Can Even Severe COVID Infection Be Cured?

Update: Very low fatality rates in US midwest

Perhaps severe COVID-19 isn’t a purely inflammatory disease, but rather a dangerous loop of ineffective human immune responses and continuous tissue inflammation, says coauthor Leif Erik Sander, an immunologist and infectious disease specialist at the Charité hospital in Berlin. ___

It is still much of a mystery. Medical clinicians and researchers are still trying to understand how this “Made in China” virus works, and how best to cure even the most severe cases of SARS CoV-2. It is a hybrid, recombinant virus, with strong suggestions of being custom-made to infect humans. Thanks, China. But how do we cure it?

One medical group in Florida thinks it may have a handle on a “cure.”

“We had no need for mechanical ventilation, and the patients all survived the discharge regardless of age and regardless of past medical history,” Norwood-Williams said about the ICAM protocol. She explained that the drug combination “works to defend the body from the most severe cases of the coronavirus.”

Norwood-Williams continued, “What we found out was that ICAM works as a strategy for super defense for the body. It doesn’t kill coronavirus, but it doesn’t need to. Viruses are self-limiting anyway. They have a very short life cycle. What kills people are the consequences of coronavirus in multiple ways.” __

The reports are sketchy, and may be describing less of a cure and more of an adjunct to other treatments, some of which are yet to be discovered.

The devil is in the details. As long as scientists and physicians are able to work free of political interference, the details will come out.

The science, such as it is so far, is fascinating. No wonder the normally competent doctors in New York City failed so badly using treatments that were never meant to succeed against this virus, which they did not understand even a little.

In a recent analysis of nearly 1,500 COVID-19 patients, Merad and her colleagues found that concentrations of IL-6, IL-8 and TNF-α in their serum upon admission correlated strongly with disease severity and death. Each cytokine could by itself predict whether a patient would survive. Interestingly, the nature of COVID-19’s cytokine response is markedly different from the cytokine storm side effect observed in some cancer patients who receive cellular immunotherapies and certain other hyperinflammatory conditions. In COVID-19 patients, concentrations of certain cytokines tend to be much lower—King’s College London immunologist Manu Shankar-Hari describes their increase as a “cytokine breeze” rather than a storm. But the increased cytokine levels are sustained over days and weeks, Merad says.

… Scientists at Yale University tracking the progression of COVID-19 patients found that the cytokine increase was followed by haphazard-seeming immune responses in severely ill patients. While people with moderate disease appeared to activate immune machinery designed to fight off viruses, those with severe disease seemed to recruit cells and proteins that are typically associated with combating parasitic worms as well as immune responses designed to go after fungi and bacteria that live outside of cells—an unusual response the team describes as “immunological misfiring,” as if the immune system is failing to activate the right program. And while the immune responses of those who recovered faded gradually over time, the heightened activity was maintained in patients with severe disease. Ultimately, their frenzied cytokine response doesn’t do much to stem the virus—based on swabs from the nose and throat, severe and moderate patients began with similar viral loads that only dropped off in the moderate group.

Trouble in the innate immune system

Severe COVID-19 is also marked by dysfunction in the immune cells that are first at the scene of a viral infection, including myeloid cells such as neutrophils and monocytes. For instance, researchers from Germany recently analyzed the properties of these cells in the blood of 109 individuals with mild, moderate, and severe COVID-19. Although patients with severe disease seemed to be manufacturing larger quantities of such cells, the cells themselves seemed to be only partially activated and dysfunctional. The neutrophils were largely immature, a feature that is thought to have a suppressive effect on the immune system, while the monocytes tended to have an inflammation-promoting phenotype and often lacked a critical surface protein (HLA-DR) needed for presenting viral material to T cells. The researchers didn’t spot these dysfunctional cells in mild or moderate cases.

… [Natural Killer (NK) cells are ] altered in severe cases of COVID-19 compared to non-severe cases, research by scientists in Sweden has shown. NK cells sense stressed cells and kill those infected with pathogens, while also releasing pro-inflammatory cytokines and influencing T cell responses. NK cells come in different flavors, from less-differentiated ones fresh out of the bone marrow—which are good at proliferating and secreting cytokines—to highly differentiated super killers specialized for taking down virally infected cells. NK cells were more skewed toward the former group in moderate disease. But “a subpopulation of NK cells that are the most terminally differentiated, that are the most skewed towards killing, they were specifically expanded in the severely sick patients,” explains senior author Niklas Björkström, an immunologist at the Karolinska Institute. Such killer cells have also been spotted in hantavirus and yellow fever virus infections, but it’s not clear if they play a deleterious role in driving further immune dysfunction or a protective role.

… COVID-19 patients also have vast quantities of antibody-secreting plasmablasts—another unusual feature of the disease. While other viral infections can provoke such a response, the increase tends to be short-lived, whereas in COVID-19 it seems to persist, Meyer adds. The blood of COVID-19 patients is also flooded with antibodies. But interestingly, new data from a study of 22 hospitalized patients suggest that although the quantity of antibodies didn’t differ between survivors and those who died, their function, and which viral proteins they targeted, correlated with severity.

Another peculiarity of the antibody response in severe COVID-19 patients is the apparent lack of a critical antibody creation process that takes place in the so-called germinal center of the lymph nodes and spleen. Ordinarily in viral infections, following a wave of initial virus-targeting antibodies that begins in the first few days of an infection, germinal centers form in the lymph nodes and spleen, where specialized B cells and T helper cells gather to produce a highly refined batch of antibody-producing cells that are crucial for lasting antibody immunity. But a study published last month demonstrated that those structures were absent in 11 COVID-19 patients who died from the disease. The germinal center formation may be stunted due to high levels of certain cytokines, the authors posit, or perhaps due to the defects of antigen-presenting cells that help drive that response, Shankar-Hari notes.

In line with those findings, data reported in a preprint by a team of Emory University researchers show that the abundance of two subtypes of B cells that create short-lived antibodies outside the germinal center correlated strongly with disease severity in 17 hospitalized patients, while those cells were barely present in healthy controls. The expansion of these B cell types has been primarily associated with flare-ups of autoimmune diseases such as systemic lupus erythematosus, where they’re reflective of an overly inflammatory state. It’s possible that this abnormal B cell response is the body’s attempt to generate antibodies after being somehow hindered from making them in germinal centers. Yet findings from autoimmune diseases also hint that “it may be that some of these cells are actually worsening the inflammatory cascade,” says Richard Ramonell, one of the study’s coauthors and a fellow in pulmonary and critical care medicine at Emory. __

Besides the cytokine levels mentioned in the above article, other blood tests may suggest which patients are at greatest risk of a potentially fatal infection.

Speculation is rampant:

Perhaps the ultimate culprit is a coagulation problem driven by the raging inflammation of blood vessels, says immunologist Niklas Björkström of the Karolinska Institute in Sweden, noting that infusions of the anticoagulant heparin reduced the fatality rate in some patient groups. “The fact that a lot of our patients have problems with clotting raises interest perhaps in the complement pathway or novel anticoagulant strategies,” Meyer says. In addition, “I do think we’re interested to know if we can perhaps intelligently intervene on this T cell activation without tipping the balance too much towards immune suppression,” she adds.

In other words, they are still largely shooting in the dark in terms of thoroughly understanding this Chinese microbe and the pandemic that triggered the hysterics of the world’s media, academic, and political classes.

But newer and possibly better treatments are being wheeled out for treating even the most severe infections, with less and less need for mechanical ventilation — unlike the initial hysterical declarations of politicians such as NY’s governor Cuomo.

In Florida, governor DeSantis is taking a more evidence-based, hard-headed approach to pandemic control, which is likely to save the state from the economic holocaust that has descended upon New York.

Families of those who were prevented from receiving treatments such as hydroxychloroquine — and who may have died as a result — are justified in suing government, public health, and media personnel to the utmost extent of the law.

Millions of people are taking or have taken hydroxychloroquine in nations that have managed to get their national pandemic under some degree of control. Two recent, large, early-use clinical trials have been conducted by the Henry Ford Health System and at Mount Sinai showing a 51% and 47% lower mortality, respectively, in hospitalized patients given hydroxychloroquine. A recent study from Spain published on July 29, two days before Margaret Sullivan’s strafing of “fringe doctors,” shows a 66% reduction in COVID mortality in patients taking hydroxychloroquine. No serious side effects were reported in these studies and no epidemic of heartbeat abnormalities.

This is ground-shaking news. Why is it not being widely reported? Why is the American media trying to run the U.S. pandemic response with its own misinformation? __ Source

The Great COVID Scam Never Stops

A scam from the beginning — this scam had the effect of spreading hysteria and economic damage to China’s enemies

A scam in the death counts — this had the effect of inflating death numbers therefore broadening the hysteria

A lockdown scam against free societies and a blow to the psychological health of people of all ages

Italics mine, to pre-confess that if I hear one more smug politician cluck glibly about “following the science” while continuing to support child-harming policies based largely on superstition and/or public sector union muscle, I’m going to lose the last of what remains of my California mellowness. Where the community spread is under control, just open the damned parks.

But they won’t because they don’t have to, and because making people suffer may provide them a political benefit.


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