Sunday, 8 November 2020

Malevolent Designer News - More Mendacity in 'Design' of SARS-CoV-2

Virus that causes COVID-19 puts a plug in cellular defenses | YaleNews

Three stories in the scientific news today show the amazingly creative intelligence of the evil genius whom creationists believe created the SARS-CoV-2 virus.

The first is about how the virus overcomes the immune system this creator allegedly created to protect us from its creations - like viruses and bacteria. According to the findings of a research team from Yale, the virus reprograms the cell to make a protein, known as non-structural protein 1 (Nsp1) which acts as as plug to block the channel in the ribosomes through which the strand of messenger RNA (mRNA) needs to pass for transcription into a protein to occur. This prevents the cell from producing the immune proteins it needs to fight infections.

According to Bill Hathaway, writing in Yale News:
One of the novel coronavirus’ most insidious tricks is that it can block the ability of cells to produce protective proteins without hindering its own ability to replicate.

Now, a multidisciplinary team of Yale researchers has discovered how SARS-CoV-2, the virus that causes COVID-19, accomplishes this trick by blocking production of cellular proteins, including immune molecules, and contributes to severe illness in its host.

“The virus essentially reprograms host cells, and by understanding this mechanism we can hopefully design new therapeutics,’’ said Yong Xiong, professor of molecular biophysics and biochemistry and co-corresponding author of the research published in the journal Molecular Cell.

Previous studies had implicated a viral protein, nonstructural protein 1 or Nsp1, in the COVID-19 virus’ ability to block cells’ ability to produce new proteins. But exactly how NsP1 works in a cell was not known.

SARS-CoV-2 protein Nsp1 plugs the messenger RNA (mRNA, the genetic blueprint) entry channel on the ribosome to block the host protein production.
Using advanced genetic screening and cryogenic electron microscopy (cryo-EM), the Yale team was able to show that Nsp1 is one of SARS-CoV-2’s most pathogenic viral proteins. In human lung cells, it can drastically alter host cell gene expression and essentially form a plug that prevents the ribosome, the cell’s protein-making machinery, from receiving genetic instructions for new proteins encoded in messenger RNA.

“This is the entry channel for genetic material, and when it is blocked no protein can be made,” Xiong explained. “We didn’t understand this mechanism before, but now we know.”

This process affects protein production in many parts of the body, and high levels of Nsp1 may help explain why some people fare poorly after infection by the virus, he said.

However, it remains unknown how the virus is still able to produce its own proteins, using the same ribosome, to replicate in the cell after it disables the cell’s ability to make normal proteins, Xiong said.

Basically, when the SARS-CoV-2 virus gains entry to a cell, the first thing it does is set about gumming up the mechanism by which the cell was designed to defend itself. ID proponents regard creating a mechanism for overcoming the defences it designed earlier, as a sign of the high intelligence of the designer!

One of Donald Trump's super-spreader events, laid on for covidiot trumpanzees during his failed 2020 re-election campaign
Source: AP
The second example is how the SARS-CoV-2 virus has been shown to be good at creating super-spreader events when people are crowded together.

Covid-19 “super-spreading” events play outsized role in overall disease transmission | MIT News | Massachusetts Institute of Technology

Writing in MIT News, the on-line news site for the Massachusetts Institute of Technology, Anne Trafton, of the MIT News Office explained:
There have been many documented cases of Covid-19 “super-spreading” events, in which one person infected with the SARS-CoV-2 virus infects many other people. But how much of a role do these events play in the overall spread of the disease? A new study from MIT suggests that they have a much larger impact than expected.

Interventions limiting superspreading may be particularly effective at controlling the ongoing COVID-19 pandemic, according to an analysis of SARS-CoV and SARS-CoV-2 superspreading events.
Credits:Image: Equinox Graphics
study of about 60 super-spreading events shows that events where one person infects more than six other people are much more common than would be expected if the range of transmission rates followed statistical distributions commonly used in epidemiology.

Based on their findings, the researchers also developed a mathematical model of Covid-19 transmission, which they used to show that limiting gatherings to 10 or fewer people could significantly reduce the number of super-spreading events and lower the overall number of infections.

“Super-spreading events are likely more important than most of us had initially realized. Even though they are extreme events, they are probable and thus are likely occurring at a higher frequency than we thought. If we can control the super-spreading events, we have a much greater chance of getting this pandemic under control,” says James Collins, the Termeer Professor of Medical Engineering and Science in MIT’s Institute for Medical Engineering and Science (IMES) and Department of Biological Engineering and the senior author of the new study.

Extreme events

For the SARS-CoV-2 virus, the “basic reproduction number” is around 3, meaning that on average, each person infected with the virus will spread it to about three other people. However, this number varies widely from person to person. Some individuals don’t spread the disease to anyone else, while “super-spreaders” can infect dozens of people. Wong and Collins set out to analyze the statistics of these super-spreading events.

“We figured that an analysis that’s rooted in looking at super-spreading events and how they happened in the past can inform how we should propose strategies of dealing with, and better controlling, the outbreak,” Wong says.


The researchers defined super-spreaders as individuals who passed the virus to more than six other people. Using this definition, they identified 45 super-spreading events from the current SARS-CoV-2 pandemic and 15 additional events from the 2003 SARS-CoV outbreak, all documented in scientific journal articles. During most of these events, between 10 and 55 people were infected, but two of them, both from the 2003 outbreak, involved more than 100 people.

Given commonly used statistical distributions in which the typical patient infects three others, events in which the disease spreads to dozens of people would be considered very unlikely. For instance, a normal distribution would resemble a bell jar with a peak around three, with a rapidly-tapering tail in both directions. In this scenario, the probability of an extreme event declines exponentially as the number of infections moves farther from the average of three.

However, the MIT team found that this was not the case for coronavirus super-spreading events. To perform their analysis, the researchers used mathematical tools from the field of extreme value theory, which is used to quantify the risk of so-called “fat-tail” events. Extreme value theory is used to model situations in which extreme events form a large tail instead of a tapering tail. This theory is often applied in fields such as finance and insurance to model the risk of extreme events, and it is also used to model the frequency of catastrophic weather events such as tornadoes.

Using these mathematical tools, the researchers found that the distribution of coronavirus transmissions has a large tail, implying that even though super-spreading events are extreme, they are still likely to occur.

“This means that the probability of extreme events decays more slowly than one would have expected,” Wong says. “These really large super-spreading events, with between 10 and 100 people infected, are much more common than we had anticipated.”

Stopping the spread

Many factors may contribute to making someone a super-spreader, including their viral load and other biological factors. The researchers did not address those in this study, but they did model the role of connectivity, defined as the number of people that an infected person comes into contact with.

To study the effects of connectivity, the researchers created and compared two mathematical network models of disease transmission. In each model, the average number of contacts per person was 10. However, they designed one model to have an exponentially declining distribution of contacts, while the other model had a fat tail in which some people had many contacts. In that model, many more people became infected through super-spreader events. Transmission stopped, however, when people with more than 10 contacts were taken out of the network and assumed to be unable to catch the virus.

The findings suggest that preventing super-spreading events could have a significant impact on the overall transmission of Covid-19, the researchers say.

“It gives us a handle as to how we could control the ongoing pandemic, which is by identifying strategies that target super-spreaders,” Wong says. “One way to do that would be to, for instance, prevent anyone from interacting with over 10 people at a large gathering.”

This finding by Felix Wong and James J Collins was published, open access, in PNAS a few days ago:


Superspreaders, infected individuals who result in an outsized number of secondary cases, are believed to underlie a significant fraction of total SARS-CoV-2 transmission. Here, we combine empirical observations of SARS-CoV and SARS-CoV-2 transmission and extreme value statistics to show that the distribution of secondary cases is consistent with being fat-tailed, implying that large superspreading events are extremal, yet probable, occurrences. We integrate these results with interaction-based network models of disease transmission and show that superspreading, when it is fat-tailed, leads to pronounced transmission by increasing dispersion. Our findings indicate that large superspreading events should be the targets of interventions that minimize tail exposure.

The third news item concerns a worrying development in Denmark, where a mutant strain of SARS-CoV-2 has been found to infect mink and other mustelids such as otters, weasles, stoats, pine martens and badgers and is transmissible to humans.

Danish Covid-19 mink variant could spark new pandemic, scientists warn | Environment | The Guardian

According to this report in the Guardian, Denmark's Prime Minister, Mette Frederiksen, said 12 people were already infected with the mutated virus and mink are now considered a public health risk, based on advice from the State Serum Institute (SSI). Denmark is the largest world producer of mink furs with some 260 mink farms, but the Danish government has ordered a cull of Denmark's 15 million plus mink in an effort to contain what could be the start of a new pandemic with a strain that has reduced sensitivity to antibodies to the original form of the virus, including those produced by the vaccines medical science is currently working on.

According to the Danish SSI:

Mutations in the mink virus

Danish mink variants of COVID-19 have been found that show signs of being less sensitive to antibodies from people who have passed a COVID-19 infection.

A new cluster of Covid-19 cases in Denmark has been traced to a mutant SARS-CoV-2 virus infecting mink in mink farms
Yesterday, Prime Minister Mette Frederiksen announced that all mink in Denmark must be killed. The reason is that infection among mink farms is increasing in number and geographical spread, without the preventive measures having worked. That people in areas with infected mink farms become infected from the mink. And that new mink variants of COVID-19 have been seen, which show reduced sensitivity to antibodies from several people with a history of infection. This is serious as it may mean that a future COVID-19 vaccine will be less effective against infection with these variants.


Pr. On 6 November, COVID-19 infection was registered in Denmark on 216 mink farms. This development has taken place despite intensive efforts by the authorities to limit the infection.

At the same time, new mink variants of COVID-19 virus have been seen in mink. This applies both among people who work with mink and in the local population. There has also been a strong geographical and temporal connection between the number of positive mink farms and the incidence of infection among people in the North Jutland Region.

Mink virus variants

Mink variants occur when there are small changes in virus genetic material (mutations). These occur continuously in connection with the virus copying itself. The more viruses that are copied, the greater the likelihood of mutations occurring.

It is well known that virus mutations can occur especially when viruses jump from one species to another, for example from humans to mink, and from mink to humans. This is done by adapting to the new species. Viruses can also mutate when transmitted between many individuals. It can be, for example, at an animal market or in a large mink farm. This results in a large virus reservoir and various virus variants.

A virus's genetic material, and thus any mutations, can be detected by whole genome sequencing (WGS).

It mutated the mink virus

So far, five different groups or clusters of mink variants have been found in Denmark (clusters 1-5).

Among these mink variants, seven different mutations have been seen in the so-called Spike protein on the coronavirus surface. And there are examples of up to four different changes in the Spike protein in the same virus.

The spike protein is essential as it is the protein that viruses use to penetrate a cell. Following a natural infection, humans develop antibodies to the Spike protein. The potential COVID-19 vaccine candidates are also based on this important protein. Therefore, there is a risk that the effect of Spike-based anti-COVID19 vaccines may be affected when there are changes in the Spike protein on the viruses that the vaccine is to fight.

A specific virus from cluster 5 has been detected with four simultaneous changes in the genes for the Spike protein in five North Jutland mink farms and in 12 patient samples. Of these, four people were directly connected to three of these farms.

To those skilled in the art, SSI may report that viruses have had the following changes in amino acids: H69del / V70del, Y453F, I692V and M1229I. Information on all variants will be uploaded in the international system GISAID.

Decreased sensitivity

Preliminary studies suggest that this virus from cluster 5 exhibits decreased susceptibility to antibodies from more individuals with past infection compared to non-mutated virus. This has been demonstrated in laboratory experiments, where it is seen that the particular mink virus is not inhibited to the same degree by antibodies from humans who have been infected with SARS-CoV-2 compared to other non-mutated SARS-CoV-2 viruses. Studies are currently underway that will further uncover the issue.

This finding is worrying as it could potentially have an impact on the future of COVID-19 vaccine against infection with this and other new mink variants. It may also pose a risk of impaired immunity to these following COVID-19 infection. It is important both for the individual and for the possibility of reinfections with mutants.

Viruses from cluster 1 have also been examined using the same method, but no evidence of reduced sensitivity to antibodies was found. The other variants (cluster 2-4) and are also being tested for sensitivity. However, these studies take time (weeks) as viruses need to be cultured first.

Mink varieties among humans

In Denmark, mink variants of the virus have been detected in 214 people among 5,102 samples that have been completely sequenced from week 24 to week 42. This is the period when there has been an outbreak of SARS-CoV-2 among mink.

During this period, a total of 37,967 infections have been detected, so that the proportion of sequenced samples is 13%. Out of the 214, these mink variants have been found in 200 people in the North Jutland Region (94%). During this period, 535 samples have been sequenced in North Jutland. This means that mink variants have been detected in 40% of the samples. In addition, 14 people have been infected with these mink variants outside North Jutland, where 4,568 samples were sequenced during the period, corresponding to 0.3% of the samples.

Cluster 5 virus was found on five mink farms and in 12 samples in August and September. Of these, 11 are from North Jutland and 1 person on Zealand.

Overall, this suggests that infection with mink variants is so far primarily a problem in North Jutland closer to the infected farms.

SSI's risk assessment

SSI has for a long time expressed concern about the mutations that occur in the Spike protein. However, concerns that there may be decreased susceptibility to antibodies from vaccines were of a theoretical nature. This concern has now become real after the trials that SSI first had results of on Monday, November 2nd.

Therefore, SSI sent a new risk assessment to the Ministry of Health on 3 November.

SSI estimated that continued mink breeding would entail a significant risk of recurrence of a large spread of infection among mink and humans, as seen in Western Denmark in 2020.

SSI estimated that this would pose a major risk to public health. Both know that the many infected mink farms can lead to a greater disease burden among humans, and know that a large virus reservoir in mink increases the risk of new virus mutations occurring again, which vaccines may not provide optimal protection against.

Overall, the immunity gained through vaccination or past infection may also be at risk of being weakened or absent.

The overall conclusion, which was also supported by the Danish Health and Medicines Authority, was therefore that continued mink breeding during an ongoing COVID-19 epidemic entails a significant risk to public health. Including the possibilities for optimally preventing COVID-19 with vaccines.

Should one be worried as a booker?

As a citizen, you do not have to worry. The mutated virus is no more dangerous than other viruses or more contagious. However, if it spreads in Denmark or internationally, it could potentially have serious consequences for the protective effect of the upcoming vaccines. The best way to get rid of this variant is generally to slow down the spread of infection. This is especially true in North Jutland, where the mink variants are most widespread, but also others in the rest of the country.

Translated from Danish using Google Translate.
So, it would appear that creationism's putative intelligent designer, if we accept that absurd notion for a moment, is already finding ingenious ways around our attempt to produce either a vaccine, or to use the almost equally absurd notion of 'herd immunity' (or 'herd mentality' as President Reject Donald J Trump once called it). It can also hide itself away in wild animals, just as I said recently, this corona virus appears to be amongst the most zoonotic viruses, and so can infect other species, not just bats.

Currently, most of our search for a vaccine is directed at producing an antibody that latches on to the virus' 'spike' proteins on it's outer surface. These are used by the virus to attach to our angiotensin conversion enzymes (ACE) on the surface of our cells to gain entry into the cell. Antibodies which attach to these 'spike' proteins inhibit the virus' ability to attach to our ACE proteins.

This means, any mutation in this 'spike' protein may reduce the ability of the antibodies to attach to them and so reduce the virus's sensitivity to the immune response. The fact that the 'mink' version has about six mutations in its 'spike' proteins and is interchangeable between mink (and presumably its wild relatives) makes this an especially serious development.

In Intelligent [sic] Design Creationist terms, their mendacious and infinitely devious designer appears to be keeping one step ahead of medical science in its determination to make as many of us sick and die as possible with its new weapon of mass destruction, SARS-CoV-2.
Sadly, this information came too late to be included in my latest book, The Malevolent Designer: Why Nature's God is not Good.

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