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New Study Belies Early Claims of ‘Silent Spreaders’ of COVID-19

by Sep 20, 2023Health Freedom, Special Reports12 comments

(Photo by Gustavo Frint, licensed under Pexels license)
A SARS‑CoV‑2 human challenge study belies the propaganda narrative that “silent spreaders” were driving community transmission.

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The Lockdown Madness

On March 16, 2020, four days after the World Health Organization (WHO) declared COVID‑19 to be global pandemic, Neil M. Ferguson and colleagues at Imperial College London, in collaboration with the WHO, published a modeling paper advocating strict “mitigation policies” ostensibly to limit the spread of SARS‑CoV‑2, the novel coronavirus that causes the disease.

That paper was highly influential and was cited by governments around the world, including the United Kingdom and the United States, as justification for implementation of authoritarian “lockdown” measures including business closures, school closures, stay-at-home orders, and mask mandates.

These lockdown measures were sold to the public based on the lie that they would be strictly temporary, just “two weeks to flatten the curve”—or, in White House parlance, “fifteen days to slow the spread”.

“Flattening the curve” meant to slow the spread enough to give hospitals time to ramp up capacity and obtain supplies so that they wouldn’t become overwhelmed with COVID‑19 patients. This concept was graphically explained to the public by the lockdown-loving New York Times with the following graph:

flatten the curve

But it was all a lie. The lockdown measures were never intended to remain in place for only two weeks. This is obvious from the fact that the Imperial College modelers advocated maintaining lockdowns until a vaccine could be developed and essentially forced upon the population.

Indeed, coerced mass vaccination is precisely what occurred once the US Food and Drug Administration (FDA) granted emergency use authorization (EUA) for the mRNA COVID‑19 vaccines.

The government systematically violated individuals’ right to informed consent by (a) deceiving people into willingly accept injection with these experimental pharmaceutical products and, failing success in that endeavor, (b) coercing people into getting vaccinated against their will.

The government lied to the public about practically everything, but, in particular, the vaccines were sold to the public on the basis of the lie that two doses would confer durable sterilizing immunity, thereby enabling “herd immunity” to be reached by stopping infection and transmission.

The vaccines were sold to the public on the basis of the lie that two doses would confer durable sterilizing immunity.

For those who weren’t deceived by false claims about the safety and effectiveness of these products, the government delivered the clear message that their freedom would remain curtailed and their ability to make a living threatened unless and until they got vaccinated—even if they had already acquired the superior immunity conferred by infection.

Policymakers implementing lockdown measures pretended to care about human lives, but we know they were really more concerned with exercising power and control over others because, just as their political calculations ignored natural immunity, they never factored the costs and predictable harms of the measures they were advocating into their thinking.

Indeed, the Imperial College modelers admitted that they “do not consider the ethical or economic implications” of the lockdown measures they advocated.

Dr. Anthony Fauci, the Director of the National Institute of Allergy and Infectious Diseases (NIAID) under the National Institutes of Health (NIH) and a top advisor to the president on the White House’s coronavirus task force, similarly admitted that he wasn’t considering the costs of the lockdowns. “I don’t give advice about economic things,” he said. “I don’t give advice about anything other than public health.”

“I don’t give advice about economic things.”

Tellingly, the rationale for the lockdowns quickly shifted from being short-term measures to “flatten the curve” by spreading out the number of newinfections over time, with the areaunder bothhypothetical curves being the same, to being long-term measures supposedly capable of not merely delaying but stopping community transmission.

In other words, under the original rationale for the measures being temporary, the only deaths hypothetically prevented were those that would otherwise occur due to people being unable to get hospital care, whereas the new rationale for the measures persisting indefinitely was that this would reduce the total number of “cases”—the official counting of which was characterized by institutionalized scientific fraud.

There was no scientific basis for this shift in rationale whereby the lockdowns were maintained on the grounds that they would reduce total case numbers. Instead, it was a faith-based policy. Policymakers deliberately shut down the economy based on the hope that this would stop community transmission and the hope that the population could ultimately be saved by mass vaccination.

That the policies were based on “hope that the vaccines would work” the way that government officials falsely claimed they would has been acknowledged in Congressional testimony by Dr. Deborah Birx, the former White House Coronavirus Response Coordinator. (Birx later claimed that she had always known that the vaccines would not prevent transmission, which is enlightening given the fact that she was among the government officials claiming that they would stop infection and transmission.)

The fact that the policy was faith-based has also been admitted by then CDC Director Rochelle Walensky. Commenting on the vast disparity between what government officials told the public and how the vaccines actually performed, she attributed it to officials like her having “wanted to be hopeful”. (Far from accepting responsibility for having deceived the public, however, she went on to essentially blame the public for taking the government’s claims at face value.)

The promised benefits of the lockdowns, of course, never manifested in the data. This includes, as recently acknowledged by Anthony Fauci, the evidence-less claim that mandatory use of masks in public places would prevent community spread.

The harms caused by these authoritarian policies, on the other hand, have incontrovertibly been devastating, with the burden of harms being disproportionately borne by children, who happen to be at very low risk from COVID‑19.

The Fearmongering about ‘Silent Spreaders’

I and many others opposed the criminal lockdown regimes and instead advocated an approach whereby people at low risk from COVID‑19 would go about their business while those at high risk remained isolated. This would result in a buildup of the population immunity that would ultimately be required to protect those at high risk and enable them to also resume their normal lives.

Lockdown advocates, on the other hand, argued that it was impossible to focus protection on those at highest risk, and so it should not be surprising that the policies they favored utterly failed to protect elderly people in nursing homes.

I was personally advocating a “focused protection” approach from the very start, six months before the Great Barrington Declaration. I don’t wish to speak for other lockdown opponents, but my own advice for slowing the spread without deliberately shutting down the economy was simple: if you feel any symptoms of illness coming on, stay home.

Lockdown advocates rejected that advice, though, and instead instilled fear into the population that people without any symptoms were the driving force behind community spread of the coronavirus.

Here is a sampling of fearmongering headlines to which we were treated about community spread being driven by people without any symptoms:

In May 2020, the CDC claimed that 40 percent of transmission occurred before those spreading the virus had any symptoms. The CDC also claimed that asymptomatic individuals were equally infectious as those who developed symptoms.

By December 2020, we could read the claim in the New York Times that “asymptomatic individuals . . . are responsible for about 50 percent of transmissions”, a brazen lie originating from the US Centers for Disease Control and Prevention (CDC), which had published a policy guidance document making the demonstrably false claim that “approximately 50% of transmission” was “from asymptomatic persons”.

The term “asymptomatic” refers to people who were infected with SARS‑CoV‑2 but never developed COVID‑19, and the CDC had absolutely no evidence to support its statement that people who never even got COVID‑19 were responsible for half of community spread of the virus.

The truth about asymptomatic transmission was told to the public by the WHO’s technical lead on the COVID‑19 pandemic, Dr. Maria Van Kerkhove, during a press conference on June 8, 2020. As she explained, the scientific evidence had indicated that viral transmission from people who were “truly asymptomatic” was “very rare”.

By December 2020, we could read the claim in the New York Times that “asymptomatic individuals . . . are responsible for about 50 percent of transmissions”.

She was very clear in her remarks to distinguish between “asymptomatic” transmission, meaning viral spread by people who never developed COVID‑19, and “presymptomatic” transmission, meaning viral spread by people before the onset of their disease symptoms.

Nevertheless, the media unfailingly mischaracterized Dr. Van Kerkhove as having said that transmission from people without symptoms was very rare, for which they baselessly criticized her on the grounds that some studies had estimated that a large proportion of transmission occurred during the presymptomatic phase of infection.

Having come under attack from the media and lockdown advocates, when Dr. Van Kerkhove subsequently tried to correct the media’s gross mischaracterization of her comments by reiterating that she had been referring specifically to asymptomatic and not presymptomatic transmission, the media doubled down on their spread of disinformation by falsely claiming that she had “walked back” her statement that asymptomatic transmission was very rare.

As she explained, the scientific evidence had indicated that viral transmission from people who were “truly asymptomatic” was “very rare”.

Estimates of the proportion of people who experience asymptomatic infection have ranged from 14 percent to 50 percent, and children are more likely than adults to experience asymptomatic infection. A systematic review and meta-analysis published by PLOS Medicine in May 2022 estimated that people with asymptomatic infection were about three times (68 percent) less likely to spread the virus than people with disease symptoms—which contrasts with the CDC’s early claim that infected individuals who never developed the disease were “100%” as infectious as people who actually had COVID‑19.

But the output of that review was only as good as the estimates from the input studies, which included modelling studies; and so it, too, may have considerably overestimated the proportion of community spread from asymptomatic individuals. Notably, when the WHO official said asymptomatic transmission was “very rare”, she was referring to very limited number of studies where investigators actually performed contact tracing as opposed to mathematical models.

The Problems with Claims of Massive Presymptomatic Transmission

Setting aside “very rare” asymptomatic transmission, probably the most influential study on presymptomatic transmission was a modeling study by Xi He et al. titled “Temporal dynamics in viral shedding and transmissibility of COVID‑19”.

The authors of that study inferred from their data that (a) infected individuals were generally contagious for more than two days before developing symptoms and (b) contagiousness peaked the day before symptoms first started to appear. From those inferences, they estimated that 44 percent of transmission occurred during the presymptomatic phase of infection.

This study was widely cited to support lockdown measures on the grounds that “silent spreaders” were major contributors to community transmission.

I provided a detailed critique of that study in an article I published in August 2020 titled “How the New York Times Lies about SARS‑CoV‑2 Transmission: Part 4”. I summarized and expanded upon that critique in an article I published in November 2022 titled “SARS‑CoV‑2 Human Challenge Study Belies Presymptomatic Transmission” (which study I’ll come back to momentarily).

To summarize very briefly, the “Temporal dynamics” modeling study, which was published in Nature Medicine in April 2020, suffered from an ascertainment bias as a result of strict isolation policies that had been implemented in China. As the authors acknowledged, the policies resulted in “substantial household clustering” of cases.

Given lockdown conditions, it is unsurprising that a high proportion of transmission occurred in the household as opposed to the community setting.

As confirmed to me by the corresponding author for the study, Eric Lau, transmission “within a household with frequent and more intensive contact, especially during a lockdown, results in shorter serial intervals.”

Given lockdown conditions, it is unsurprising that a high proportion of transmission occurred in the household as opposed to the community setting.

Consequently, this ascertainment bias would result in an underestimated “serial interval”, which is the duration between the point in time that a person first develop symptoms and the time that they transmit the virus to someone else.

Additionally, the authors acknowledged that relying on patients’ recollections of when their symptoms first appeared introduced “recall bias” that would tend to result in an overestimation of the “incubation period”, which is the duration between the point in time that a person becomes infected and the time that they experience their first symptom.

By underestimating the serial interval and overestimating the incubation period, the study was biased toward overestimation of presymptomatic transmission.

In other words, the lockdown measures themselves were a confounding factor that predictably resulted in an overestimation of the rate of presymptomatic transmission that would otherwise occur in the absence of policies like compulsory quarantine or executive “stay-at-home” orders”.

Ironically, lockdown advocates effectively employed circular reasoning by citing such artifactually high estimates as justification for continuing those same policies.

Another problem with the “Temporal dynamics” study is that the authors used “cycle threshold” (Ct) values from PCR tests as a proxy measure for “viral load”. They did not have any data on viral loads before symptom onset in any patients. Rather, all samples were collected from patients after they had already developed symptoms.

They did not have any data on viral loads before symptom onset in any patients.

Moreover, while the authors described viral loads as “high” at the earliest time points, with subsequent decreases, their data show that most PCR test results indicated an initially low viral load, with Ct values over 30.

As the New York Times finally admitted in August 2020, “up to 90 percent of people testing positive” with PCR tests were unlikely to be contagious. This is because most tests were being run at such high Ct values that they were returning positive results for detection of non-infectious fragments of viral RNA.

Anthony Fauci had similarly acknowledged in July 2020 that “positive” PCR tests with Ct values of 35 or more were almost certain to be false positives. At such high Ct values, Fauci admitted, “the chances of it being replication competent are miniscule”, and “you almost never can culture” the virus in cell culture experiments.

Another problem with the “Temporal dynamics” study is that the date of symptom onset was rounded to the nearest day. As noted by the authors of a systematic review of studies on asymptomatic and presymptomatic transmission published in June 2020 on the preprint server medRxiv (emphasis added):

This is especially problematic because the difference in serial interval and incubation period calculated in these studies often differed by less than a day. It is therefore not possible to ascertain if the difference between calculated serial interval and incubation period are true differences, or an artefact of rounding error.

Furthermore, since the confidence intervals for the estimated serial interval fell entirely within the confidence intervals for the incubation period, the data were also “compatible with the hypothesis that infectious appears to emerge at symptom onset.”

Notwithstanding such methodological weaknesses, the fear of “silent spreaders” served as the basis for “following the science” with mask mandates and widespread testing of people who had no symptoms, which admittedly resulted in “up to 90 percent of people testing positive” despite having no active infection with SARS‑CoV‑2 at the time of testing.

As reported by David Zweig in May 2023, during an annual conference the prior month at the Society for Healthcare Epidemiology of America, researchers from Stanford University presented findings from a study they conducted using a special PCR test they developed that not only indicated whether viral RNA was present in a sample but also whether it was likely to represent infectious virus.

As Zweig reported, “the researchers found that 96 percent of people who were PCR-positive but without symptoms were not infectious.” (Emphasis added.)

A Human SARS‑CoV‑2 Challenge Study Belies Presymptomatic Transmission

On March 31, 2022, a SARS‑CoV‑2 human challenge study was published in Nature Medicine. Among its authors were researchers from Imperial College London, including Neil Ferguson.

Among the purposes of their study was to investigate transmission dynamics and duration of viral shedding in a controlled environment that would overcome the many inherent limitations of the types of studies that had previously been done.

The subjects deliberately exposed to SARS‑CoV‑2 were 36 healthy volunteers between the ages of 18 and 29. All were inoculated with an early strain of the virus that predated the emergence of variants given names from the Greek alphabet (Alpha, Beta, Delta, Omicron, etc.). The inoculation dose was sufficient to produce infection in 53 percent of subjects.

I reported about the findings of that study in my November 2022 article “SARS-CoV-2 Human Challenge Study Belies Presymptomatic Transmission”.

One striking conclusion we can draw from the findings of the challenge study is that, while subjects continued to test positive by PCR, they were unlikely to have been contagious after one week since exposure to the virus, which meant that they were unlikely to spread the virus after about three to five days since developing symptoms.

This highlights the erroneously burdensome nature of the CDC’s previous recommendation for people to isolate themselves for ten days after testing positive, which the CDC didn’t revise downward to five days until the end of December 2021.

As I pointed out in my previous article, the authors claimed that their findings were “consistent with modeling data indicating that up to 44% of transmissions occur before symptoms are noted”, which was a reference to the “Temporal dynamics” study, even though their own data directly contradicted the basis for that 44 percent estimate.

Whereas the “44%” estimate was based on the estimate that the time from infection until symptom onset—or the “incubation period”—was about five days, the human challenge study showed that symptoms had already peaked by five days into an infection.

As I explained in my prior article:

Thus, the incubation period observed in the human challenge study was days shorter than that used by Xi He et al. to estimate the proportion of presymptomatic transmission. Since this makes the estimated serial interval relatively longer, as explained by Eric Lau, this must mean that the likelihood of presymptomatic transmission is considerably lower than their estimate of 44 percent—even setting aside the other problems with that modeling study biasing it toward overestimation.

Rather than symptoms only beginning to appear shortly after peak viral loads, indicating that a very large proportion of people must have been contagious before they ever started showing symptoms, significant symptoms in the human challenge study were already apparent between days 2 and 3, consistent with the hypothesis that infectiousness begins around the same time as the first symptoms appear, and symptoms peaked at around the same time as viral loads (about a day later than peak viral loads in the throat but a day before peak viral loads in the nose), indicating that symptoms are a reasonable proxy measure of contagiousness.

. . . The remark by the study authors that their findings are “consistent” with the estimate of 44 percent presymptomatic transmission is a useful example of how conclusions drawn by researchers are frequently either unsupported or directly contradicted by their own findings.

Now, however, the team of researchers who conducted the human challenge study have published a follow-up study walking back their earlier claim that their findings were “consistent” with the estimate that 44 percent of transmission occurred during the presymptomatic phase of infection.

How the Challenge Study Reveals the Folly of Lockdowns

The new study is titled “Viral emissions into the air and environment after SARS‑CoV‑2 human challenge: a phase 1, open label, first-in-human study”, published in Lancet Microbe on June 9, 2023.

Ironically, the authors—which again included Neil Ferguson—begin by stressing the importance of “understanding who is contagious and when” to be able to implement effective strategies “to curb SARS‑CoV‑2 transmission”.

While Ferguson et al. were happy to advocate lockdowns without having that knowledge back in March of 2020, the authors of the challenge study understandably refrain from trying to justify extreme lockdown measures and instead recommend precisely the alternative approach that I and many others had advocated: “isolation upon awareness of first symptoms”.

Of course, when those of us who opposed harmful lockdowns suggested this very approach early into the pandemic, we were shouted down by lockdown advocates who falsely proclaimed to be “following the science”, and we were censored for correcting official government disinformation.

Study participants were isolated for two weeks while samples were taken from their nose and throat as well as the air and environmental surfaces. The researchers also used cell culture to determine whether positive results represented viable virus.

No viable virus was detected in air samples, although the authors caution against drawing any conclusions from this about airborne transmission since the sampler they used “is not designed nor expected to preserve infectivity of SARS‑CoV‑2.”

One important finding of the study was that symptom severity did not correlate well with viral emissions. People with more severe symptoms did not tend to shed more virus than those with mild symptoms.

Viral load from nasal samples correlated more strongly with emitted virus than viral load from throat samples, indicating that contagiousness should not be estimated from the latter.

“However,” the authors noted, “even nasal viral load is not a perfect predictor of how much virus a person emits into the environment. For example, we identified participants with relatively low nasal viral load who emitted large amounts of virus.”

This finding suggests that using PCR test Ct values as a proxy measure of viral load is not a reliable surrogate measure of infectiousness.

To illustrate the folly of earlier claims that “silent spreaders” were driving community transmission, take the Forbes article I mentioned earlier titled “A New Study Shows Children Are Silent Spreaders of Covid‑19”.

That headline and all the others like it were false. The referenced study, which was published in the Journal of Pediatrics, did not show that. Rather, the study authors fallaciously assumed this to be true based on the finding that children with COVID‑19 had “a significantly higher level of virus in their airways than adults who were hospitalized for Covid‑19 treatment.”

“According to the authors,” Forbes reported, “this finding suggests that . . . children can still carry a high viral load and are therefore more contagious.” (Emphasis added.)

As demonstrated by the findings of the human challenge study, that conclusion was a non sequitur fallacy: the conclusion that children were more contagious than adults didn’t logically follow from the finding that children tended to have a higher “viral load” as measured by PCR test Ct values.

Another of the findings from the challenge study supports the conclusion that a minority of infected individuals are responsible for the majority of community transmission.

As Benjamin Cowling and Dillon Adam reported in June 2020 in a New York Times article titled “Just Stop the Superspreading”, Cowling’s team of researchers in Hong Kong had found that “just 20 percent of cases, all of them involving social gatherings, accounted for an astonishing 80 percent of transmissions.”

“Seventy percent of the people infected”, they additionally reported, “did not pass on the virus to anyone.”

The authors of the challenge study observed that just two of the eighteen participants who became infected “generated 86% of total airborne viral RNA detected on only 3 days.”

This heavy viral shedding by just two subjects “coincided mostly (but not exclusively) with times of high nasal viral load.”

Disingenuously, they state that this finding is “consistent with previous descriptions of presymptomatic transmission identified through modelling studies.”

The researchers also found that “around one third of emissions occurred before participants met the WHO suspected case criteria that would have triggered symptoms-based testing.”

Disingenuously, they state that this finding is “consistent with previous descriptions of presymptomatic transmission identified through modelling studies.” With that statement, they refer specifically and exclusively to the “Temporal dynamics” study by Xi He et al.

To see why this is so disingenuous, this finding of their study must be understood within the context of what it means to be a “suspected case” according to WHO guidelines.

The WHO’s case definition for a “suspected case of SARS‑CoV‑2 infection” is a person who has: (a) both a fever and cough; (b) any three or more of the following symptoms: fever, cough, general weakness/fatigue, headache, myalgia, sore throat, coryza, dyspnoea, nausea/diarrhoea/anorexia”; or (c) severe acute respiratory illness.

Instructively, while still trying vainly to maintain that their findings were “consistent” with the estimate that 44 percent of transmission occurred before symptom onset, the study authors also explicitly acknowledged that such modeling estimates were likely to have overestimated the proportion of transmission occurring during the presymptomatic phase of infection.

As they diplomatically put it:

However, self-isolation after symptoms would prevent transmission that might otherwise have occurred and lead to an underestimation of the post-symptomatic component in epidemiological studies.

This was a necessary admission because, unlike with the WHO’s case definition, it only took one symptom for study participants to be symptomatic.

That is, just because around one-third of viral emissions occurred before subjects met the WHO’s case definition for suspected COVID‑19 does not mean that one-third of viral emissions occurred during the presymptomatic phase of infection.

Consequently, the statement that their finding was “consistent” with an estimate of 44 percent presymptomatic transmission is false and dishonest.

No doubt, in the unlikely event you see this human challenge study reported in the mainstream media, they will tell you that its findings were “consistent” with the whole “silent spread” narrative. Don’t be fooled.

On the contrary, what the study actually found was that only 7 percent of viral emissions into the air and environment occurred before the first reported symptom, which indicated that “most contagiousness occurred after the participant first felt unwell.”

In other words, 93 percent of viral emissions occurred after symptom onset.

And that, of course, is not at all consistent with earlier modeling studies used to support the mainstream narrative that the community transmission was being driven by “silent spreaders”.

Aside from that, the study found that the WHO’s suspected case definition and onset of fever were both “relatively poor definers of the onset of contagiousness.”

The authors reiterate that viral emissions “mostly occurred after participants developed early symptoms and began to test positive” by lateral flow test, otherwise known as a rapid antigen test.

Although prominent lockdown advocate Neil Ferguson was among their numbers, instead of concluding that their findings offer justification for those extreme authoritarian measures, the study authors state that their findings indicate that “a heightened awareness of early symptoms prompting self-testing could identify a large proportion of infectiousness.”

As they reiterate, lateral flow tests “effectively detected the contagious period”, and therefore, “for healthy individuals with mild infections in the community, awareness of early symptoms prompting daily self-testing by LFT could be a valuable tool to avert community transmission.”

Additionally, their findings “suggest roles for hand hygiene and surface cleaning in reducing transmission risk.”

As summarized in a Twitter post by Dr. Monica Gandhi, a professor of medicine at the University of California, San Francisco, the takeaway lesson from the study is “Stay home when sick”.

As David Zweig has observed, the new study “upends the logic behind the pandemic response”, indicating that “Forced masking and distancing of healthy people may have had little societal benefit.”

Indeed, it seems clear that the simple advice for people to just stay home if you feel any symptoms of illness would have sufficed in lieu of the dangerously extreme authoritarian policies whereby healthy people were ordered to close their businesses, stay home from work, keep their children home from school, and wear a facemask when going out in public.

So, next time you hear policymakers advocating authoritarianism on the grounds that they are “following the science”, just remember how this phrase is a euphemism meaning to demonically exercise power and control over others by implementing devastatingly harmful authoritarian measures that are completely unsupported by scientific evidence.

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  • JB says:

    Great well presented and timely article for all to read. Thank you!

  • Asymptomatic transmission happens all the time and cannot be stopped any more than we can stop the ocean tides. The PCR test proved that. Millions of people tested positive for the presence of viral genetic material and never displayed a single symptom. The particles transmit, the symptoms don’t. Whether a person displays symptoms or not depends more on the condition of their immune system than the presence of the virus. Trying to eliminate the virus is a battle between God’s natural design and man than man cannot win. Man must learn about how the immune system works, where the protection of infection is, and how to bolster that cellular protection that does not rely on the creation of serum antibodies from injections.

    • Kevin,

      With respect, it is evident to me from your comment that you didn’t read the article before commenting. The article explains why your belief that the PCR test proved that asymptomatic transmission occurs all the time is incorrect, so I do encourage you to read it.

  • The PCR test is indeed a bad example due to high false positive rates and nonstandard cycling. Trying to use any test to determine the levels of contagiousness based on viral loads is complicated. The simple point I was trying to make is that you can find viral genetic material in the mucosa of people who are ill, and people who are not ill. We are exposed to pathogens all the time, the source of which can be the environment, shedding from people who are ill, transmission in the atmosphere from people who are infected but not displaying symptoms, and exchange from people who are not infected at all. The pathogens always move between us, the symptoms don’t.

    • I appreciate that clarification, Kevin, and you are certainly right to emphasize the distinction between infection and disease (as I also do in the above article), but it still appears to me that you have not read the article since the human challenge study I discuss showed that individuals’ viral loads were indicative of viral shedding mostly after symptom onset. Only 7% of shedding occurred during the presymptomatic phase of infection.

  • I did read it, several times. Viral loads fluctuate for sure depending upon whether the person doing the shedding is infected and presymptomatic, asymptomatic, or symptomatic. So, where’d ya get that virus? Hard to say.

    • Kevin, I have shown you the best study to date for understanding viral loads and viral shedding, and it supports my conclusion. If you are going to insist that my conclusion is incorrect, please show me where I got any facts wrong or employed any logical fallacies, and also support your opposing conclusion with scientific evidence.

  • Bernd Hartke says:

    Thanks for this great text (and I love its length and richness of details). While I am not claiming to have seen every nuance of the c19 “dissident” discussion, my personal view is that the issues of how important (or un-important) asymptomatic and presymptomatic transmission are have not been discussed sufficiently before. I am only a chemist, not a biologist (and hence “not an expert”), but to me a low importance of asymptomatic/presymptomatic spread makes much more sense than the official claim that these were the true c19 pandemic drivers. After all, in contrast to bacteria, viruses cannot multiply by themselves, they need the biochemical machinery of living cells (cells of my body) for that, leading to these cells being killed (by total viral capture, or by the immune system) or at least being severely impaired in their functions. And although in some abstract sense one single virus particle may be sufficient to infect someone else, I do hear and understand the message that the viral load has to be quite high to really become infected (for various reasons, among them cross-immunity, and the probability of a virus particle successfully entering a cell and overtaking its machinery being much less than 100% upon contact, etc.). In other words, to be infectious to others I have to produce LOTS of fully functional viral particles, which means that lots of my cells have to die or become seriously incapacitated. I will notice that as “symptoms”. — This is a believable “mechanism story”. The asymptomatic/presymptomatic story fails to deliver a plausible mechanism, i.e., it is a bare claim, without sufficient biochemical background, in flat contradiction to the “follow the science” mantra.

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