Is anyone even listening to them any more ?
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Either for giggles or when they see something they want to see.
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Beyond a widespread phenomenon of magical (confirmation-bias fueled) thinking and speaking in an all too willing to hyperbolically theatricalize click-bait “press” (lauded and shrilly cited when they appeal to confirmation-bias filters, and shrilly excoriated with equal passions when their reporting happens to activate de-confirmation-bias filters), engendering episodes of acute phantasmagoria, …
… note that out of 382 swab-sampled PCR SARS-CoV-2 tests, only 5 samples registered as “positive”, and only one single incidence of the described genetic mutation was found. Note that researcher Efrem Lim indicates that the functional implications of that mutation (in SARS-CoV-2) are not presently understood. Also note that less than 0.5% of SARS-CoV-2 strains circulating worldwide have had their genomes sequenced (as of May 4, 2020). From those findings, SARS-CoV-2 genomes have been found to be relatively stable (as is acknowledged in the referenced research paper). Thus, all of this frenetic fuss is highly speculative.
Efrem Lim leads a team at ASU that looks at how the virus may be spreading, mutating and adapting over time. … using a pool of 382 nasal swab samples obtained from possible COVID-19 cases in Arizona, Lim’s team has identified a SARS-CoV-2 mutation that had never been found before, where 81 of the letters have vanished, permanently deleted from the genome. … “One of the reasons why this mutation is of interest is because it mirrors a large deletion that arose in the 2003 SARS outbreak,” said Lim, an assistant professor at ASU’s Biodesign Institute. During the middle and late phases of the SARS epidemic, SARS-CoV accumulated mutations that attenuated the virus. Scientists believe that a weakened virus that causes less severe disease may have a selective advantage if it is able to spread efficiently through populations by people who are infected unknowingly. … The ASU team is now hard at work performing further experiments to understand the functional consequences of the viral mutation. The viral protein is thought to help SARS-CoV-2 evade human defenses, eventually killing the cell. … Lim points out that only 16,000 SARS-CoV-2 genomes have been sequenced to date, which is less than 0.5% of the strains circulating.
Source: https://neurosciencenews.com/coronavirus-mutation-16327
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The research paper referenced (May 1, 2020):
From: https://jvi.asm.org/content/early/2020/04/30/JVI.00711-20/article-info
Out of 382 NP swabs collected from January 24 to March 25, 2020, we detected SARS CoV-2 in 5 swabs in the week of March 16 to 19. … further experiments are needed to determine the functional consequences of the ORF7a deletion. … global NGS efforts indicate that SARS-CoV-2 genomes are relatively stable …
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(Johns Hopkins University, June 9, 2020):
“The virus has had very few genetic changes since it emerged in late 2019,” says Peter Thielen, a molecular biologist at the Johns Hopkins Applied Physics Laboratory and JHU Doctor of Engineering candidate, who, with colleagues from other areas of the Hopkins research community, has been sequencing the viral genome to better understand its makeup. …
… Coronaviruses - of which there are hundreds, most of them occurring in animals - typically mutate more slowly than many other viruses. Influenza, for example, mutates quickly, which is why people must be inoculated annually against changing flu strains. Data from SARS-CoV-2 samples the researchers have examined from the Baltimore and Washington region are similar to those from other parts of the world. “So far, the genetic changes accumulating as the virus spreads are not resulting in different strains of the virus,” Thielen says. …
… “SARS-CoV-2 … is changing slowly, and because there is no existing immunity to the virus, it doesn’t have any evolutionary pressure to change as it spreads through the population.” …
… “There are very small regions of the spike protein that make direct contact with the receptor on a human cell, and these are the highest likelihood targets for vaccine developers. To date, no changes have been observed to these parts of the virus in any of the more than 20,000 samples that have been sequenced globally.”
… JHU scientists say they have seen fewer than two dozen mutations between the current versions they are studying and original viral isolates from China, which is a very small number.
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I’m not discounting what Lars posted, but it seems to me (too busy to research, link drop), that they have been growing very GOOD at reversing themselves, specifically during the COVID-19 incident.
So, apparently a team of scientists at the university of Copenhagen has had success in mice with their SARS-CoV-2-vaccine. Apparently they use a cVLP or vCLP (viral Capsid-Like Particle) to carry SARS-CoV-2-antigens into the host. The host then reacts and makes antibodies.
They expect to start tests in humans this year.
Article in Danish:
I bet they release an English one soon…
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The have a company called AdaptVac, and they did do an English press release:
Hørsholm, Denmark, June09, 2020 –AdaptVac, a PREVENT-nCoV consortium member, today announced that its COVID-19 cVLP vaccine induced high levels of virus neutralizing antibodies in an animal model. The vaccine elicited antibodies in mice which effectively prevented live SARS-CoV-2 virus from infecting and killing human cells in an in vitro assay.
The press release itself in PDF-format:
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Found the article (English translated) published by the University of Copehangen:
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(New York Times, June 9, 2020):
… on Monday, Dr. Maria Van Kerkhove, the W.H.O.’s technical lead for coronavirus response, said that “it still seems to be rare that an asymptomatic person actually transmits onward to a secondary individual.”
Her statement provoked an immediate backlash from scientists, who noted that study after study had shown transmission of the virus from people before they ever felt symptoms. …
… A key point of confusion is the difference between people who are “pre-symptomatic” and will go on to develop symptoms, and those who are “asymptomatic” and never feel sick. Dr. Van Kerkhove suggested that her comments were about people who are truly asymptomatic.
A widely cited paper published in April suggested that people are most infectious up to two days before the onset of symptoms, and estimated that 44 percent of new infections were a result of transmission from people who were not yet showing symptoms.
W.H.O. refers to such people as pre-symptomatic. “OK, technically fine,” Dr. Jha said. “But for all intents and purposes, they are asymptomatic - they are without symptoms.”
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The above-referenced paper:
(Nature, April 15, 2020):
“Temporal dynamics in viral shedding and transmissibility of COVID-19”
We estimated that 44% (95% confidence interval, 25-69%) of secondary cases were infected during the index cases’ presymptomatic stage, in settings with substantial household clustering, active case finding and quarantine outside the home. Disease control measures should be adjusted to account for probable substantial presymptomatic transmission. …
… we have estimated that viral shedding of patients with laboratory-confirmed COVID-19 peaked on or before symptom onset, and a substantial proportion of transmission probably occurred before first symptoms in the index case.
@Mikser I’m hearing FRESH reports from the “News”, claiming and uptick, and citing the protests as the source/cause. If that WERE to be the case, do we publicly condemn those who embraced protesting ?
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(Ars Technica, June 11, 2020):
While this is a draft paper and should be viewed cautiously, the results are largely in line with a separate draft study of 175 patients done by an unrelated group of researchers in China. This also saw high levels of variability and a small subset of patients that had no detectable antibodies to SARS-CoV-2. Another group based in New York found even higher levels of variability, but it found neutralizing antibodies in most patients, even if they were rare. There have also been a number of draft studies that suggest that the levels of antibody produced correlate roughly with the severity of COVID-19 symptoms that a person experienced. …
… SARS-CoV-2 infection isn’t necessarily producing a robust immunity. We don’t really know what levels of neutralizing antibodies are actually protective, but it’s clear that a lot of people don’t produce many of them after an infection. Which means any plans for generating herd immunity by allowing a controlled level of infection have to be viewed with extreme skepticism at this point. And vaccine developers will need to ensure that the injections produce a consistently high-level response that includes neutralizing antibodies.
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(Washington Post, June 11, 2020):
“Lots of us are infected by the coronavirus - and don’t know it.
Here’s what that means.”
Evidence is accumulating, though it remains inconclusive, that the novel coronavirus can indeed spread silently, transmitted through infected people who will never experience symptoms, just as it is transmitted by the presymptomatic before they become ill. Covid-19’s dual nature - often benign, yet sometimes deadly - puts it in a rare category among the common pathogens that afflict humanity.
Since mid-April, we have been tracking an ever-increasing number of medical studies and news reports that have clarified the prevalence of asymptomatic infection by SARS-CoV-2, the virus that causes covid-19. In our recent review published in the Annals of Internal Medicine, we collected data from 16 sources, spanning the globe and in settings as diverse as cruise ships, nursing homes, homeless shelters and prisons.
In assessing the overall rate of asymptomatic infection, we found some dramatic outliers. For example, among 3,277 prison inmates in four states who tested positive for the coronavirus, an astounding 96 percent had no symptoms at the time of testing. At the other end of the spectrum, a mere 6 percent of 48 infected nursing home residents remained asymptomatic. It appears that a variety of factors, perhaps including age and previous exposure to other, more benign coronaviruses, may account for these extremes. …
… we have been impressed by the uniformity of data from the three representative samples in our collection. … three studies have yielded asymptomatic infection percentages of 42 percent, 43 percent and 45 percent. Knowing that some people in these cohorts went on to have symptoms, we concluded that the overall rate of asymptomatic infection is likely at least 30 percent and could be as high as 40 percent to 45 percent.
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Here such a wide definitional net is cast that distinctions seem nearly meaningless:
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(The Guardian, June 7, 2020):
From the beginning, Covid-19 struck unevenly across the globe, and scientists have been trying to understand the reasons. Why are some populations or sectors of a population more vulnerable than others? Or to turn the question around, why are some groups relatively protected? …
… One thing seems clear: there are many reasons why one population is more protected than another. Theoretical epidemiologist Sunetra Gupta of the University of Oxford thinks that a key one is immunity that was built up prior to this pandemic. “It’s been my hunch for a very long time that there is a lot of cross-protection from severe disease and death conferred by other circulating, related bugs,” she says. Though that cross-protection may not protect a person from infection in the first place, it could ensure they only experience relatively mild symptoms. …
… Antibody testing, as we know, was slow to get going and unreliable to begin with, and the results to date suggest that the percentages of populations carrying antibodies to the Covid-19 virus are often in single or low-double digits. New, more sensitive antibody tests that have become available in recent weeks could soon provide a much more accurate picture if deployed widely enough, but there are already hints that the results to date may be underestimates. …
… cross-reactivity doesn’t necessarily translate into immunity. … If exposure to other coronaviruses does protect against Covid-19, Gupta says, then variability in that exposure could explain much of the difference in fatality rates between countries or regions. Exposure to the related virus that caused the epidemic of severe acute respiratory syndrome (Sars) in 2002-4 might have afforded some protection to east Asians against Covid-19, for example. …
… We know some of those vulnerability factors. Age is the most obvious one. Unlike with the 2009 flu, elderly people are particularly vulnerable to Covid-19 - a fact that might reflect the history of exposure to coronaviruses of different age cohorts. Comorbidity is another, and a third is being male. … Socioeconomic status, climate, culture and genetic makeup could also shape vulnerability, as could certain childhood vaccines and vitamin D levels. And all of these factors can vary between countries. …
… Friston’s models … suggest that immunity in the population is higher than data indicates, but for him it’s not clear how long that immunity will last …
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Another super interesting video from MedCram - Looks like HFCS also has a (bad) role to play!
Way before this pandemic, I’ve steered clear (as much as I could) of HFCS-stuff. Fortunately it’s not that widely used here in Europe! I also avoid artificial sweeteners as much as I can - I have no problem using regular sugar - after all, I don’t use a lot of it.
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I can not use hfcs either… something in it does not do my body good at all!
I have found cane sugar to be the best, pure and raw, and I rarely use it either.
I might go thru a 1/4 bag of 8oz in a year.
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Sucrose (“regular sugar” consists of a fructose molecule and a glucose molecule):
Sucrose is common sugar. It is a disaccharide, a molecule composed of two monosaccharides: glucose and fructose. … In humans and other mammals, sucrose is broken down into its constituent monosaccharides, glucose and fructose … Sucrose is digested rapidly, but has a relatively low glycemic index due to its content of fructose, which has a minimal effect on blood glucose.
Source: https://en.wikipedia.org/wiki/Sucrose
Glucose (also known as Dextrose) is not itself very sweet (at all, to my palate). I use a bit of it to mildly boost blood (glucose) sugar levels on occasion (including a few grams in my morning tea). I use Sucralose (~600 times sweeter than Sucrose) to sweeten foods/beverages - which does not appear to be a harmful substance.
(2016): “Artificial sweeteners as a sugar substitute: Are they really safe?”
(2009): “An overview of the safety of sucralose”
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A 2017 paper regarding Fructose metabolism; possible implications upon health:
Fructose is associated with the biochemical alterations that promote the development of metabolic syndrome (MetS), nonalcoholic fatty liver disease, and type 2 diabetes. … Fructose has not been a main focus of glycation research because of the difficulty in measuring its adducts, and, more importantly, because although it is 10 times more reactive than glucose, its plasma concentration is only 1% of that of glucose. In this focused review, I summarize exogenous and endogenous fructose metabolism, fructose glycation, and in vitro, animal, and human data. Fructose is elevated in several tissues of diabetic patients where the polyol pathway is active, reaching the same order of magnitude as glucose. It is plausible that the high reactivity of fructose, directly or via its metabolites, may contribute to the formation of intracellular AGEs and to vascular complications. The evidence, however, is still unconvincing.
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High Fructose Corn Syrup (HFCS) is extensively used in many processed foods (because it’s far less expensive per perceived unit of “sweetness” than Sucrose). (In the US), there is no requirement to disclose it’s presence in processed/prepared foods. Anything whatsoever that states “sugar(s)” as ingredient(s) may contain it.
I already avoided HFCS like the plague as I knew how it was made. Seeing all the lobbying commercials stating how safe it was, made that decision even easier, but once I found the connection with “leaky gut syndrome” I started lobbying ALL of my friends, family, co-workers to abstain as well.
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