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HE funded. What did HE decide to fund?
HE funded. What did HE decide to fund?
The research that was conducted. As you say he must be too stupid to know or understand what the research was about.
He should resign today for being an imbecile.
What research was conducted?The research that was conducted. As you say he must be too stupid to know or understand what the research was about.
He should resign today for being an imbecile.
From that science article.
Ecohealth reported the progress of the research including the GOF:
"These (research) data were reported as soon as we were made aware, in our year 4 report in April 2018. NIH reviewed those data and did not indicate that secondary review of our research was required, in fact year 5 funding was allowed to progress without delay. We are also working to answer any questions NIH has about the research on this R01 grant, which is not currently ongoing.”
Fauci knew (or was too stupid to care/understand).
So you know where it originated.
Please tell us because we dont know which is why we want access to Wuhan and the labs that were working on possibly close relatives in bats and other animals.
Fauci was NOT head of the NIH.
Bozo.
Hater....
Read your source again.
Fauci really does never lose.
I don't know what hater's latest conspiracy theory is (he doesn't either) but nothing is going to happen to Fauci.
HATER:
"Fearless in his efforts to be consistently wrong."
Collins, who is conveniently stepping down lol, was head of the NIH.
At issue with Fauci is his statement to congress on NIH funding.
In a testy exchange with Senator Rand Paul last July, Dr. Fauci asserted flatly, "The NIH [National Ins ute of Health] has not ever and does not now fund gain-of-function research in the Wuhan Ins ute of Virology."
That wasn't true. The NIH has conceded that EcoHealth and the Wuhan Ins ute of Virology did in fact conduct controversial gain-of-function experiments. Fauci, perhaps unknowingly, misled Congress in denying that.
https://www.newsweek.com/firing-dr-f...umbers-1641690
Transmission of airborne pathogens can be mitigated by ventilation. Design and engineering solutions to improve indoor air quality are available.
Urbanization led to regulation of public water sources and sanitation in the 20th century, and the deterioration of outdoor air quality led to anti-pollution laws. The regulation of indoor air quality would seem to be a blind spot. ~ 8 billion people spend 90% of their time indoors. Shoring up indoor air quality would seem to be a significant hindrance to future and present respiratory pandemics.
https://onlinelibrary.wiley.com/doi/...1111/ina.12928The four basic observations are made from study of the general population. Thus, we deduce that in the general population, short-range inhalation transmission mostly occurs in poorly ventilated spaces. The transmission risk is considerably lower if the indoor space is well-ventilated. If ventilation is poor, transmission throughout the indoor space (ie, “long-range” inhalation transmission) can occur. Long-range inhalation can infect many people simultaneously, whereas short-range transmission only infects those in close contact. Physical space constraints limit the number of susceptible individuals that an infected person can be in close contact with at any time. This feature is consistent with the observation that the number of secondary infections is generally small in this pandemic and supports the idea that close-contact indoor transmission is predominant.
This reasoning supports an important conclusion: that SARS-CoV-2 transmission does not occur everywhere, but mostly indoors in poorly ventilated spaces. The effect of ventilation rate on infection risk is continuous. The choice of a threshold ventilation rate depends on our definition of acceptable risk. Ventilation alone cannot prevent all infections. Instead, it should be viewed as one layer of protection in a multi-layered or multi-route approach, used in combination with other methods such as occupancy limitations, physical distancing, and mask wearing. Appropriate threshold ventilation rates remain to be determined.
The underlying axiomatic statement in the above analysis is that COVID-19 infection is mainly due to respiratory droplets. During heavy physical activities, an infectious person would exhale more air and produce higher shear stress at the epithelial surface, consequently releasing more infectious droplets. During physical exertion, a susceptible individual also inhales more. The net effect for infection transmission risk is a double multiplier. In an office setting, by contrast, both the infectious and the susceptible breathe at lower rates. Assume in the case of an office, an appropriate ventilation rate is 10 L/s per person. Then, in a gym, the infectious would exhale more, say by 5×, and the susceptible would also inhale more, also by 5×. The exposure rate to exhalations could likely be 25× the office value, and a rational ventilation requirement might therefore also 25× the office value, that is, about 250 L/s per person. ASHRAE Standard 62.1 currently only recommends a ventilation rate of about 20 L/s per person for gyms. This modest increment above office conditions reflects an important fundamental fact: outside of healthcare settings, existing ventilation standards do not account for infection control. Gyms designed and operated following ASHRAE Standard 62.1, then their ventilation rates are significantly lower than what is required for infection control. This scaling analysis can help explain why high activity spaces such as gyms have been observed to have high attack rates. Ventilation requirement for health is a complex topic9 and is also affected by exposure time and viral loads when infection is considered.
The dominant view in public health toward fearful airborne transmission fails to account for the power of dilution. Sufficient dilution of airborne infectious aerosols is the key to reducing inhalation transmission, both at close range and at room scale. Sufficient ventilation and filtration reduce infection to be as low as outdoors. A paradigm shift10 is needed toward a new ventilation standard accounting for managing infection risk. This goal should also apply to other respiratory viruses, such as influenza and the common cold.
Someone is always going to take the fall for big bureaucracies not keeping up.
And imo, gain of function research is vitally important in learning how to create an appropriate idea of how a virus works. thus down the line helps get vaccines much quicker. There are some other techniques apparently coming up that might let us eliminate these types of experiments. But that is debatable. These experiments will go on.
ANd there is NO FKN way a researcher could have dreamed up the virus that caused THIS pandemic. There is NO WAY to tell this virus would be so incredibly effective in infecting people. We know its genetic sequence and its protein makeup intimately and you just cant tell AHEAD of the game. No one dreamt this virus up molecularly. They put in way too many natural fk ups in the right places that would mimic an unknowing mutational mechanism.
And thats ultimately what most of this is all about. Scaring people. And getting Fauci.
Otherwise it might be an incredibly boring bureaucratic failure.
Yup. Its a toss up wether hes too stupid to understand or was lying.
Associate VP of Peter Daszak's EcoHealth Alliance going ham
https://www.linkedin.com/feed/update...9986359767041/
https://www.linkedin.com/feed/update...2161477222400/
https://www.linkedin.com/posts/aghuf...01114112-wvxF/
An appeal for an objective, open, and transparent scientific debate about the origin of SARS-CoV-2
On July 5, 2021, a Correspondence was published in The Lancet called “Science, not speculation, is essential to determine how SARS-CoV-2 reached humans”.1
The letter recapitulates the arguments of an earlier letter (published in February, 2020) by the same authors,2
which claimed overwhelming support for the hypothesis that the novel coronavirus causing the COVID-19 pandemic originated in wildlife. The authors associated any alternative view with conspiracy theories by stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin”. The statement has imparted a silencing effect on the wider scientific debate, including among science journalists.3
The 2021 letter did not repeat the proposition that scientists open to alternative hypotheses were conspiracy theorists, but did state: “We believe the strongest clue from new, credible, and peer-reviewed evidence in the scientific literature is that the virus evolved in nature, while suggestions of a laboratory leak source of the pandemic remain without scientifically validated evidence that directly supports it in peer-reviewed scientific journals”. In fact, this argument could literally be reversed. As will be shown below, there is no direct support for the natural origin of SARS-CoV-2, and a laboratory-related accident is plausible.
There is so far no scientifically validated evidence that directly supports a natural origin. Among the references cited in the two letters by Calisher and colleagues,1
, 2
all but one simply show that SARS-CoV-2 is phylogenetically related to other betacoronaviruses. The fact that the causative agent of COVID-19 descends from a natural virus is widely accepted, but this does not explain how it came to infect humans. The question of the proximal origin of SARS-CoV-2—ie, the final virus and host before passage to humans—was expressly addressed in only one highly cited opinion piece, which supports the natural origin hypothesis,4
but suffers from a logical fallacy:5
it opposes two hypotheses—laboratory engineering versus zoonosis—wrongly implying that there are no other possible scenarios. The article then provides arguments against the laboratory engineering hypothesis, which are not conclusive for the following reasons. First, it assumes that the optimisation of the receptor binding domain for human ACE2 requires prior knowledge of the adaptive mutations, whereas selection in cell culture or animal models would lead to the same effect. Second, the absence of traces of reverse-engineering systems does not preclude genome editing, which is performed with so-called seamless techniques.6
, 7
Finally, the absence of a previously known backbone is not a proof, since researchers can work for several years on viruses before publishing their full genome (this was the case for RaTG13, the closest known virus, which was collected in 2013 and published in 2020).8
Based on these indirect and questionable arguments, the authors conclude in favour of a natural proximal origin. In the last part of the article, they briefly evoke selection during passage (ie, experiments aiming to test the capacity of a virus to infect cell cultures or model animals) and acknowledge the do ented cases of laboratory escapes of SARS-CoV, but they dismiss this scenario, based on the argument that the strong similarity between receptor binding domains of SARS-CoV-2 and pangolins provides a more parsimonious explanation of the specific mutations. However, the pangolin hypothesis has since been abandoned,9
, 10
, 11
, 12
so the whole reasoning should be re-evaluated.
• View related content for this article
Although considerable evidence supports the natural origins of other outbreaks (eg, Nipah, MERS, and the 2002–04 SARS outbreak) direct evidence for a natural origin for SARS-CoV-2 is missing. After 19 months of investigations, the proximal progenitor of SARS-CoV-2 is still lacking. Neither the host pathway from bats to humans, nor the geographical route from Yunnan (where the viruses most closely related to SARS-CoV-2 have been sampled) to Wuhan (where the pandemic emerged) have been identified. More than 80 000 samples collected from Chinese wildlife sites and animal farms all proved negative.13
In addition, the international research community has no access to the sites, samples, or raw data. Although the Joint WHO-China Study concluded that the laboratory origin was “extremely unlikely”,13
WHO Director-General Tedros Adhanom Ghebreyesus declared that all hypotheses remained on the table including that of a laboratory leak.14
A research-related origin is plausible. Two questions need to be addressed: virus evolution and introduction into the human population. Since July, 2020, several peer-reviewed scientific papers have discussed the likelihood of a research-related origin of the virus. Some unusual features of the SARS-CoV-2 genome sequence suggest that they may have resulted from genetic engineering,15
, 16
an approach widely used in some virology labs.17
Alternatively, adaptation to humans might result from undirected laboratory selection during serial passage in cell cultures or laboratory animals,5
, 18
, 19
including humanised mice.20
Mice genetically modified to display the human receptor for entry of SARS-CoV-2 (ACE2) were used in research projects funded before the pandemic, to test the infectivity of different virus strains.21
Laboratory research also includes more targeted approaches such as gain-of-function experiments relying on chimeric viruses to test their potential to cross species barriers.17
, 22
A research-related contamination could result from contact with a natural virus during field collection, transportation from the field to a laboratory,23
characterisation of bats and bat viruses in a laboratory, or from a non-natural virus modified in a laboratory. There are well-do ented cases of pathogen escapes from laboratories.24
, 25
, 26
, 27
Field collection, field survey, and in-laboratory research on potential pandemic pathogens require high-safety protections and a strong and transparent safety culture. However, experiments on SARS-related coronaviruses are routinely performed at biosafety level 2,22
, 28
which complies with the recommendations for viruses infecting non-human animals, but is inappropriate for experiments that might produce human-adapted viruses by effects of selection or oriented mutations.
Overwhelming evidence for either a zoonotic or research-related origin is lacking: the jury is still out. On the basis of the current scientific literature, complemented by our own analyses of coronavirus genomes and proteins,5
, 15
, 16
, 18
, 29
, 30
we hold that there is currently no compelling evidence to choose between a natural origin (ie, a virus that has evolved and been transmitted to humans solely via contact with wild or farmed animals) and a research-related origin (which might have occurred at sampling sites, during transportation or within the laboratory, and might have involved natural, selected, or engineered viruses).
An evidence-based, independent, and prejudice-free evaluation will require an international consultation of high-level experts with no conflicts of interest, from various disciplines and countries; the mandate will be to establish the different scenarios, and the associated hypotheses, and then to propose protocols, methods, and required data in order to elucidate the question of SARS-CoV-2's origin. Beyond this issue, it is important to continue debating about the risk–benefit balance of current practices of field and laboratory research, including gain-of-function experiments, as well as the human activities contributing to zoonotic events.
Scientific journals should open their columns to in-depth analyses of all hypotheses. As scientists, we need to evaluate all hypotheses on a rational basis, and to weigh their likelihood based on facts and evidence, devoid of speculation concerning possible political impacts. Contrary to the first letter published in The Lancet by Calisher and colleagues,2
we do not think that scientists should promote “unity” (“We support the call from the Director-General of WHO to promote scientific evidence and unity over misinformation and conjecture”). As shown above, research-related hypotheses are not misinformation and conjecture. More importantly, science embraces alternative hypotheses, contradictory arguments, verification, refutability, and controversy. Departing from this principle risks establishing dogmas, abandoning the essence of science, and, even worse, paving the way for conspiracy theories. Instead, the scientific community should bring this debate to a place where it belongs: the columns of scientific journals.31
, 32
https://www.thelancet.com/journals/l...?rss%3Dyes#%20
Also, tuberculosis.
Still a top 10 killer globally.
https://www.thelancet.com/journals/l...625-X/fulltextGlobally in 2016, among HIV-negative individuals, the number of incident cases of tuberculosis was 9·02 million (95% uncertainty interval [UI] 8·05–10·16) and the number of tuberculosis deaths was 1·21 million (1·16–1·27). Among HIV-positive individuals, the number of incident cases was 1·40 million (1·01–1·89) and the number of tuberculosis deaths was 0·24 million (0·16–0·31).
After Republicans push anti-mask policies, Arizona's COVID death rate now as high as New York's
Arizona has reached New York in COVID-19 deaths per capita
as the state leads efforts to fight vaccine mandates
https://www.salon.com/2021/10/26/aft...-as-new-yorks/
Repug politics valued more than their own voters' lives
Desantis offering UN-vaccinated, out-of-state cops $5000 to move the Florida.
There's no evidence that this time that there was.
My turn, why do you keep falling for these conspiracies over and over again?
Soon he's going to go so far down this rabbit hole he'll end up commiting to the same theory he always does which is basically baby eating Democrats.
Happens every time.
Facts so far: "that research did not cause Covid"Fauci s: "that research did not cause Covid"
Everyone else: "Falsuchi lied to congress. Thats a felony"
Fauci s: "but that research didnt cause Covid"
Falsuchi s.
Trump s: "Falsuchi lied to congress. Thats a felony"
Facts so far: "Fauci didn't lie to congress"
Trump s: "Alternate facts!"
Trump s.
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