DISPATCHES FROM MOON OF ALABAMA, BY "B"
This article is part of an ongoing series of dispatches from Moon of Alabama
In an utterly corrupt empire, everything is for sale and everything is politicized. Truth and science, too.
[dropcap]D[/dropcap]r. Fauci, the director of the National Institute of Allergy and Infectious Diseases, recently declared the anti-viral drug remdesivir as a "standard of care" based on unpublished trials. But the judgment was sketchy and has come under question as it seems that the government moved the goalposts to achieve this outcome:
Instead of counting how many people taking the drug were kept alive on ventilators or died, among other measures, the National Institute of Allergy and Infectious Diseases said it would judge the drug primarily on a different outcome: how long it took surviving patients to recover.
Death and other negative outcomes were moved to secondary measure status: They would still be tracked, but they would no longer be the key measure of remdesivir’s performance. The switch — which specialists said is unusual in major clinical trials but not unheard of — was publicly disclosed on the government’s clinicaltrials.gov website on April 16 but did not receive much attention at the time.
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“It raises a lot of flags, and it requires a lot of answers,” Walid F. Gellad, a professor of health policy and management at the University of Pittsburgh’s Department of Medicine, said in an interview, “especially when people start saying it’s become the standard of care, and all we saw was a news release in a trial with an outcome that was changed two weeks ago. It really is striking."
A Chinese double blind study of remdesivir, previously published in Lancet, had come to the conclusion that the drug had no statistically noticeable influence on the length of recovery and the outcome.
One wonders how much White House influence was used to push that drug. White House influence may also have been used in this ventilator acquisition that was paid for but never received the goods.
Children are less prone to catch the Covid-19 disease. Within households in China their chance of getting infected was only 30% of the average chance for all household members. For individuals over 65 years of age the chance was 150% of the household average. Children who catch the Coronavirus have in general only very mild symptoms. But they carry the same load of viruses as grownups do. That means that they are generally as infectious as adults.
During a normal school day a child will have often intense contact with some 47 other individuals. Typical adults only have some 15 inter-human contacts during a normal work day. That is why children, even when less susceptible to the disease, are still a very important epidemic vector. While closing schools can not completely interrupt an epidemic and is expensive it can lower the epidemic's peak by some 60%.
There were reports from South Korea that recovered Covid-19 patients had again caught the disease. This was always unlikely to be true. To test the patients the usual RT-PCR test was used. That test does not directly look for the virus but for distinct sections of its genetic RNA code.
We know that people can be infectious two days after they were infected. Around day five the first symptoms occur. Eight days later the infected persons will have stopped infecting other people.
But recovered patients may continue to shed non-infectious virus debris for several month. Professor Drosten, the now famous German coronavirus specialist, explained in one of his podcasts that it takes a while until clotted parts of the lungs reopen. When they do the virus debris contained in those parts will be shed just by normal breathing. An RT-PCR test may show these patients as positive but we can be sure that they are cured.
South Korea has now used other tests to confirm that those 're-infected persons' were indeed cured and no longer infectious.
Another Chinese study found that all people they tested who successfully recuperated from Covid-19 had developed antibodies:
Within 19 days after symptom onset, 100% of patients tested positive for antiviral immunoglobulin-G (IgG). Seroconversion for IgG and IgM occurred simultaneously or sequentially. Both IgG and IgM titers plateaued within 6 days after seroconversion.
The study used a special laboratory test, not the less reliable fast blood tests, to confirm the results.
That both types of antibodies reliably occur is very good news. We know from human reactions to other coronaviruses that these antibodies give immunity for at least a year. Even after that the body will react to a new infection much faster to find and kill the virus than in people who catch the virus for the first time. The symptoms of the second infection will therefore be much milder than those of the first one.
It is likely that the immunity will stay even longer than a year because the novel Coronavirus is so far less prone to mutate than the typical influenza viruses:
In fact, researchers have found that the coronavirus is mutating relatively slowly compared to some other RNA viruses, in part because virus proteins acting as proofreaders are able to fix some mistakes. Each month, a lineage of coronaviruses might acquire only two single-letter mutations.
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That bodes well for vaccines currently in development for Covid-19. If people get vaccinated in 2021 against the new coronavirus, they may well enjoy a protection that lasts for years.
The genetic code of the novel Coronavirus is about 30,000 letters long. Two modifications per month per strain are unlikely to change its immune-system appearance or function. A vaccine that creates sufficient antibodies will likely be long lasting.
The evidence is piling up that severe cases of the Covid-19 disease are related to an unusual immune system response caused by the SARS-CoV-19 virus:
Benjamin tenOever at the Icahn School of Medicine at Mount Sinai in New York City and his colleagues found that cells infected with SARS-CoV-2 produce unusually low levels of antiviral proteins called interferons compared with cells infected with other respiratory viruses (D. Blanco-Melo et al. Cell https://go.nature.com/3bWE82b, 2020). But levels of some proteins, such as IL-6, that activate more general immune responses are higher in infected ferrets and people than in uninfected controls.
During the outbreak in Hubei province one local Chinese hospital tested a new way to keep its staff healthy. It used the human interferon alpha, an immune system related messenger substance, in nasal drops applied four times a day. Out of nearly 3,000 staff, a third of whom cared for Covid-19 cases, none got infected. While this was not a randomized double blind study it points into an interesting direction.
Nicotine can also play a role in balancing the immune system response in Covid-19 cases. Smokers have been the accidental guinea pigs that allowed for these findings:
A quarter of French adults smoke. Many people were surprised, therefore, when researchers reported late in April that only 5% of 482 covid-19 patients who came to the Pitié-Salpêtrière hospital in Paris between February 28th and April 9th were daily smokers. The ratios of smokers to non-smokers in earlier tallies at hospitals in America, China and elsewhere in France varied. But all revealed habitual smokers to be significantly underrepresented among those requiring hospital treatment for the illness.
A new paper in Science Direct explains in detail why this may indeed happen. If the SARS-CoV-19 virus is not defeated early and replicates in huge numbers it imbalances the mixture of chemical messengers substances that keep the immune system under control. Then a so called cytokine storm happens and the immune system starts to attack the inner organs. This explains why doctors see such a wide range of different organ failures in critical Covid-19 cases. The authors of the study conclude:
Once someone is infected with SARS-CoV-2, the immune system is mobilized. As the virus replicates, cell and viral debris or virions may interact with the nAChRs blocking the action of the cholinergic anti-inflammatory pathway. If the initial immune response is not enough to combat the viral invasion at an early stage, the extensive and prolonged replication of the virus will eventually block a large part the cholinergic anti-inflammatory pathway seriously compromising its ability to control and regulate the immune response. The uncontrolled action of pro-inflammatory cytokines will result in the development of cytokine storm, with acute lung injury leading to ARDS, coagulation disturbances and multiorgan failure. Based on this hypothesis, COVID-19 appears to eventually become a disease of the nicotinic cholinergic system. Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm.
Some groups in France have started randomized studies with nicotine patches as therapy for Covid-19 cases.
Other researchers have investigated old and well known drugs that might be useful to influence the interaction between virus proteins and human ones. They found a few that work well in monkey cells and will now go on human trial. But they also found an often used drug that may help the virus. One is of serious concern:
Interestingly, a seventh compound – an ingredient commonly found in cough suppressants, called dextromethorphan – does the opposite: Its presence helps the virus. When our partners tested infected cells with this compound, the virus was able to replicate more easily, and more cells died.
This is potentially a very important finding, but, and I cannot stress this enough, more tests are needed to determine if cough syrup with this ingredient should be avoided by someone who has COVID-19.
Dextromethorphan or the derivative dextromethorphanhydrobromid is not only used in cough suppressants but also in combination drugs that are regularly used against the flu. The last time I caught a bad flu I used "Wick MediNait", a Procter & Gamble product. It is a combination of paracetamol, dextromethorphanhydrobromid and some other ingredients. If the next 'flu-like' disease hits me I will be back to pure paracetamol to suppress the fever and to syrup with thyme extracts to lighten the cough.
Posted by b on May 2, 2020 at 19:15 UTC | Permalink
I think this remdesivir authorization was a genius move by the Trump administration. So genial even Dr. Fauci must have immediately understood the catch and endorsed it, as it is probable the drug must not have any grave collateral effects on the patients (as is the case with hydroxycloroquine).
First of all, remdesivir helps one of America's biggest pharmaceuticals (Gilead). Therefore, it will also help American capitalist reproduction.
Second, it will trigger a nationwide placebo effect thanks to widespread optimism and petit-bourgeois euphoria, thus lowering the death rates (though not the infection rates), and giving Trump an election boost in crucial areas (by the astroturf protests pattern, important swing states in the Midwest).
Third, by the time the efficacy of remdesivir is debunked, the Trump administration can simply state they acted with good will, with the "evidence" available at the time, and gently apologize. It is the perfect plausible deniability.
Fauci should be fired for promoting this crap research on remdesivir. Changing the primary endpoint is verboten, plain and simple. The only reason to change the primary endpoint is to cherry-pick data in order to claim "success". Honest journals, if they still exist, will not publish this rubbish, as it contravenes their industry's "Committee on Publication Ethics" guidelines. The control arm of the trial was halted, another giant red flag, so there is nothing to compare their cherry-picked data against.
This trial is now at the quality level of the rubbish research that "proves" homeopathy "works". How can Fauci not be totally embarrassed by this? There must be powerful financial forces behind this. No amount of air freshener can cover up the stink...
Posted by: Trailer Trash | May 2 2020 19:44 utc | 3
Trailer Trash,
FAUCI is now prohibited by Trump admin from testifying before Congress on the COVID debacle. This criminal co-conspirator of Billy Goats owns the patents on the same HIV genes that just happened to be found as gain-of-function additions to the genome of the Corona virus. PROVING it is a lab made bioweapon. W/ Fauci's signature all over creation of this WMD. He should get the electric chair for genocide.
Posted by: NWOdna | May 2 2020 19:57 utc | 4
Looks like Artemisia, a plant common in Madagascar and South Africa may have good potential as a cure or at least prophylactic. Senegal, Guinea Bissau, Equatorial Guinea and Congo Brazzaville are ordering Covid-Organics from Madagascar..
Posted by: Lozion | May 2 2020 20:00 utc | 5
Recent developments and insights point out that SARS-COV-2 is not primarily a respiratory virus, it is mostly an epithelial virus. The lung surface is composed of epithelial cells, but so are many other organs in the body.
The virus binds to ACE2 receptors that are richly expressed in epithelial cells. ACE2 stands for the angiotensin II converting enzyme. By this binding action, it disables the function of this enzyme and therein lies the mechanism of the problems it causes in the body.
A cascade of reactions surrounding the angiotensin system results in the creation of, and exacerbation of pre-existing oxidative stress at the cellular level. This is why the actual risk categories turn out not to be asthmatics and other pulmonary patients, but instead diabetics, hypertensics and people with coronary disease.
Many COVID-19 victims die not from ARDS, but from sudden heart attacks, strokes and renal failure, in many cases systemic blood clotting is found. The "ground glass" lung photos are in fact showing pervasive alveolar bleeding.
Check out the latest of many highly informative MedCram videos on the topic:
https://m.youtube.com/watch?v=gzx8LH4Fjic
Posted by: Lurk | May 2 2020 20:01 utc | 6
Thanks b.. a lot of good info... i am not following this nearly as closely, but i thought of what @1 laguerre has said as particularly relevant to the conversation..
@ 6 lurk.. i had to look up that word - epithelial.. thanks for your post..
Posted by: james | May 2 2020 20:14 utc | 7
Professor Drosten, the now famous German coronavirus specialist,
Fascinating article indeed. Point taken, no tap beer for me, ever.
So he is trying these drugs:
But Drosten wants his research to save lives. Large cardboard boxes in his office hold supplies of two medicines waiting to be tried in the clinic. One is camostat mesylate, a pancreatitis drug approved in Japan that Drosten and others found can prevent both SARS-CoV and SARS-CoV-2 from entering cells. The other drug is niclosamide, used to treat tapeworms and other parasites. In a paper posted on the preprint server bioRxiv this month, Drosten's colleague Marcel Müller showed that SARS-CoV-2 interferes with the cellular recycling process called autophagy. It's unclear how exactly that benefits the virus, but niclosamide counters the interference. Treatment with the compound reduced SARS-CoV-2's growth in cell culture by 70%, the authors write. Drosten hopes to start to enroll patients soon in a trial to test a combination of the two drugs.
Posted by: hopehely | May 2 2020 20:20 utc | 8
OK, comment no.1 is now out of my system.
Two days ago I watched a bio on French TV of Didier Raoult, the controversial champion of hydroxychloroquine as a treatment for covid-19, broadcast just before an interview with the man himself. I knew already what he himself thinks. Hydroxychloroquine along with an anti-biotic whose name I forget is useful in the first week or so of infection, when the virus is massively increasing, but not useful in the second week when the viral mass is decreasing but you're still heading for death.
What interested me from the bio was that apart from his somewhat entrepreneurial foundation of his own institute, no doubt with much help from French big pharma, he'd once been invited to consult on a virus that had broken out in Briançon. It was localised to the abattoir, and he solved it with Hydroxychloroquine. So he's just been repeating what was done before.
In the end, Hydroxychloroquine is an ancient medicine, discovered nearly a century ago, with well-known secondary effects, and some benefits. Quite why Remdesivir is now being boosted totally escapes me.
Posted by: Laguerre | May 2 2020 20:22 utc | 9
"b" is Moon of Alabama's founding (and chief) editor. This site's purpose is to discuss politics, economics, philosophy and blogger Billmon's Whiskey Bar writings. Moon Of Alabama was opened as an independent, open forum for members of the Whiskey Bar community. Bernhard )"b") started and still runs the site. Once in a while you will also find posts and art from regular commentators. You can reach the current administrator of this site by emailing Bernhard at MoonofA@aol.com.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Remdesivir is the case I always thought would come. A drug of dubious use, but it's in patent, and costs a lot. The campaign against hydroxychloriquine was always because it's cheap and out of patent, and worse, made by the French.
Posted by: Laguerre | May 2 2020 19:27 utc | 1