When they tested white-tailed deer in the US, they found SARS-COV-2 antibodies in 3 samples from January 2020 - ie predating the supposed US index case, which I read was a scientist or researcher returning from Wuhan via a somewhat circuitous route. This evidence of early wild deer infection only merits a casual mention in articles about these animals being a possible reservoir, and the risks that presents, eg NatGeo: https://www.nationalgeographic.com/animals/article/wild-us-deer-found-with-coronavirus-antibodies
The Santa Claus reindeers got if from the packaging of Wuhan made toys just that christmas & spread it immediately to all the other deers - makes sense. I suppose the elves & obese comorbid Santa took Ivermectin, Vit C & Zinc.
“Exactly how deer may have been exposed to the virus remains uncertain, though researchers suspect they were infected by humans. “Multiple activities could bring deer into contact with people, including captive cervid operations, field research, conservation work, wildlife tourism, wildlife rehabilitation, supplemental feeding, and hunting,” the USDA researchers wrote. Other possibilities include that they contracted it through contaminated wastewater or from exposure to other infected species like mink.“
A group of researchers conducted more advanced genomic analysis on more recent samples from one specific group of these wild deer and detected a predominant strain previously found among humans in California, a considerable distance away. They suggested the logical explanation was that these deer had eaten contaminated (inference: by humans) bait, most likely sweetcorn.
However if the source is indeed zoonotic, I'm not ready to set aside a possible mink/ferret/etc connection, not least because the Pfizer veterinary research spin-off, Zoetis, with its US govt funding and connections to EHA, has been beavering away in the background this whole time. Zoetis projects include eg mRNA SARS-COV-2 Spike vaccination programmes for primates in zoos and shelters.
What about waste water, leak, deer drink water and zoonotic jump?
Here’s another interesting part from the study:
“To evaluate the in vivo competition between the ancestral lineage A (SARS-CoV-2/human/USA/WA1/2020) and the alpha VOC (SARS-CoV-2/human/USA/CA-5574/2020) strains, cDNA products of SARS-CoV-2 RNA extracted from swabs and tissue homogenates were sequenced on the Illumina NextSeq platform. While the intent was to use a 1:1 titre ratio of the two strains, we were limited in our ability to obtain an exact 1:1 ratio since our only means to quantify virus was through virus titrations. Subsequently, sequencing analysis showed the inoculum used for infection was 60% alpha VOC B.1.1.7 and 40% lineage A WA1. Nasal swabs collected at 1 DPC revealed the proportion of lineage A strain ranged from 0.7-40.0% and of alpha VOC B.1.17 strain from 60.0-99.3% in the 4 principal infected deer (Table 3, Supplementary Figure 5). In contrast, one of the oral swabs from a principal infected deer (#905) at 1 DPC showed 51.0% lineage A WA1 and 49.0% VOC B.1.1.7, while the other oral swab contained 5.4% lineage A and 94.6% VOC B.1.1.7. By 3 DPC, the composition of all nasal and most oral swabs was entirely alpha VOC B.1.1.7, with the exception of a 4 DPC oral swab collected from deer #905 that showed 2.9% lineage A and 97.1% VOC B.1.1.7. Swab and tissue samples collected from sentinel deer were also dominated by the alpha VOC B.1.1.7 strain. The B.1.1.7 strain was also dominant in tissues collected from the two primary challenged deer at 4 DPC, with a maximum lineage A percentage of 20.9% found in the nasopharynx of deer #905 (Table 3, Supplementary Figure 5). Virus genome analysis was only possible in a few tissues collected from principal (nasopharynx and tonsil) and sentinel (retropharyngeal lymph node) deer at 18 DPC; the results revealed a >95% presence of alpha VOC B.1.1.7 genomic sequences. These results indicate a competitive advantage of the alpha VOC B.1.1.7 isolate over the lineage A WA1 isolate.”
Two or more of the events you mention are possible, even within a relatively short time frame, since we've seen how quickly new VOCs emerge, and there are papers describing a jump "back" eg from humans to mink.
What a fantastic deep dive, fab resource thanks! Because good stuff tends to vanish I have saved at Wayback and encourage you to make sure your other research and references are protected for posterity! :~)
“ Michael Gasaway, principal of Madison Consolidated High School (MCHS), said the teachers fell ill while monitoring an area in the school’s C-wing. They were taken to hospital as an apparently precautionary measure along with three other students who also displayed minor symptoms.”
“ As of Feb. 4, the Centers for Disease Control and Prevention reported that vaping-related lung injury has hospitalized a total of 2,758 people nationally and resulted in the deaths of 64.”
so, seems no evidence of onwards transmission, which is bizarre if it was Covid-19. This aspect solidly supports the hypothesis that it was indeed a disease caused by toxic ingredients in vaping products, confined to the individuals who used them, and not a human to human transmissible respiratory disease.
Now-now, the Vitamin E Acetate stuff is a scam of proportions greater than that of the Wet Market Origin multiplied by the Pangolins trail divided by Kristian G's candor.
There was never any VEA in aqueous Nicotine Vape cartridges, there can't be (aqueous, VEA not water soluble => mayonnaise).
"The hazardous agent was soon identified. This was a cutting agent, Vitamin E Acetate (VEA), added to dilute viscous cannabis oils for criminal economic reasons. This agent was identified in September 2019 and confirmed beyond doubt in early 2020 (Blount et al, NEJM, 2020). VEA cannot be added to nicotine e-liquids (Kozlovich et al, 2021) and would serve no useful purpose even if it could. The outbreak ended because US-based illicit THC vape producers removed the harmful agent or ceased production because they were arrested. No remedial action was taken by manufacturers of nicotine vapes because none was necessary or possible, and yet the outbreak still ended."
you have been caught out telling lies before, so not surprising that you continue to do so, as for middle names we can call you Alberto "Paranoid Pinocchio" Silva and why do you think I have a grant and am connected to "Anderson"? Such a foolish person you are.
“Cytotoxic effects of Vitamin E acetate on macrophage and epithelial cell functions in the lung may have additive or synergistic effects with the SARS-CoV-2 virus, and further amplify lung injury and inflammation in vapers. The increased inflammation promoted by combined injury from the SARS-Co-V-2 cytokine release and inflammation induced by vaping induced epithelial cell injury in the lung may worsen the likelihood of cytokine release and systemic inflammation with an associated increase in systemic manifestations such as fever, myalgias, fatigue, and headache.“
-The previously mentioned Layden et al. article reported pathology from 17 of the 53 cases, which included 14 BALs and three transbronchial biopsies. Seven of the BALs reported lipid-laden macrophages: 7 of 53.
- however neither study (36,37) demonstrated findings of exogenous lipid pneumonia
COVID-19: characterized in detail as exactly the same as Evali.
PLUS:
Check out n°37 & 43 (Kansas 25% maybe THC, CO half of them)
EVALI's clinical presentation, apart from ground-glass opacities in the lungs, runs counter to what we know about COVID-19 epidemiology, as you say.
No Pro-CoV2 near-ancestor would target the same population that is largely protected from SARS-CoV-2 because of TMPRSS2 expression differences between 20 year-old lungs & 70 year-old lungs [in addition to several other epid. incongruities].
A link to the VA nursing home deaths is far more plausible
EVALI clusters also spread geographically from hot spots.
Anecdotally:
wisconsin story below.
Plus some more bread crumbs: Remember about that boiler that exploded in Baltimore, that serviced that specific BW research establishment with no incinerator, that was recruiting for in-vivo aerosolization testing & was flooded in May 2018?
When they tested white-tailed deer in the US, they found SARS-COV-2 antibodies in 3 samples from January 2020 - ie predating the supposed US index case, which I read was a scientist or researcher returning from Wuhan via a somewhat circuitous route. This evidence of early wild deer infection only merits a casual mention in articles about these animals being a possible reservoir, and the risks that presents, eg NatGeo: https://www.nationalgeographic.com/animals/article/wild-us-deer-found-with-coronavirus-antibodies
1 sample was from someone returning from Wuhan but the other 2 samples in Washington aren’t described as to their connection.
The Santa Claus reindeers got if from the packaging of Wuhan made toys just that christmas & spread it immediately to all the other deers - makes sense. I suppose the elves & obese comorbid Santa took Ivermectin, Vit C & Zinc.
“Exactly how deer may have been exposed to the virus remains uncertain, though researchers suspect they were infected by humans. “Multiple activities could bring deer into contact with people, including captive cervid operations, field research, conservation work, wildlife tourism, wildlife rehabilitation, supplemental feeding, and hunting,” the USDA researchers wrote. Other possibilities include that they contracted it through contaminated wastewater or from exposure to other infected species like mink.“
A group of researchers conducted more advanced genomic analysis on more recent samples from one specific group of these wild deer and detected a predominant strain previously found among humans in California, a considerable distance away. They suggested the logical explanation was that these deer had eaten contaminated (inference: by humans) bait, most likely sweetcorn.
However if the source is indeed zoonotic, I'm not ready to set aside a possible mink/ferret/etc connection, not least because the Pfizer veterinary research spin-off, Zoetis, with its US govt funding and connections to EHA, has been beavering away in the background this whole time. Zoetis projects include eg mRNA SARS-COV-2 Spike vaccination programmes for primates in zoos and shelters.
What about waste water, leak, deer drink water and zoonotic jump?
Here’s another interesting part from the study:
“To evaluate the in vivo competition between the ancestral lineage A (SARS-CoV-2/human/USA/WA1/2020) and the alpha VOC (SARS-CoV-2/human/USA/CA-5574/2020) strains, cDNA products of SARS-CoV-2 RNA extracted from swabs and tissue homogenates were sequenced on the Illumina NextSeq platform. While the intent was to use a 1:1 titre ratio of the two strains, we were limited in our ability to obtain an exact 1:1 ratio since our only means to quantify virus was through virus titrations. Subsequently, sequencing analysis showed the inoculum used for infection was 60% alpha VOC B.1.1.7 and 40% lineage A WA1. Nasal swabs collected at 1 DPC revealed the proportion of lineage A strain ranged from 0.7-40.0% and of alpha VOC B.1.17 strain from 60.0-99.3% in the 4 principal infected deer (Table 3, Supplementary Figure 5). In contrast, one of the oral swabs from a principal infected deer (#905) at 1 DPC showed 51.0% lineage A WA1 and 49.0% VOC B.1.1.7, while the other oral swab contained 5.4% lineage A and 94.6% VOC B.1.1.7. By 3 DPC, the composition of all nasal and most oral swabs was entirely alpha VOC B.1.1.7, with the exception of a 4 DPC oral swab collected from deer #905 that showed 2.9% lineage A and 97.1% VOC B.1.1.7. Swab and tissue samples collected from sentinel deer were also dominated by the alpha VOC B.1.1.7 strain. The B.1.1.7 strain was also dominant in tissues collected from the two primary challenged deer at 4 DPC, with a maximum lineage A percentage of 20.9% found in the nasopharynx of deer #905 (Table 3, Supplementary Figure 5). Virus genome analysis was only possible in a few tissues collected from principal (nasopharynx and tonsil) and sentinel (retropharyngeal lymph node) deer at 18 DPC; the results revealed a >95% presence of alpha VOC B.1.1.7 genomic sequences. These results indicate a competitive advantage of the alpha VOC B.1.1.7 isolate over the lineage A WA1 isolate.”
https://www.independent.co.uk/news/world/americas/virus-biological-us-army-weapons-fort-detrick-leak-ebola-anthrax-smallpox-ricin-a9042641.html
Two or more of the events you mention are possible, even within a relatively short time frame, since we've seen how quickly new VOCs emerge, and there are papers describing a jump "back" eg from humans to mink.
My point is that the ancestral strain would disappear! Convenient.
What a fantastic deep dive, fab resource thanks! Because good stuff tends to vanish I have saved at Wayback and encourage you to make sure your other research and references are protected for posterity! :~)
https://web.archive.org/web/20220318011521/https://therequestor.substack.com/p/is-wuhan-a-red-herring?r=7in29&s=r
Did any of the known "evali" patients transmit "evali" to family or medical workers, etc?
https://therequestor.substack.com/p/is-wuhan-a-red-herring-addendum
“ Michael Gasaway, principal of Madison Consolidated High School (MCHS), said the teachers fell ill while monitoring an area in the school’s C-wing. They were taken to hospital as an apparently precautionary measure along with three other students who also displayed minor symptoms.”
“ As of Feb. 4, the Centers for Disease Control and Prevention reported that vaping-related lung injury has hospitalized a total of 2,758 people nationally and resulted in the deaths of 64.”
Interesting case fatality rate isn’t it?
https://abcnews.go.com/amp/US/hospitalized-vaping-device-found-wisconsin-school/story?id=69067857
so, seems no evidence of onwards transmission, which is bizarre if it was Covid-19. This aspect solidly supports the hypothesis that it was indeed a disease caused by toxic ingredients in vaping products, confined to the individuals who used them, and not a human to human transmissible respiratory disease.
Now-now, the Vitamin E Acetate stuff is a scam of proportions greater than that of the Wet Market Origin multiplied by the Pangolins trail divided by Kristian G's candor.
There was never any VEA in aqueous Nicotine Vape cartridges, there can't be (aqueous, VEA not water soluble => mayonnaise).
The VEA was in THC based vapes (not nicotine vapes) used as a viscous oil to cut the THC, all explained here in great detail: https://clivebates.com/e-cigarette-risk-perceptions-an-american-crime-scene/?print=print
"The hazardous agent was soon identified. This was a cutting agent, Vitamin E Acetate (VEA), added to dilute viscous cannabis oils for criminal economic reasons. This agent was identified in September 2019 and confirmed beyond doubt in early 2020 (Blount et al, NEJM, 2020). VEA cannot be added to nicotine e-liquids (Kozlovich et al, 2021) and would serve no useful purpose even if it could. The outbreak ended because US-based illicit THC vape producers removed the harmful agent or ceased production because they were arrested. No remedial action was taken by manufacturers of nicotine vapes because none was necessary or possible, and yet the outbreak still ended."
VEA hypothesis "potentially applicable" to 1/15 of cases. Equivalent to wet market x pangolin/K candor.
Pure BS, is your maiden name Billy G. Anderson? You got a nice grant?
you have been caught out telling lies before, so not surprising that you continue to do so, as for middle names we can call you Alberto "Paranoid Pinocchio" Silva and why do you think I have a grant and am connected to "Anderson"? Such a foolish person you are.
“Cytotoxic effects of Vitamin E acetate on macrophage and epithelial cell functions in the lung may have additive or synergistic effects with the SARS-CoV-2 virus, and further amplify lung injury and inflammation in vapers. The increased inflammation promoted by combined injury from the SARS-Co-V-2 cytokine release and inflammation induced by vaping induced epithelial cell injury in the lung may worsen the likelihood of cytokine release and systemic inflammation with an associated increase in systemic manifestations such as fever, myalgias, fatigue, and headache.“
https://journals.sagepub.com/doi/full/10.1177/21501319211062672
Please read this, key info further down.
https://www.nature.com/articles/s41379-021-00915-6
Nature:
Evali:
- pathology of EVALI was poorly defined
-The previously mentioned Layden et al. article reported pathology from 17 of the 53 cases, which included 14 BALs and three transbronchial biopsies. Seven of the BALs reported lipid-laden macrophages: 7 of 53.
- however neither study (36,37) demonstrated findings of exogenous lipid pneumonia
COVID-19: characterized in detail as exactly the same as Evali.
PLUS:
Check out n°37 & 43 (Kansas 25% maybe THC, CO half of them)
https://archive.is/54Zy7#selection-10767.15-10767.272
https://twitter.com/SixandLaura/status/1402900673545617412
from CDC Lung Injury Response: Special Syndromic Surveillance Call 09/20/2019
“discharge coding tends to be very non-specific”
”shortness of breath,” “cough”
but one code that did pop out..“respiratory failure with hypoxemia”
..seems to start to *increase in our data around 2017.*
..we see it increasing in ages 10-30 the most..”
EVALI's clinical presentation, apart from ground-glass opacities in the lungs, runs counter to what we know about COVID-19 epidemiology, as you say.
No Pro-CoV2 near-ancestor would target the same population that is largely protected from SARS-CoV-2 because of TMPRSS2 expression differences between 20 year-old lungs & 70 year-old lungs [in addition to several other epid. incongruities].
A link to the VA nursing home deaths is far more plausible
Quick question. What is the difference between EVALI and Covid?
Still waiting for that comparison. Do you know of any differences in the clinical presentation, as you say?
Page 6:
https://www.nature.com/articles/s41420-022-00855-3.pdf
.Hmm, nice work here. Hello Fony. Some more bread crumbs here for you.
Hello Billy: Yes, EVALI manifested in "clusters".
CDC: geographical clustering of cases.
E-cigarette, or Vaping, Product Use–Associated Lung Injury Among Clusters of Patients Reporting Shared Product Use — Wisconsin, 2019
=>https://archive.is/GPsfg
https://www.cdc.gov/mmwr/volumes/69/wr/mm6909a4.htm
EVALI clusters also spread geographically from hot spots.
Anecdotally:
wisconsin story below.
Plus some more bread crumbs: Remember about that boiler that exploded in Baltimore, that serviced that specific BW research establishment with no incinerator, that was recruiting for in-vivo aerosolization testing & was flooded in May 2018?
=>https://archive.is/ZJQfn
https://twitter.com/amicocolorido/status/1338618385396068353
https://twitter.com/amicocolorido