirus, but rather with the chronically ill and other emergency cases whose treatment has been delayed because of coronavirus,” said Ran Yaron, a spokesperson for PHRI.

Israeli doctors, part of a delegation to Gaza organized by Physicians for Human Rights – Israel, arrive in the Strip on Thursday, December 3, 2020 (Credit: Mu’ataz Azayza)

According to PHRI, the delegation will remain in the Strip for two days before returning to Israel.

All of the delegation’s treatment will be provided for free, Yaron said. The doctors arriving from within Israel were volunteers as well, and were not being compensated for their participation in the delegation.

While the coastal enclave had managed to avoid a wide-scale coronavirus outbreak since the pandemic began, the past few weeks have seen a sharp rise in cases.

The Gaza Strip had 10,321 total active infections on Thursday. Three weeks ago, in mid-November, the number hovered around 2,000. Another 827 cases were recorded in Gaza over the past 24 hours. Over 30% of coronavirus tests administered came back positive, indicating that the virus could be spreading widely undetected.

Health officials in the Hamas-ruled territory have warned that Gaza’s fragile health system cannot bear much more strain and is close to collapse.

Around 87% of hospital beds with ventilators for coronavirus patients in critical condition were occupied as of Thursday morning, a World Health Organization told The Times of Israel.

An Israeli doctor treats a Palestinian patient in Gaza as part of a medical delegation organized by Physicians for Human Rights – Israel on December 3, 2020 (Credit: Mu’ataz Azayza)

The Gaza Strip’s healthcare system has been battered by a 13-year-blockade by Egypt and Israel and several wars between Israel and the Hamas terror group.

Israel has argued that the blockade — which places strict limitations on materials entering and exiting the Gaza Strip — is essential to stop Hamas, which avowedly seeks to destroy the Jewish state, from arming itself.

Critics of the restrictions have argued that it has had devastating impacts on ordinary Gazans.

“This delegation is not just a humanitarian action, but also a reminder that the Gaza Strip is not simply confronting coronavirus, but also the continuing blockade which hurts the ill, medical staff, and the entire civilian population in Gaza,” said PHRI director Ran Goldstein.


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Common sense model for COVID

Common Sense Model professor: ‘COVID-19 management’s wrong; learn from the haredim’

“As I explained, the morbidity is not in percentages that scared us in February or March. If we knew then the data we know today, no country in the world would go into lockdown because it doesn’t really work. We think we did something, we open the lockdown, and then go back and repeat it.”

By Mordechai Sones

Tel Aviv University Faculty of Medicine Department of Microbiology and Clinical Immunology immunologist Prof. Moti Gerlic is part of an initiative by doctors and scientists called the ‘Common Sense Model‘, and criticizes the “war on coronavirus”.

“Management looking at the epidemic is wrong in general. The tools we use to measure coronavirus are relevant to verified patients. The tests that give us a measure of people who have probably met the virus do not give us a true measure of patients. A person who tests positive for the virus should be distinguished from a patient.” Says Gerlitz in an interview with Arutz Sheva.

“The system, in the end, is run according to the numbers of people who encountered the virus and not according to the state of the patients in the economy and tends to lean towards the side of panic. It’s stuck in the same concept as in February and March.”

Prof. Gerlic argues that the health care system creates pressure on the public while the situation should be much less stressful. “Today we’re talking about a third lockdown and the collapse of the health system, and I just want to mention that at the height of the second closure, 800 critical patients were dealt with and we aren’t close to that number at all. The numbers that were defined four months ago as a red line have gone down. What we dealt with before is now a problem to deal with, and already with 2,000 verified patients a day there’s talk of closure. The conduct is extreme. We know more about the virus every day and the treatments are better; we should have been less panicked.”

The team of researchers and physicians who established the Common Sense Model include:

  • Dr. Uri Gavish, physicist, expert in algorithms and models inspection, and a consultant in the field of biomedicine.
  • Prof. Ariel Munitz, immunologist in the Department of Microbiology and Clinical Immunology in the Faculty of Medicine at Tel Aviv University, and head of the Coronavirus Laboratory at Tel Aviv University.
  • Prof. Motti Gerlic, immunologist in the Department of Microbiology and Clinical Immunology in the Faculty of Medicine at Tel Aviv University.
  • Prof. Udi Qimron, microbiologist and head of the Department of Microbiology and Clinical Immunology at the Faculty of Medicine at Tel Aviv University,

and they are joined by several prominent Israeli physicians.

The program is based on several principles:

  • First, “government identification and recognition of people belonging to at-risk groups and helping people from these groups protect themselves” on the one hand, and lead a normal life on the other. For example, allocating hours designated for them only in pharmacies and food stores, giving priority in line, allocating space on public transportation, and providing full compensation to those whose work cannot be done remotely.
  • Second, “stopping the enormous waste of resources currently spent on mass testing and forced quarantine”, and directing them to protecting nursing homes and medical staff, thus increasing hospitalization capacity and training staff.
  • In addition to these, “the whole economy needs to be re-opened”, including cultural and sports activities, and regular flights. Above all, re-opening the educational system, from kindergarten to universities.

Prof. Gerlic presents the Model he and his friends have created: “We know the virus severely attacks very defined populations – the elderly, and those with background diseases. Once this figure is in front of us and we know how to map this population, we can use the benefits of the Israeli health system. It’s probably 15%-18% of the population and once we make efforts to protect them, the rest of the citizens can return to work and school better. All the capsules that prevent schools or businesses from actually opening regularly can be avoided.

“As I explained, the morbidity is not in percentages that scared us in February or March. If we knew then the data we know today, no country in the world would go into lockdown because it doesn’t really work. We think we did something, we open the lockdown, and then go back and repeat it.

“In our opinion, one can look and learn from success stories like those of haredi society. They haven’t been shut down for two months, the education systems are back in full operation, and the fears of health system decision makers that there will be a total collapse haven’t materialized. At the moment we’re still captive to the same concept and the Health Ministry wants to see fewer verified people a day, and I don’t know why this is the index,” he concludes.

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Sidney Powell describes voter fraud

Sidney Powell at ‘Stop the Steal’: Massive voter fraud exists, money traced back to China | NTD

Youtube channel

Sidney Powell said that massive voter fraud exists in the country, and it’s in the DNA of all software in voting systems used across America. She said some algorithms changed votes at a rate of 90% for Biden and 10% for Trump. She said a lot of the money behind the fraud is traced back to China.

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