Posted on 06/06/2021 7:57:55 AM PDT by Enlightened1
The Pfizer and Moderna vaccines are based on "messenger" RNA. The RNA is encapsulated in a lipid layer consisting of propylene glycol (a petrochemical).
This is the biological definition of a virus. (In this case a synthetic virus.)
Medical Microbiology, 4th Edition:
Virus Structure and Function
Viruses are small obligate intracellular parasites, which by definition contain either a RNA or DNA genome surrounded by a protective, virus-coded protein coat. Viruses may be viewed as mobile genetic elements, most probably of cellular origin and characterized by a long co-evolution of virus and host. For propagation viruses depend on specialized host cells supplying the complex metabolic and biosynthetic machinery of eukaryotic or prokaryotic cells. A complete virus particle is called a virion. The main function of the virion is to deliver its DNA or RNA genome into the host cell so that the genome can be expressed (transcribed and translated) by the host cell. The viral genome, often with associated basic proteins, is packaged inside a symmetric protein capsid. The nucleic acid-associated protein, called nucleoprotein, together with the genome, forms the nucleocapsid. In enveloped viruses, the nucleocapsid is surrounded by a lipid bilayer derived from the modified host cell membrane and studded with an outer layer of virus envelope glycoproteins.
https://www.ncbi.nlm.nih.gov/books/NBK8174/
Great question. No one knows.....especially the Quacker/FR VPs.
Time will tell :-(
Thanks!
New post by Sebastian Rushworth M.D.
Can asymptomatic people spread covid-19?
by Sebastian Rushworth, M.D.
If anyone answers your question, it might be from this
medical stat genius: Sebastian Rushworth M.D.
Can asymptomatic people spread covid-19?
by Sebastian Rushworth, M.D.
One of the most contentious issues when it comes to covid-19 is whether or not people who are asymptomatic can spread the disease. The reason is that there are major ramifications depending on the answer. If only those with symptoms spread the disease, then telling people who are completely symptom free to stay at home and avoid social contacts makes zero sense. But if even those without symptoms can spread the disease, then there is at least some theoretical basis for quarantining asymptomatic people, a.k.a. lockdowns.
My personal intuition has been that covid probably does spread asymptomatically. This intuition is based on the fact that the virus has spread so rapidly and successfully around the world, and also on the complete and utter uselessness of lockdowns (I’ll explain my thinking on this further along in the text). This is very diferent from MERS and SARS, which were both rapidly and easily contained, probably because there was no asymptomatic spread, thus making it easy to identify and quarantine those who were infectious.
Back in November I wrote an article about a study conducted on US marine corps recruits. These recruits were forced to quarantine at home for two weeks before beginning their training, and were only allowed to begin the training if they had been symptom free during that entire two week period. In spite of this, the virus was able to sneak in to the training camp and spread among the recruits. Of the recruits that were determined to have brought the virus in to the camp, most remained symptom free throughout. To me, this in itself is pretty powerful evidence that asymptomatic spread does happen. But of course, 18 year olds are not known for being reliable - maybe they were so keen to start their military careers that they went to the training camp in spite of a sore throat and head ache, and just pretended to be asymptomatic.
Since then, however, more data has been published, which can perhaps help to answer the question more definitively. And to be fair, we don’t just want to know if asymptomatic spread can happen, we also want to know to what extent it happens in reality, and what the difference in infectiousness is between people who are symptomatic or pre-symptomatic and those who stay asymptomatic.
If people with symptoms are 100 times more infectious than people without symptoms, then that is for all practical intents and purposes the same as if people without symptoms are not infectious, because it means that it should be enough to contain only those with symptoms in order to effectively stop the spread of the disease. If on the other hand they’re only slightly more infectious, then efforts to contain the disease by quarantining only those with symptoms are unlikely to be successful.
An article was published in The Lancet in January that sought to establish the relative infectiousness of people with symptomatic as opposed to asymptomatic disease. It used data from Singapore’s screening and track and trace programs. Singapore screens large segments of the population for covid-19 on a regular basis. When someone tests positive for covid through the screening program, all recent contacts that have spent more than half an hour within two meters of that person are also tested. Both the “index case” and the contacts are then placed in quarantine until they test negative.
This has allowed the Singaporean government to catch a lot of people with asymptomatic infection, and to see the extent to which they are able to pass the infection on to others. This data can then be compared with the data from people who have symptomatic infection and their close contacts. So, what the authors of the study did was to take the data on everyone who spent time in quarantine as a result of being a close contact of someone with covid between August 1st and October 11th 2020, and compare the relative rates of secondary infection among those exposed to someone with symptomatic covid and those exposed to someone with asymptomatic covid, as diagnosed by PCR.
A total of 628 index cases and 3,790 close contacts were identifed (roughly six close contacts per index case). 5.2% of the contacts of symptomatic index cases developed covid-19 (i.e. switched from having a negative to a positive PCR test) during their quarantine period, as compared with 1.6% of asymptomatic index cases. On the face of it, this would suggest that people with symptomatic disease are roughly three times more infectious than those with asymptomatic disease.
Of course, there is a factor that makes this result more difficult to interpret, and that is the false positive rate of the PCR test. Data from real world testing suggests that the false positive rate of the PCR test is well below 1%. In Australia, as few as 0.2% of tests have been positive for much of the pandemic. If we assume that this number is in the ballpark, and subtract 0.2% from the two numbers provided above from the Singaporean data, that would give us 5.0% infected among contacts of symptomatic people, and 1.4% infected among contacts of asymptomatic people, which would still suggest that people with symptomatic infection are roughly three to four times more infectious than people with asymptomatic infection.
One major issue with this study, however, is the fact that all of this is observational data. The contacts haven’t only been in close contact with the known index cases. They’ve interacted with lots of other people too. How do we know that the supposed index case is the person that actually infected them? We don’t. So technically, it could actually be the case that every single one of the people that became infected after spending time with an asymptomatic person was actually infected by someone else who was symptomatic. If that’s the case, then people who are symptomatic are infinitely more infectious than people who are asymptomatic. It’s impossible to know for certain.
In order to be able to figure that part out, you would need a randomized trial, where you keep your study objects in a cage and cut them off from all contact with other people for a month or so, then introduce them to someone with either symptomatic or asymptomatic covid-19 and see if they become infected. Well... I guess it doesn’t have to be a cage...
Since that trial design would be difficult to get approved by an ethical review board, we have to look around for an observational study that accomplishes something similar. Luckily, a Japanese study, recently published in the International Journal of Infectious Diseases, does just that. Like Singapore, Japan has had an extensive track and trace system in place since the beginning of the pandemic. The study describes the first cluster of cases identified in Japan, back in January 2020. At that time there was virtually zero societal spread in Japan, so for anyone who was a close contact of a known index case, and who subsequently developed covid-19, we can be reasonably certain that it was the known index case that infected them.
It began with a tourist from Wuhan. The tourist infected a person who subsequently went to a party in Tokyo on January 18th, at which ten people were infected, four with symptomatic covid, and six with asymptomatic disease (it must have been quite a party!). Of the six asympomatic people, one went on to infect two people. One of these developed symptomatic disease while the other remained asymptomatic. The asymptomatic person then went on to infect two more people, both of whom developed symptomatic disease, one of whom died.
What does this prove? Well, it’s observational data, so it’s hard to say that it proves anything. But considering how little societal spread there was at the time, it seems highly likely that the people identified as having spread the infection to others further down the chain actually were the spreaders. This study therefore provides pretty strong support to the notion that people with asymptomatic disease, who remain asymptomatic (i.e. who aren’t just pre-symptomatic), can spread the disease on to others, who then go on to develop symptoms.
Overall, 36 people were identified in the cluster of infections arising from the tourist from Wuhan. 23 of these were symptomatic, while 12 remained asymptomatic (one had unknown symptom status). Overall, people with symptomatic infection were estimated to be 3.7 times more infectious than people with asymptomatic infection. However, the confidence interval was wide due to the small number of cases, with the lower bound estimate being that people with symptomatic disease are over thirty times more infectious than those with asymptomatic disease, while the upper bound estimate is that people with asymptomatic disease are almost as infectious as those with symptomatic disease.
When taken together, I think these two studies show that people with asymptomatic covid-19 can and do spread the disease, and the best estimate from both studies is that those with symptomatic disease are about three to four times more infectious than those with asymptomatic disease. That is not a huge difference. Even though people with symptoms are a couple of times more infectious than people without symptoms, those without symptoms could still be causing more infections overall.
The reason is that people with symptomatic disease will for the most part stay at home and avoid contact with other people, at least from the moment they start to have symptoms (by which time they could, of course, already have infected plenty of other people). People who are asymptomatic, on the other hand, will continue to lead their lives as normal, for example going to work at a care home or hospital, where they will come in to close physical contact with frail elderly people for extended periods. Considering that the evidence from randomized trials shows that face masks provide little to no benefit, they will then likely spread the infection on regardless of how rigorously they follow mandates to wear face masks at work. And that’s probably why lockdowns haven’t had any noticeable effect on the number of people dying of covid. Telling 30 year old office workers to work from home won’t stop the virus circulating in hospitals and care homes. Those at risk of serious disease will therefore still be exposed and infected.
“…whence do they obtain the lipid proteins…
********************************
Oops… “lipid proteins” should only read “lipids”.
Luc Montagnier Did NOT Say Vaccine Would Kill People in Two Years - Here’s What he DID Say (Video)
Nobel Prize Winner Reveals - Covid Vaccine is ‘Creating Variants’
Exactly.
He NEVER said that, but....he has done wonderful work (on AIDS, other studies) and has sounded the warning.
I’m glad that the group who translated his original interview has confirmed, for all, that he didn’t say that.
His interview is a must see. Thanks for posting the link.
“A virus requires the host cell for replication. That’s exactly what the “vaccines” are doing. Using the host cell to replicate spike proteins.”
No they are not replicating.
The snippet of COVID spike protein head that is produced in the ribosomes (not the nucleus), is not the mRNA vaccine.
The mRNA itself degrades (half life ten hours), and is not replenished or reproduced in any way.
I inject 3rd generation synthetic insulin every day.
It works much better than “real” insulins.
All vaccines today use a dead virus. But you need to grow them alive first.
So replicating a real virus or synthetic virus, would a synthetic virus be safer to make?
I guess what I’m saying or asking is, perhaps synthetic isn’t bad?
Does it matter? Just gotta fool the body to become immune.
Bret and Heather 83rd DarkHorse Podcast Livestream: Doing Science in an Emergency
https://youtu.be/pQiv8I9Peqk
=> Ivermectin efficacy.
The viral spike proteins that viral m-RNA forces your cells to produce is the virulent part of the covid virus structure. It is NOT staying in your deltoid muscle as they thought it would. It is getting into your circulation and exposing every organ in your body to this pathological part of the covid virus, including crossing the blood brain barrier and is DEFINITELY causing damage! These pathological spike proteins also get into the bone marrow.
End of story.
I did not recommend them to my patients when they came out.
Out of those who have received them, many have had serious complications.
“What incredible IGNORANCE you are promoting.”
Yes! There is great IGNORANCE. But, it is coming from your keyboard!
Vaccine researcher admits ‘big mistake,’ says spike protein is dangerous ‘toxin’
https://bit.ly/3fOwz2d
Exposing the Media’s Plot to Hide Record Vaccine Deaths and Deceive Americans —
https://bit.ly/3wRbIRq
A mild cousin of the disfiguring and often lethal smallpox was just the ticket in 1796!
Haha!
Oh yeah you got it all figured out..... (sarcasm off)
Aren’t all vaccines just watered down versions of the actual virus that enable your body’s immune system to fight it.
Provocation thought !, and open for comments
Since the mRNA injection, bypasses one's own "natural immunity system", and we don't know the long-lasting reaction to the human body,
we need to ask ourselves how our immune system will react to future viri, or even bacteriologal infections.
Will it require future "booster shots" for commonly occurring infections ? or viruses ?
Enlightened1 wrote: “Oh, yeah you got it all figured out..... (sarcasm off)”
It’s easy to figure out once you drop the anti-vaxxer cult conspiracy theories.
“ Aren’t all vaccines just watered down versions of the actual virus that enable your body’s immune system to fight it.”
——————————————————————————-
Yes. But you can’t just come out and say that.
You need to walk them through it as they themselves make the astounding discovery.
If you have had one vaccination, do NOT get another one.
I am doing a study of my own and it’s grisly outcome clotting, neurological, bone, lung, cardiac and GI issues are chilling.
One of my patients fell down a rocky embankment at the coast and his lower leg shattered after 2 vaccinations. Bowel necrosis and sepsis, seizures in a 25 year old woman.
You absolutely should not even get one shot if you have any kind of autoimmune disorder.
I could go on and on.
Is the lottery worth it, or a frickin’ free beer?
I am totally astounded that state governors are pushing these after the first round of injections started.
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