The idea is planted in people’s mind that this virus is mutating in such a way as to evade prior immunity. This is completely unfounded, certainly as regards immunity..
In a number of Sunday papers:
Scientific advisers said it was “hard to see” when the restrictions would end as new variants continued to emerge, delivering a potentially devastating blow to the travel industry. The prime minister said that after progress with vaccinations...
The idea is planted in people’s mind that this virus is mutating in such a way as to evade prior immunity. This is completely unfounded, certainly as regards immunity..
To mutations & variants. Many viruses are error-prone when they replicate in your cells. They make “typos” so the virus which results is...
Why these incorrect stories are being spun, I’ve no idea, that not being a scientific matter. But spin & completely inappropriate & severe restrictions...
More from Yardley Yeadon
I urge all followers who have read my criticisms of PCR mass testing in U.K. to carefully read Mr Fordham’s carefully worded letter. Note that the innovation minister in the Lords, Lord Bethel, already admitted that the PCR system doesn’t have the equivalent of an MOT. https://t.co/zXzeDMKCBb
Without this information it’s impossible to interpret any result. If the oFPR is 4%, for example, and if the true prevalence is 0.3% (it’s probably less), then for every 10,000 tests, 400 positives would be false & 30 positives would be genuine. So 93% of positives are false.
As Mr Fordham points out, almost all policies pivot on PCR mass testing. Hancock previously admitted on talkRADIO to Julia Hartley-Brewer in late summer that the FPR was “just under 1%”. That was a flat lie (possibly inadvertent but he’s never corrected the record). The reason...
...we are sure Hancock told a lie is that they have never known the FPR. Those including Hancock who believe that the oFPR can be estimated by inspection of the lowest positivity ever recorded, while logical, is completely wrong. Changes in personnel, throughout, testing...
...architecture & the like can radically alter the oFPR. Since Hancock’s remark in late summer, PCR mass testing has moved into the Lighthouse Labs & this creates a new & urgent need to continually assess oFPR. I’ve good reason to believe it’s now VERY much higher now that the...
So I wrote back to @lucyfrazermp for another go. Here\u2019s my letter.
— Edmund Fordham (@EdmundFordham) November 28, 2020
They don\u2019t understand how serious this is.
If they can\u2019t tell us the oFPR, our PCR testing is worthless. (thread) pic.twitter.com/zHJ8SJCzf1
Without this information it’s impossible to interpret any result. If the oFPR is 4%, for example, and if the true prevalence is 0.3% (it’s probably less), then for every 10,000 tests, 400 positives would be false & 30 positives would be genuine. So 93% of positives are false.
As Mr Fordham points out, almost all policies pivot on PCR mass testing. Hancock previously admitted on talkRADIO to Julia Hartley-Brewer in late summer that the FPR was “just under 1%”. That was a flat lie (possibly inadvertent but he’s never corrected the record). The reason...
...we are sure Hancock told a lie is that they have never known the FPR. Those including Hancock who believe that the oFPR can be estimated by inspection of the lowest positivity ever recorded, while logical, is completely wrong. Changes in personnel, throughout, testing...
...architecture & the like can radically alter the oFPR. Since Hancock’s remark in late summer, PCR mass testing has moved into the Lighthouse Labs & this creates a new & urgent need to continually assess oFPR. I’ve good reason to believe it’s now VERY much higher now that the...
@ukiswitheu I invite people to run the thought experiment: “what if the ‘cases’ data is inaccurate?”
Ignore ‘cases’, look instead only at excess deaths (per M Levitt’s tweet). Does that look characteristic of an epidemic? It’s completely diff from spring or any winter flu outbreak.
London:
Can anyone explain why there is no ‘2nd wave’ of excess deaths in London, without invoking herd immunity?
It’s not lockdown. See NW England:
This is the largest #SecondaryRipple (which I predicted).
https://t.co/b0rT5Lq9HI
Now check the 3 predictions I made months ago. They’ve all happened. Compare predictions from SAGE’s statements: they’re all wrong.
Even neutrals at this point might ask themselves “if he’s been right on all predictions, maybe he’s correct now?”
I’ve been saying since the Lighthouse Labs got up & running that I’m deeply sceptical about the trustworthiness of their ‘cases’ data. I showed how, at low virus prevalence, the PCR mass testing data was throwing out potentially 90% positives being
https://t.co/t4qQN4rH0u
I got ‘fact checked’ a LOT over that statement. This paper just published, about precisely that time period I speculated about. Turns out that high-80s% of Dr Healy’s positives by PCR were FALSE. This alone is sufficient in my view to throw severe doubt...
Ignore ‘cases’, look instead only at excess deaths (per M Levitt’s tweet). Does that look characteristic of an epidemic? It’s completely diff from spring or any winter flu outbreak.
London:
Can anyone explain why there is no ‘2nd wave’ of excess deaths in London, without invoking herd immunity?
It’s not lockdown. See NW England:
This is the largest #SecondaryRipple (which I predicted).
https://t.co/b0rT5Lq9HI
Now check the 3 predictions I made months ago. They’ve all happened. Compare predictions from SAGE’s statements: they’re all wrong.
Even neutrals at this point might ask themselves “if he’s been right on all predictions, maybe he’s correct now?”
I’ve been saying since the Lighthouse Labs got up & running that I’m deeply sceptical about the trustworthiness of their ‘cases’ data. I showed how, at low virus prevalence, the PCR mass testing data was throwing out potentially 90% positives being
https://t.co/t4qQN4rH0u
I got ‘fact checked’ a LOT over that statement. This paper just published, about precisely that time period I speculated about. Turns out that high-80s% of Dr Healy’s positives by PCR were FALSE. This alone is sufficient in my view to throw severe doubt...
More from Science
Localized Surface Plasmon Resonance - an overview | ScienceDirect Topics
https://t.co/mzS7vVSREJ
https://t.co/353PdAX2fa
https://t.co/3yBImjOdd4
In some cases, almost 100% of the light energy can be converted to the second harmonic frequency. These cases typically involve intense pulsed laser beams passing through large crystals, and careful alignment to obtain phase matching.
https://t.co/mzS7vVSREJ
https://t.co/353PdAX2fa
https://t.co/3yBImjOdd4
In some cases, almost 100% of the light energy can be converted to the second harmonic frequency. These cases typically involve intense pulsed laser beams passing through large crystals, and careful alignment to obtain phase matching.
Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).
Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.
You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.
The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.
In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.
The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.
Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.
Feels like the next thing we're going to need is a ranking system for how concerning "variants of concern\u201d actually are.
— Kai Kupferschmidt (@kakape) January 15, 2021
A lot of constellations of mutations are concerning, but people are lumping together variants with vastly different levels of evidence that we need to worry.
You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.
The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.
In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.
The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.
1/ Automobiles and Intake Fraction. Since cars are back in the news I thought I would retweet this model result I offered in early April 2020. I focused only on 1 micron particles & accounted for windows completely closed & cracked slightly open.
2/ Related air exchange rates were based on experimental results in literature for mid-sized sedans. Particle deposition to indoor surfaces were accounted for, as the surface to volume ratio in a 3 m3 cab is large. An important outcome was the intake fraction (IF)
3/ Here, IF is the number of particles (or virions in collective particles) inhaled by a receptor DIVIDED BY the number or particles (or virions in collective particles) emitted by an infector.
4/ Integrated over the two hour drive (in this example) the IF for all windows closed & a receptor at rest is 0.08 (8% of what comes out of the infectors respiratory system ends up in the respiratory system of the receptor). 8%! That is a very high intake factor.
5/ With additional ventilation from cracking a window open drops the IF to 0.012 (1.2%) still relatively high. Can get lower by opening more windows.
Simulation: Riding in car for 120 min w/ infected passenger who seems fine other than a cough every few mins. (1) a lot of SARS-CoV-2 virus (in fine aerosol particles) accumulation in car cabin w/ windows closed; (2) cracking window open slightly = dramatic reduction. #COVID19 pic.twitter.com/bCmrmnLUPG
— Dr. Richard Corsi (@CorsIAQ) April 4, 2020
2/ Related air exchange rates were based on experimental results in literature for mid-sized sedans. Particle deposition to indoor surfaces were accounted for, as the surface to volume ratio in a 3 m3 cab is large. An important outcome was the intake fraction (IF)
3/ Here, IF is the number of particles (or virions in collective particles) inhaled by a receptor DIVIDED BY the number or particles (or virions in collective particles) emitted by an infector.
4/ Integrated over the two hour drive (in this example) the IF for all windows closed & a receptor at rest is 0.08 (8% of what comes out of the infectors respiratory system ends up in the respiratory system of the receptor). 8%! That is a very high intake factor.
5/ With additional ventilation from cracking a window open drops the IF to 0.012 (1.2%) still relatively high. Can get lower by opening more windows.
https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get
A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from
The Taq. https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals
Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.
The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get
A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from
The Taq. https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals
Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.
The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
