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Epidemiologist Who Triggered Worldwide Lockdowns Admits:
Without Instituting Full Lockdown, Sweden Essentially Getting Same Effect
By Hank Berrien Jun 2nd, 2020 DailyWire.com
https://www.dailywire.com/news/epidemiologist-who-triggered-worldwide-lockdowns-admits-without-instituting-full-lockdown-sweden-essentially-getting-same-effect?itm_source=parsely-api?utm_source=cnemail&utm_medium=email&utm_content=060320-news&utm_campaign=position1 

On Tuesday, Professor Neil Ferguson, of Imperial College London, whose bleak projections of future deaths from COVID-19 influenced governments around the world to institute massive lockdowns, admitted of Sweden, which did not institute harsh lockdowns, “It is interesting that adopting a policy which is short of a full lockdown – they have closed secondary schools and universities and there is a significant amount of social distancing, but it’s not a full lockdown – they have got quite a long way to the same effect.”

Speaking before a House of Lords Science and Technology Committee, the man who half a million Britons could die from Covid-19 spoke of Sweden, whose 436 people per million mortality rate from the coronavirus is significantly lower than the UK’s 575 people per million. The Daily Mail noted, “As well as fewer deaths, Sweden’s GDP actually grew in the first quarter of 2020, suggesting it might avoid the worst of the economic fallout from the crisis"

Ferguson admitted, “’There are differences in how science has influenced policies in different countries. I have the greatest respect for scientists there [in Sweden]. They came to a different policy conclusion but based really on quite similar science.” Asked why 4,000 people had died in Sweden instead of the 90,000 that had been forecast, he answered, “I think it’s an interesting question. It’s clear there have been significant social distancing in Sweden. Our best estimate is that that has led to a reduction in the reproduction number to around 1.” He cautioned, “It’s clear that when you look at their mortality, they are not seeing the rate of decline most European countries are seeing.”

He admitted, “But nevertheless it is interesting that adopting a policy which is short of a full lockdown… they’ve gone quite a long way to [achieving] the same effect,” while adding, “’Although there is no evidence of a rapid decline in the same way in other European countries. That is something we’re looking at very closely.” Then he acknowledged, “Lockdown is a very crude policy and what we’d like to do is have a much more targeted approach that does not have the same economic impacts.”

Ferguson added, “I suspect though, under any scenario that levels of transmission and numbers of cases will remain relatively flat between now and September, short of very big policy changes or behavior changes in the community. The real uncertainty then is if there are larger policy changes in September, of course we move into time of year when respiratory viruses tend to transmit slightly better, what will happen then. And that remains very unclear.”

The Imperial College London model headed by Ferguson surmised as many as 2.2 million Americans could have died from the virus if no action were taken. It also suggested 510,000 people would die in the U.K. without a lockdown and 250,000 if mitigating steps were taken.

Business Insider noted, “In 2009, one of Ferguson’s models predicted 65,000 people could die from the Swine Flu outbreak in the UK — the final figure was below 500.” Business Insider also noted, “Michael Thrusfield, a professor of veterinary epidemiology at Edinburgh University, told the paper he had ‘déjà vu’ after reading the Imperial paper, saying Ferguson was responsible for excessive animal culling during the 2001 Foot and Mouth outbreak. Ferguson warned the . . .


In Luce tua Videmus Lucem KRK
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5 years ago
kind of long, but interesting....explains alot:

Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
Many of the infection’s bizarre symptoms have one thing in common
Dana G Smith May 29 · 8 min read

https://elemental.medium.com/coronavirus-may-be-a-blood-vessel-disease-which-explains-everything-2c4032481ab2 

In April, blood clots emerged as one of the many mysterious symptoms attributed to Covid-19, a disease that had initially been thought to largely affect the lungs in the form of pneumonia. Quickly after came reports of young people dying due to coronavirus-related strokes. Next it was Covid toes — painful red or purple digits.

What do all of these symptoms have in common? An impairment in blood circulation. Add in the fact that 40% of deaths from Covid-19 are related to cardiovascular complications, and the disease starts to look like a vascular infection instead of a purely respiratory one.

Months into the pandemic, there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.

“All these Covid-associated complications were a mystery. We see blood clotting, we see kidney damage, we see inflammation of the heart, we see stroke, we see encephalitis [swelling of the brain],” says William Li, MD, president of the Angiogenesis Foundation. “A whole myriad of seemingly unconnected phenomena that you do not normally see with SARS or H1N1 or, frankly, most infectious diseases.”

“If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.

In a paper published in April in the scientific journal The Lancet, Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.

“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra.

A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.

A one-of-a-kind respiratory virus

SARS-CoV-2 is thought to enter the body through ACE2 receptors present on the surface of cells that line the respiratory tract in the nose and throat. Once in the lungs, the virus appears to move from the alveoli, the air sacs in the lung, into the blood vessels, which are also rich in ACE2 receptors.

“[The virus] enters the lung, it destroys the lung tissue, and people start coughing. The destruction of the lung tissue breaks open some blood
vessels,” Mehra explains. “Then it starts to infect endothelial cell after endothelial cell, creates a local immune response, and inflames the endothelium.”

A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.

Benhur Lee, MD, a professor of microbiology at the Icahn School of Medicine at Mount Sinai, says the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.

“In SARS1, the protein that’s required to cleave it is likely present only in the lung environment, so that’s where it can replicate. To my knowledge, it doesn’t really go systemic,” Lee says. “[SARS-CoV-2] is cleaved by a protein called furin, and that’s a big danger because furin is present in all our cells, it’s ubiquitous.”

Endothelial damage could explain the virus’ weird symptoms

An infection of the blood vessels would explain many of the weird tendencies of the novel coronavirus, like the high rates of blood clots. Endothelial cells help regulate clot formation by sending out proteins that turn the coagulation system on or off. The cells also help ensure that blood flows smoothly and doesn’t get caught on any rough edges on the blood vessel walls.

“The endothelial cell layer is in part responsible for [clot] regulation, it inhibits clot formation through a variety of ways,” says Sanjum Sethi, MD, MPH, an interventional cardiologist at Columbia University Irving Medical Center. “If that’s disrupted, you could see why that may potentially promote clot formation.”

Endothelial damage might account for the high rates of cardiovascular damage and seemingly spontaneous heart attacks in people with Covid-19, too. Damage to endothelial cells causes inflammation in the blood vessels, and that can cause any plaque that’s accumulated to rupture, causing a heart attack. This means anyone who has plaque in their blood vessels that might normally have remained stable or been controlled with medication is suddenly at a much higher risk for a heart attack.

“Inflammation and endothelial dysfunction promote plaque rupture,” Sethi says. “Endothelial dysfunction is linked towards worse heart outcomes, in particular myocardial infarction or heart attack.”

Blood vessel damage could also explain why people with pre-existing conditions like high blood pressure, high cholesterol, diabetes, and heart disease are at a higher risk for severe complications from a virus that’s supposed to just infect the lungs. All of those diseases cause endothelial cell dysfunction, and the additional damage and inflammation in the blood vessels caused by the infection could push them over the edge and cause serious problems.

The theory could even solve the mystery of why ventilation often isn’t enough to help many Covid-19 patients breathe better. Moving air into the lungs, which ventilators help with, is only one part of the equation. The exchange of oxygen and carbon dioxide in the blood is just as important to provide the rest of the body with oxygen, and that process relies on functioning blood vessels in the lungs.

“If you have blood clots within the blood vessels that are required for complete oxygen exchange, even if you’re moving air in and out of the airways, [if] the circulation is blocked, the full benefits of mechanical ventilatory support are somewhat thwarted,” says Li.

A new paper published last week in the New England Journal of Medicine, on which Li is a co-author, found widespread evidence of blood clots and infection in the endothelial cells in the lungs of people who died from Covid-19. This was in stark contrast to people who died from H1N1, who had nine times fewer blood clots in the lungs. Even the structure of the blood vessels was different in the Covid-19 lungs, with many more new branches that likely formed after the original blood vessels were damaged.

“We saw blood clots everywhere,” Li says. “We were observing virus particles filling up the endothelial cell like filling up a gumball machine. The endothelial cell swells and the cell membrane starts to break down, and now you have a layer of injured endothelium.” Finally, infection of the blood vessels may be how the virus travels through the body and infects other organs — something that’s atypical of respiratory infections.

“Endothelial cells connect the entire circulation [system], 60,000 miles worth of blood vessels throughout our body,” says Li. “Is this one way that Covid-19 can impact the brain, the heart, the Covid toe? Does SARS-CoV-2 traffic itself through the endothelial cells or get into the bloodstream this way? We don’t know the answer to that.”

In another paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival.

If Covid-19 is a vascular disease, the best antiviral therapy might not be antiviral therapy

An alternative theory is that the blood clotting and symptoms in other organs are caused by inflammation in the body due to an over-reactive immune response — the so-called cytokine storm. This inflammatory reaction can occur in other respiratory illnesses and severe cases of pneumonia, which is why the initial reports of blood clots, heart complications, and neurological symptoms didn’t sound the alarm bells. However, the magnitude of the problems seen with Covid-19 appear to go beyond the inflammation experienced in other respiratory infections.

“There is some increased propensity, we think, of clotting happening with these [other] viruses. I think inflammation in general promotes that,” Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that just because [the infection] is just that much more severe? I think those are all really good questions that unfortunately we don’t have the answer to yet.”

Anecdotally, Sethi says the number of requests he received as the director of the pulmonary embolism response team, which deals with blood clots in the lungs, in April 2020 was two to three times the number in April 2019. The question he’s now trying to answer is whether that’s because there were simply more patients at the hospital during that month, the peak of the pandemic, or if Covid-19 patients really do have a higher risk for blood clots.

“I suspect from what we see and what our preliminary data show is that this virus has an additional risk factor for blood clots, but I can’t prove that yet,” Sethi says.

The good news is that if Covid-19 is a vascular disease, there are existing drugs that can help protect against endothelial cell damage. In another New England Journal of Medicine paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival. Statins reduce the risk of heart attacks not only by lowering cholesterol or preventing plaque, they also stabilize existing plaque, meaning they’re less likely to rupture if someone is on the drugs.

“It turns out that both statins and ACE inhibitors are extremely protective on vascular dysfunction,” Mehra says. “Most of their benefit in the continuum of cardiovascular illness — be it high blood pressure, be it stroke, be it heart attack, be it arrhythmia, be it heart failure — in any situation the mechanism by which they protect the cardiovascular system starts with their ability to stabilize the endothelial cells.”

Mehra continues, “What we’re saying is that maybe the best antiviral therapy is not actually an antiviral therapy. The best therapy might actually be a drug that stabilizes the vascular endothelial. We’re building a drastically different concept.”



In Luce tua Videmus Lucem KRK
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5 years ago
They are always wrong, so I am not sure how relevant this is....but it would seem temperature and masks in crowds could go a long way in preventing the spread.

CNBC reported

Asymptomatic spread of coronavirus is ‘very rare,’ WHO says
PUBLISHED MON, JUN 8 20201:05 PM EDT UPDATED 43 MIN AGO
William Feuer @WILLFOIA Noah Higgins-Dunn @HIGGINSDUNN

KEY POINTS
[list]

  • Government responses should focus on detecting and isolating infected people with symptoms, the World Health Organization said.
  • Preliminary evidence from the earliest outbreaks indicated the virus could spread even if people didn’t have symptoms.
  • But the WHO says that while asymptomatic spread can occur, it is “very rare.”[/list]WHO: Coronavirus patients who don’t show symptoms aren’t driving the spread of the virus
  • Coronavirus patients without symptoms aren’t driving the spread of the virus, World Health Organization officials said Monday, casting doubt on concerns by some researchers that the disease could be difficult to contain due to asymptomatic infections.
    Some people, particularly young and otherwise healthy individuals, who are infected by the coronavirus never develop symptoms or only develop mild symptoms. Others might not develop symptoms until days after they were actually infected.

    Preliminary evidence from the earliest outbreaks indicated that the virus could spread from person-to-person contact, even if the carrier didn’t have symptoms. But WHO officials now say that while asymptomatic spread can occur, it is not the main way it’s being transmitted.

    “From the data we have, it still seems to be rare that an asymptomatic person actually transmits onward to a secondary individual,” Dr. Maria Van Kerkhove, head of WHO’s emerging diseases and zoonosis unit, said at a news briefing from the United Nations agency’s Geneva headquarters. “It’s very rare.”


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