“Viral” load is a common measure that one often hears about from the CDC/WHO/MSM when discussing “Covid-19” and disease severity. It is considered an estimation of the amount of “virus” that is within a person’s body fluid. This is primarily determined through calculations based off the Cycle Threshold (Ct) Value from a PCR test. Virologists assume that if a person has a low Ct value, they have a high “viral” load and vice versa. They also assume that a low Ct value/high “viral” load equates to more severe disease. However, looking through various sources shows that correlation does not equal causation no matter how hard virologists may want that to be the case:
This first article states that various studies have found no difference in the “viral” load between those who have symptoms of “Covid-19” and those who are considered asymptomatic. They also note that there is no difference in “viral” loads between kids and adults, with kids being primarily asymptomatic. This clearly shows that a person’s supposed “viral” load (i.e. amount of “virus” estimated to be in the body) has no relation to disease severity whatsoever:
“Scientists have cleared up many mysteries surrounding the coronavirus, but one question still inspires debate: Does a person’s viral load, the amount of the virus in their body, determine how sick they get?
Common sense suggests the answer should be yes, higher viral loads produce a more severe outcome. But the coronavirus hasn’t always neatly followed that rule.
Studies have found little difference between the viral loads of patients who show symptoms and those who don’t. Scientists also haven’t found much difference in the viral loads of adults versus children, even though infected kids are more likely to be asymptomatic.”
“To measure viral loads, they relied on cycle threshold values: a measure of how much virus is detected within a sample from a standard PCR test. Patients with lower viral loads tend to have a higher threshold, since it takes more cycles to amplify the virus’ genetic material in order to detect it.”
“But the researchers offered a few caveats to these findings. When comparing outcomes, they didn’t examine confounding factors such as age or preexisting conditions, so more studies are needed. Cycle threshold values can also vary widely depending on how a sample is collected and how quickly it gets analyzed.“
However, one source is surely not good enough to make any definitive conclusions regarding the validity of a “viral” load. Let’s see what else we can find.
A study from January 2021 found no correlation between “viral” load and disease severity. In fact, mild cases had lower Ct values (suggesting higher “viral” loads) than those with severe disease. The use of “viral” loads as an estimate for disease severity was questioned as there were numerous factors that influenced the outcome of the Ct results, even with varying Ct results using the same sample and kit:
No correlation between Ct values and severity of disease or mortality in patients with COVID 19 disease
“In our small study we could not demonstrate any correlation between Ct values and severity of disease. Though patients with mild disease had lower Ct values and possibly higher viral loads they had also been tested earlier (median 3 days) than those with severe disease (median 5 days). However in patients with severe disease the Ct values of those who died were significantly lower than those who survived; but at the same time these patients had shorter duration of symptoms before testing (median 3 days as against 5 days). While it is difficult to draw conclusions from these results, it appears that time since onset of symptoms has a stronger relationship with the Ct values as compared to the severity of disease.”
“Recently the ability of Ct values to reflect the true viral load has been questioned . Experts state that the Ct values for a specimen vary between different kits and techniques (including target genes, primers and threshold fluorescence values) and Ct values may vary between different runs of the same kit.  The Ct value also depends on the method of collection of the sample and hence there may be variation in Ct values between two different samples obtained from the same person on the same day and run on the same kit. The Ct values also depend on the timing of sample collection in relation to onset of symptoms; samples collected earlier in the illness will have lower Ct values than those collected later in the illness . Therefore, the time of sampling since onset of illness has to be controlled while comparing Ct values between mild and severe disease. Our study proves the same point.”
What is interesting about this next study from June 2021 is the two instances where the researchers point out that there is a class of scientists who currently disagree with the use of PCR as the “gold standard” diagnostic tool for “SARS-COV-2.” Maybe the aforementioned scientists are ones who are intellectually honest and understand the severe limitations of the technology? The authors concluded that it is of the utmost importance to develop reliable and efficient methods to estimate “viral” load. They acknowledged that further studies are needed in order to depict the relationship between “viral” loads with viable “viruses” and disease severity/infectivity and that questions and knowledge gaps remain regarding any correlation between Ct values and disease severity. In other words, “viral” load estimates are absolutely meaningless:
Viral Dynamics and Real-Time RT-PCR Ct Values Correlation with Disease Severity in COVID-19
“Abstract: Real-time RT-PCR is considered the gold standard confirmatory test for coronavirus disease 2019 (COVID-19). However, many scientists disagree, and it is essential to understand that several
factors and variables can cause a false-negative test.”
“However, there are some ambiguities, such as whether it is best to use Ct values in predicting the level of infectivity and disease severity in patients infected with SARS-CoV-2. In addition, one class of scientists has questioned whether RT-PCR be termed a gold standard technique for the detection of SARS-CoV-2 infection [29,30].”
“In the future, there is an utmost need to develop reliable and efficient methods to estimate viral load, and further studies depicting the relationship between viral loads with viable viruses and disease severity/infectivity are also needed. It should also be considered that decisions about predicting the severity of disease, fatality rate, and viral dynamics should be based on a wide range of clinical parameters such as age, co-morbidities, and biomarkers, namely lymphocyte counts, C-reactive protein level, and D-dimer level, as there are several question marks and knowledge gaps associated with a positive correlation between Ct values and disease severity, which is yet to be explored.“
This study from July 2021 showed again that there is no difference between “viral” loads of asymptomatic and symptomatic “Covid” patients. Obviously, this would go against logic. If one has no symptoms, it would be assumed that they would have less “virus” in their bodies and those with symptoms would have more “virus” within them. However, this is demonstrated over and over again not to be the case. There are asymptomatic cases with high “viral” loads and severe cases with low “viral” loads:
Viral Load Difference between Symptomatic and Asymptomatic
COVID-19 Patients: Systematic Review and Meta-Analysis
“Results: Overall, 703 COVID-19 patients (553 symptomatic and 150 asymptomatic) were analyzed. Five investigations reported the mean age of patients, evidencing that asymptomatic patients were younger than symptomatic patients (34.0 vs. 40.3 years, respectively). Pooled data regarding the levels of expression of the RdRp gene revealed no significant difference between symptomatic and asymptomatic subjects. Similarly, no differences were observed comparing the mean Ct values for the E and N genes. Based on real-time RT-PCR data, no differences exist in the viral load between symptomatic and asymptomatic COVID-19 subjects considering Ct values for RdRp, E and N genes’ expression. Asymptomatic subjects may represent a reservoir of the infection and significantly contribute to the maintenance of the pandemic.”
“Our analysis evidenced that symptomatic and asymptomatic SARS-CoV-2 patients have the same viral load since no differences were observed in terms of mean Ct values for the RdRp, E and N genes among the two groups. As it was recommended by the World Health Organization (WHO), the RdRp, E and N genes represent the targets for the detection of SARS-CoV-2, specifically the E gene for first-line screening, the RdRp gene for the confirmatory assay and the N gene for the additional confirmatory assay .”
It is clear from the above sources that “viral” load is an utterly useless measure. Together, they are pretty damning. Yet, as a final nail in the coffin for how PCR can not be used to determine a so-called “viral” load, the Association for Public Health Laboratories released a rather informative guide in November 2020 from which I have provided a few highlights:
Is there variability in Ct values?
Short answer: Yes.
The number of cycles required for detectable amplification of viral RNA is dependent on a long list of variables beyond simply how much viral RNA is present in a patient specimen. The relative impacts of these variables on the Ct value differs between test platforms and can vary widely.
Variables that can impact Ct values include but are not limited to:
• Efficiency of the collection of specimen
• Time of collection of specimen after onset of infection
• Specimen type—matrix effect
• Specimen type – level of viral RNA in different specimen types (e.g., upper vs. lower respiratory tract) can differ between specimens from the same patient at the same time
• Storage and transport conditions of specimen prior to testing
• Age of specimen
• Nucleic acid extraction efficiency
• Amount of viral RNA in the specimen
• Nature of the target RNA and design of the primer/probe sequences
• Efficiency of the real-time PCR chemistry in the assay (singleplex, multiplex)
• Method for defining/determining Ct value
I can get a quantitative test for HIV, why can’t I get one for COVID-19?
Short answer: They are not currently commercially available in the US.
Quantitative viral load assays are specifically designed for this purpose. They are run on specimen types that mitigate the impact of variables on the Ct value and include controls and calculations to assess viral load. For example, an HIV quantitative viral load assay is performed on a blood specimen. This specimen is homogenous and can be collected in a very standardized manner. The real-time PCR assay used to calculate viral load includes a set of controls to “standardize” the specimen (e.g., a control for specimen adequacy) and a set of standards (i.e., known dilutions of virus for calibration). Ct values of the patient specimen are compared to those of the standard curve to calculate the viral load in a standardized specimen.
This type of assay is not yet available for SARS-CoV-2. Respiratory specimens are not homogeneous and are challenging to standardize. The collection process of a respiratory specimen does not lend itself to quantifying the amount of virus present. Each swab collection is different and does not assure that the same amount of sample is collected. Quality of specimen collection is impacted by other variables including the skill of the collector, which nostril is swabbed first, or whether the patient recently ate or drank. Many COVID-19 diagnostic real-time PCR assays do not include specimen adequacy controls, and those that do still lack the standardization necessary to calculate viral load.
Cts and infectiousness—can we infer one from the other?
Short answer: No.
There are a number of reasons that Ct values should not be used to determine how infectious someone is. The first relate to the nature of the available testing methods and the inherent variability of Ct values:
• The available assays are qualitative, not quantitative. Qualitative tests are not designed to provide an indication of possible infectivity.
• There are many variables that impact Ct value that are unrelated to the amount of viral RNA in a specimen (see
• The only method available for determining the presence of live virus in a specimen is inoculating the virus into cell culture to determine if the virus can grow there. This is a very insensitive and qualitative method, may not detect low levels of infectious virus and does not necessarily correlate with infectiousness.
There are also simply not enough data at this time to infer a correlation between detectable SARS-CoV-2 viral RNA and infectiousness. We do not know how much virus (as measured by detecting viral RNA) is needed in a respiratory specimen for a person to be able to transmit it to someone else. We also do not know what the “cutoff” is for a person to no longer be infectious (i.e., at what point the amount of virus in a person’s respiratory specimen is too little for them to be able to infect others).
Do Ct values correlate with viral load?
Short Answer: Often, but not always.
There is a relationship between Ct values and amount of virus in a patient specimen, but they are not equivalent. There are many variables that impact Ct values (see above). Although Ct may be used as a proxy for viral load, caution must be taken when interpreting in this manner. A high Ct value often correlates with a low viral load, but not always.
A specimen could have a very high viral load, but also a high Ct value (i.e., it took more cycles to detect the viral RNA) because the extraction was inefficient, the patient just drank something that inhibited the real-time PCR reaction, or the specimen was packaged inappropriately and reached a high temperature during transportation to the lab and the viral RNA in the specimen degraded in the heat.
Any specimen that generates a result that is defined as “positive” by the test manufacturer is considered positive. As with any diagnostic test, the result should be interpreted in the clinical context.
The process of viral replication and infection must be taken into consideration as well. If a specimen is collected very close to the time of the initial infection the viral load may be very low as the virus has not had a lot of time to replicate; a specimen collected in the coming days may have a much higher viral load. A specimen collected many days to weeks after the initial infection may have a low viral load, and viral RNA can be detectable for many weeks after infection in some patients. Limited epidemiological and culture data indicate that patients are not infectious more than 10-15 days post-onset of symptoms.
Can I compare a Ct value from one test method to another?
Ct values and cutoffs are assay- and method-specific. A specimen with a Ct of 35 by one assay will not necessarily have the same Ct value by other assays. These values can vary up to two to three logs from test to test due to how the tests are designed.1
There can be a difference in the relative sensitivities of FDA authorized tests which may also impact Ct values. According to comparison data recently published by FDA using a standard panel, there can be as much as a 1000-fold difference between the various assays.2“
That was yet another scathing warning regarding the use of Ct values to determine a so-called “viral” load. Perhaps it’s because of the scientific data (or lack thereof) that the CDC has also said the same regarding Ct values and “viral” load.
According to a CDC study:
“The exact RT-PCR Ct values associated with the presence of infectious SARS-CoV-2 is unknown“
According to the CDC Q & A:
Q. Can cycle threshold (Ct) values be used to access when a person is no longer infectious?
A. No. Although attempts to culture virus from upper respiratory specimens have been largely unsuccessful when Ct values are in high but detectable ranges, Ct values are not a quantitative measure of viral burden. In addition, Ct values are not standardized by RT-PCR platform nor have they been approved by FDA for use in clinical management. CDC does not endorse or recommend use of Ct values to assess when a person is no longer infectious.“
The CDC understands as well that there can be no correlation between Ct values, “viral” load, and disease severity/infectivity. The data does not exist and what is out there contradicts their narrative. However, even though they admit that there is no correlation, this does not stop the CDC/WHO/MSM from constantly using “viral” load to drum up evidence-less and inaccurate headlines/conclusions in order to generate fear.
- Studies have found little difference between the “viral” loads of patients who show symptoms and those who don’t
- Scientists also haven’t found much difference in the “viral” loads of adults versus children
- Cycle threshold values used to determine “viral” load can vary widely depending on how a sample is collected and how quickly it gets analyzed
- One small study from India could not demonstrate any correlation between Ct values and severity of disease
- Patients with mild disease had lower Ct values and possibly higher “viral” loads
- The ability of Ct values to reflect the true “viral” load has been questioned
- Experts state that the Ct values for a specimen vary between different kits and techniques (including target genes, primers and threshold fluorescence values) and Ct values may vary between different runs of the same kit
- Many scientists are disagreeing that RT-PCR should be considered the gold standard confirmatory test
- There is an utmost need to develop reliable and efficient methods to estimate “viral’ load, and further studies depicting the relationship between “viral” loads with viable “viruses” and disease severity/infectivity are also needed
- There are several question marks and knowledge gaps associated with a positive correlation between Ct values and disease severity, which is yet to be explored
- A meta-analysis revealed, based on real-time RT-PCR data, that no differences exist in the “viral” load between symptomatic and asymptomatic “COVID-19” subjects considering Ct values for RdRp, E and N genes’ expression
- Their analysis showed symptomatic and asymptomatic “SARS-CoV-2” patients have the same “viral” load
- According to the Association for Public Health Laboratories, there is wide variability in Ct values and they are dependent on a long list of variables beyond simply how much “viral” RNA is present in a patient specimen
- These include Pre-analytic Variables such as:
- Efficiency of the collection of specimen
- Time of collection of specimen after onset of infection
- Specimen type—matrix effect
- Specimen type – level of viral RNA in different specimen types (e.g., upper vs. lower respiratory tract) can differ between specimens from the same patient at the same time
- Storage and transport conditions of specimen prior to testing
- Age of specimen
- They also include Analytic Variables such as:
- Nucleic acid extraction efficiency
- Amount of “viral” RNA in the specimen
- Nature of the target RNA and design of the primer/probe sequences
- Efficiency of the real-time PCR chemistry in the assay (singleplex, multiplex)
- Method for defining/determining Ct value
- Quantitative assays are not yet available for “SARS-CoV-2”
- Respiratory specimens are not homogeneous and are challenging to standardize
- The collection process of a respiratory specimen does not lend itself to quantifying the amount of “virus” present
- Many “COVID-19” diagnostic real-time PCR assays do not include specimen adequacy controls, and those that do still lack the standardization necessary to calculate “viral” load
- The APHL admits there are a number of reasons that Ct values should not be used to determine how infectious someone is
- They claim cell culture is a very insensitive and qualitative method, may not detect low levels of infectious “virus” and does not necessarily correlate with infectiousness
- It is not known how much “virus” (as measured by detecting “viral” RNA) is needed in a respiratory specimen for a person to be able to transmit it to someone else
- It is also not known what the “cutoff” is for a person to no longer be infectious
- Ct values and “viral” loads are not equivalent and do not always correlate
- Although Ct may be used as a proxy for “viral” load, caution must be taken when interpreting in this manner
- A specimen with a Ct of 35 by one assay will not necessarily have the same Ct value by other assays
- According to comparison data recently published by FDA using a standard panel, there can be as much as a 1000-fold difference between the various assays
- The CDC has stated that the exact RT-PCR Ct values associated with the presence of infectious “SARS-CoV-2” is unknown
- The CDC also states:
- Ct values are not a quantitative measure of “viral” burden
- Ct values are not standardized by RT-PCR platform nor have they been approved by FDA for use in clinical management
- It does not endorse or recommend use of Ct values to assess when a person is no longer infectious
Kary Mullis, the creator of the PCR test, repeatedly warned against using his invention as a quantitative measurement of “viral” burden:
“Kary Mullis … is thoroughly convinced that HIV is not the cause of AIDS. With regard to the viral-load tests, which attempt to use PCR for counting viruses, Mullis has stated:
“Quantitative PCR is an oxymoron.” PCR is intended to identify substances qualitatively, but by its very nature is unsuited for estimating numbers. Although there is a common misimpression that the viral-load tests actually count the number of viruses in the blood, These tests cannot detect free, infectious viruses at all; they can only detect proteins that are believed, in some cases wrongly, to be unique to HIV. The tests can detect genetic sequences of viruses, but not viruses [(29), p. 3].”
“I think misuse PCR is not quite, I don’t think you can misuse PCR. The results, the interpretation of it, If they could find this virus in you at all, and with PCR, if you do it well, you can find almost anything in anybody. It starts making you believe in the sort of Buddhist notion that everything is contained in everything else. Right, I mean, because if you can amplify one single molecule up to something which you can really measure, which PCR can do, then there’s just very few molecules that you don’t have at least one single one of them in your body, okay. So that could be thought of as a misuse of it, just to claim that it’s meaningful.”
“It’s [PCR] just a process that’s used to make a whole lot of something out of something. That’s what it is. It doesn’t tell you that you’re sick and it doesn’t tell you that the thing you ended up with really was going to hurt you or anything like that.”
He would have torn these studies and articles apart were he alive today. It’s clear that “viral” load estimates are inaccurate, are not standardized, are influenced by numerous variables outside of the quantity of RNA, and that they have no correlation to disease severity/infectivity.
Don’t fall for their lies.
It’s time to flush virology down the toilet with the rest of the crap.
“Asymptomatic subjects may represent a reservoir of the infection and significantly contribute to the maintenance of the pandemic.” Really. So if someone has tested positive yet is asymptomatic, and continue to roam freely since they feel fine, you might have a real killer on the loose? Resevoir of infection. We are so dirty, aren’t we? I hear grown adults discuss viral load as if it means something. Nope. As if it can be somehow measured, quantified. Nope. Thanks again Mike! Nice to read Kary’s words, have heard them many times and they are so spot on. He knew the con, the lie, didn’t he?
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Yes, I believe Kary did. I think he was taken off the board early as he would have blown this Testing Pandemic open right off the bat.
They want us fearful of each other hence the asymptomatic carrier BS. It is downright stupid to think healthy people can spread disease, especially since they can’t even prove sick people can transmit disease (i.e. Gallops/Angel Island circa 1918). There is so much wrong with virology I could probably keep doing daily posts for the rest of my life and still not have uncovered it all.
All I would say about Asymptomatic spread ( and it is not very scientific ) is that if I were a virus , it is how I would do it.
Enjoy the site very much , BTW
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Thanks for the kind words and support! I really appreciate it. 🙂
I wonder what makes “AIDS” patients’ reported “viral load” go down when they have “retroviral” drugs.
In general there’s a slew of questions I have about the mainstream of the form, “This is obviously an unscientific process, but how do we account for the apparent uniformity in results?”
Of course the trick is frequently something like that they interpret “test” results subjectively, circular-reasoning-based reporting guidelines bias the data, or they just plain have no pattern in the results but say they do anyway; but it seems important rhetorically to establish what does account for the apparently uniformity or apparent solidity of the mainstream edifices. Otherwise it leaves edge cases where the mainstream could seem “right for the wrong reason.”
…..(sigh)….Mike you keep SCREWING UP with this Mullis CRAP! And you’re digging an even deeper HOLE for itself with this latest effort of yours! When are you going to LISTEN TO ME…???!!! You’ve cited an EXTREMELY **EDITED** version of the video of Mullis’ comments he spoke that day in front of that red brick wall. AGAIN, I WAS FREAKIN’ **THERE** when he said these things in 1997 since I helped to PRODUCE that freakin’ event!! Mullis’ comments were ANSWERS to questions that my friend asked Mullis and felt compelled to REPEAT and RE-WORD his questions to Mullis because Mullis was NOT understanding the original QUESTION! I am LOATHE to cite the complete version of this video because, for MANY reasons, the WHOLE THING should NEVER have been posted anywhere on the internt in the first place! However, you think you clearly KNOW IT ALL about all of this, so, I think it may be necessary to show people the COMPLETE version of Mullis’ comments which is HERE:
As was par for the course with Mullis in our “AIDS” dissident movement, Mullis EQUIVOCATES ALL of his “radical” sounding or “dissident” quotes with OTHER statements that are in support of the ORTHODOXY!! For example, one of the times my friend re-phrases his questions was when he asked (at ~ 1:54 in the youtube link above): “is it an estimation?”
Mullis IMMEDIATELY replies: “It’s NOT an estimation. It’s a REALLY QUANTITATIVE thing”!!
In fact, Mullis’ arguments he was making that day were ALL *QUANTITATIVE* in nature and NOT qualitative! Mullis ALWAYS believed in the existence of that virus (so-called “HIV”) AND his PCR’s ability to DETECT it “down to one molecule” which he ALSO states in the FULL-length version of his comments.
Furthermore, with all due respect Mike, you make another fundamental MISTAKE in your MIS-QUOTING of Mullis from the Goodson paper which makes me question your reading skills. Also, Goodson’s paper WAS RETRACTED, FYI (for other reasons and not because Goodson mis-quoted Mullis which she DID). Mullis’ ONLY legitimate quote in Goodson’s paper WAS “quantitative PCR is an oxymoron”. However, NO ONE can find the EXACT citation for that quote. ALL OF THE OTHER CRAP you have “quoted” Mullis as saying was NOT, I repeat *NOT* said by HIM!! It was WRITTEN by Lauritsen in his original article from 1996 which Goodson used as her ref. # “[(29), p. 3].”
I KNEW Lauritsen who passed away earlier this year, and when I first saw Goodson’s paper being used by well-meaning but STUPID COVID dissidents, I reached out to Lauritsen (in April 2020) to confirm what I already suspected. Lauritsen, who was NOT a scientist, confirmed for me that his article was NOT an interview of Mullis and that the ONLY actual quote FROM MULLIS HIMSELF was the “quantitative PCR is an oxymoron”. ALL OF THE REST of the “quotes” from that paragraph some of which you’ve chosen to post IN BOLD are from *LAURITSEN* and NOT from Mullis!! You even INCLUDE Lauritsen’s “close quotes” after the word “oxymoron” in YOUR article above!! This is a simple matter of READING skills!! Lauritsen SHOULD have done a better job of separating Mullis’ quote from HIS own thoughts, but Lauritsen DID include the “close quotes”.
See: http://www.virusmyth.com/aids/hiv/jlprotease.htm for the ORIGINAL article by Lauritsen.
More importantly, as I have tried in vain to impress upon you NUMEROUS times, Mullis’ ALWAYS managed to NEGATE ANY “dissident”-sounding “quotes” he ever said, contradicting himself MANY times in the process. Sometimes he did so in the course of a few seconds, as he did at that seminar in front of the red brick wall in 1997. And sometimes Mullis contradicted himself over the span of years, as he also did in his comments from our 1997 seminar when he emphatically insisted that PCR is “NOT an estimation! It’s a really QUANTITATIVE THING”!
This obviously contradicted his aforementioned comment he said earlier “Quantitative PCR is a OXYMORON”….None of us old-timers can locate the exact time and place where and when Mullis said that, and with Mullis, it of course DOES MATTER where and when he said something, in light of the fact that he DID contradict himself so freakin’ MUCH!!! Lauritsen could not find an original source for Mullis “oxymoron” quote, either, when I asked him do so in 2020, and unfortunately, Lauritsen never cited a source or reference for it in his original article back in 1996. It WAS quite widely known that Mullis said it back then, and I think I may have narrowed it down to a AAAS conference the dissidents had in San Francisco in 1994 (it was definitely PRIOR to 1995 when Mullis said that).
At any rate, you keep choosing to invoke Mullis when I’ve warned you that there is enough evidence to show that he was ORTHODOX more so than he EVER was supposedly “dissident”. IMHO, Mullis would NOT be a help nowadays to ANY dissident movement. FWIW, Dr. Tom Cowan also agrees with me. Mullis was NOT that big of a help to us in our old “AIDS” dissident movement, and nowadays he would probably refer to all of us who are on #teamnovirus as “Half-wits”!! And, IMHO, Mullis would be CORRECT about that in many cases! “Half-wit” is exactly what Mullis called our REAL hero Stefan Lanka when the two men met each other back in 1997, just a few months after Mullis’ seminar in front of the red brick wall. Were Mullis still alive today, it’s doubtful that he would have spoken up at all, since all we have of his “dissident” comments were from **TWENTY YEARS** or more prior to his death. If Mullis were alive and if he were to “speak out”, he would probably be saying CONTRADICTORY things, given his very **WELL-DOCUMENTED** contradictory comments he made during his tenure as a so-called “AIDS” dissident!!
At the very best, NO ONE in ANY current dissident movement ever needs to cite Mullis as a “shining example” of dissident science. One can certainly cite Mullis for any of a number of ORTHODOX papers he published in his career, including but not limited to the original ORTHODOX paper that demonstrated….wait for it….wait for it….the use of PCR in “HIV research”! Other than that, one can and one SHOULD, IMHO, go MUCH farther than the very SHALLOW efforts that Mullis made as a dissident and more closely examine his invention, the PCR process itself!! Again, I refer everyone to this critical review article on the PCR:
“Mullis ALWAYS believed in the existence of that virus (so-called “HIV”) AND his PCR’s ability to DETECT it “down to one molecule” which he ALSO states in the FULL-length version of his comments.”
Rod, first of all, this is an old article based on a post I did in October 2020.
Second, I did not say that Mullis did not believe in “viruses.” The point in using his quotes was to show that the PCR results are meaningless.
“Also, Goodson’s paper WAS RETRACTED, FYI (for other reasons and not because Goodson mis-quoted Mullis which she DID). Mullis’ ONLY legitimate quote in Goodson’s paper WAS “quantitative PCR is an oxymoron”.”
Goodson’s paper being retracted has zero to do with anything. It was retracted due to the fact that the editors felt it was (rightfully) making people doubt the HIV=AIDS story. From the retraction:
“Our conclusion today is that the continued attention that this article garners of which almost none consider the necessary context provided in the critical commentaries itself PRESENTS A POTENTIAL PUBLIC HEALTH RISK BY LENDING CREDIBILITY to refuted claims that place doubt on the HIV causation of AIDS.”
I already know that Mullis’ quote was only the statement regarding quantitative PCR being an oxymoron. The rest was Lauritsen which did a great job expanding on the Mullis quote.
“Mullis’ ALWAYS managed to NEGATE ANY “dissident”-sounding “quotes” he ever said, contradicting himself MANY times in the process”
Whether Mullis contradicted himself or not really does not matter if we can use the pertinent quotes against the mainstream PCR narrative.
“At any rate, you keep choosing to invoke Mullis when I’ve warned you that there is enough evidence to show that he was ORTHODOX more so than he EVER was supposedly “dissident”.”
As I’ve told you before, I feel that Mullis’s words carry weight and have meaning, especially in regards to PCR. Whether he believed in “viruses” or not does not matter when his quotes can be used to destroy aspects of the mainstream narrative.
“If Mullis were alive and if he were to “speak out”, he would probably be saying CONTRADICTORY things, given his very **WELL-DOCUMENTED** contradictory comments he made during his tenure as a so-called “AIDS” dissident!!”
I agree that Mullis may not be a hero. My past speculation that he would have spoken out about the misuse of the PCR is based on his comments implying that the results are meaningless and can not tell one anything about illness/disease. He may have accepted the “virus” narrative but I do not think, based on his quotes, that he would have agreed to how PCR is being used today. Again, that is speculation on my part. I understand that you may disagree, but I feel that Mullis’s words help our cause more than they hurt it.
“Whether Mullis contradicted himself or not really does not matter if we can use the pertinent quotes against the mainstream PCR narrative.”
Mike, what is not getting through your thick skull is the fact that the orthodoxy is saying essentially the same thing in reference to the pseudo-dissident statements that Mullis made:
“Whether Mullis made some semi-dissident statements many years ago really does not matter if we can use the pertinent quotes from him IN FAVOR OF the mainstream PCR narrative.”
“Mike, what is not getting through your thick skull is the fact that the orthodoxy is saying essentially the same thing in reference to the pseudo-dissident statements that Mullis made:”
Then I guess both sides can use Mullis’s quotes to support our arguments. However, his more recent statements against the use of PCR as a diagnostic tool are far more powerful than the INTENDED use listed in a 1985 patent.
“It’s absolutely clear from this document that Mullis and his fellow researchers/inventors intended the technology to be used to detect the presence of pathogens that cause infectious diseases.”
Patents are often submitted and granted even if the invention does not work as intended. Mullis may have intended for PCR to detect and diagnose “viruses” in 1985 but he clearly changed his stance on its ability to do so later on in his life.
For instance, in the 1985 patent, it seems clear that PCR’s use for diagnosis is theoretical as the technology was not where it needed to be at the time:
“For diagnostic applications in particular, the target nucleic acid sequence may be only a small portion of the DNA or RNA in question, so that it may be difficult to detect its presence using nonisotopically labeled or end-labeled oligonucleotide probes. Much effort is being expended in increasing the sensitivity of the probe detection systems, BUT LITTLE RESEARCH HAS BEEN CONDUCTED on amplifying the target sequence so that it is present in quantities SUFFICIENT TO BE READILY DETECTABLE USING CURRENTLY AVAILABLE METHODS.”
“Routine clinical use of DNA probes for the diagnosis of infectious diseases would be simplified considerably if non-radioactively labeled probes could be employed as described in EP No. 63,879 to Ward. In this procedure biotin-containing DNA probes are detected by chromogenic enzymes linked to avidin or biotin-specific antibodies. This type of detection is convenient, BUT RELATIVELY INSENSITIVE. The combination of specific DNA amplification by the present method and the use of stably labeled probes COULD PROVIDE the convenience and sensitivity required TO MAKE THE FALKOW AND WARD PROCEDURES USEFUL IN A ROUTINE CLINICAL SETTING.”
Click to access US4683195.pdf
So while the patent lists diagnostic capabilities as an intention for the PCR invention, that does not mean it was possible nor that the results would have any practical use clinically.