Posted on 12/07/2020 3:09:02 PM PST by HogsBreath
A nurse who took part in Pfizer Inc's late-stage coronavirus vaccine trial said she experienced several side effects, leading her to worry she may have contracted the disease.
(Excerpt) Read more at dailymail.co.uk ...
That’s about kkke saying blue eyes DNA is the DNA that forms blue eyes. The point is there is no particular actual mechanism like mRNA or tRNA.
This was my general recollection too. I think that this amounts to something just short of human experimentation.
I think the risk of taking the vaccine vastly outweighs the risks of contracting the Chinese Bioweapon.
One of our TN legislators is introducing a bill to forbid the vaccine from becoming mandatory. It’ll be interesting to see how that shakes out. They were interviewing him this morning and he made some good sense.
It seems that the word was out that at least one of the vaccines did work by altering a person’s DNA in some way. I didn’t pay much attention; I won’t take it.
I personally agree. Treatments ought to be evaluated in terms of risk vs benefit.
Especially since there are treatments which work very well if administered early:
https://principia-scientific.com/covid19-dr-zelenkos-statement-to-u-s-senate-committee-homeland-security/
FauXi is a bureaucrat and politician with major conflicts of interest with big pharma. He is expert at using fear, guilt, bullying, and trashing the careers of those who raise questions about his recommendations. All done under the guise of a kindly, caring, public health servant.
Nature Reviews Drug Discovrey 17, (2018):
261-79,
https://doi.org/10.1038/nrd.2017.243
The poly(A) tail also plays an important regulatory role in mRNA translation and stability25; thus, an optimal length of poly(A)24 must be added to mRNA either directly from the encoding DNA template or by using poly(A) polymerase. The codon usage additionally has an impact on protein translation. Replacing rare codons with frequently used synonymous codons that have abundant cognate tRNA in the cytosol is a common practice to increase protein production from mRNA29, although the accuracy of this model has been questioned30.
Maybe you have different understanding of the meaning of "directly from the encoding DNA template "?
I’m not certain about the Shingrix vaccine itself, but typically reactions are either due to the components of the drug/vaccine itself (e.g. there may be some sort of irritant) or they’re due to the immune system’s response. For the latter, this can include things like T-cells and/or macrophages overreacting to the change in environment and signaling all kinds of swelling and inflammation, or even attacking otherwise healthy tissue temporarily. Your immune system’s general defense against invaders includes raising your body temperate (fever), and other things that can disrupt normal body functions.
The idea with things like that is yes, it’s uncomfortable for you, but if the invading pathogen has a narrower scope of livable conditions than you do, you can survive with a fever and it can’t. Differences in things like genetics, underlying conditions, existing allergies, and other factors can play into why different people experience different reactions to the same drug or vaccine.
thanks..I am going into it expecting the worst so as to be prepared and if I have no reaction then I will be pleasantly surprised
Which one? If you say it’s the Russian or Chinese one, I almost might believe that. But then my next question would be: exactly what modifications are made to which chromosomes at which sites, and how are those modifications being made to all the cells of the body when the vaccine doses don’t typically include 20 lbs of vaccine material.
However, none of the vaccines being tested or used in any western nation make any changes to any DNA. They don’t have the ability to do so. You can’t change my computer by asking my printer to print a new picture.
Reactions to vaccines in general are less common than most people realize. If you get 5% of people developing noticeable reaction symptoms (e.g. headache, fever, body aches), that’s pretty high. A particular reaction could be seen in fewer than 1% of people, but you include that because 1% of 330 million is still nominally a large number, even if it’s unlikely you - as an individual - will experience it.
I always say expect the worst; hope for the best. It leaves you prepared for when things go poorly, but still with a sunny disposition about life in general.
WHOLEHEARTEDLY AGREE!
No, this is simply the next step in vaccine development and it's been researched, studied, and tested for over a decade. Moderna was founded over 10 years ago with the sole purpose of creating vaccines on the mRNA platform. Other biotech companies have been working on the mRNA platform even longer.
Gen 1 vaccines used killed or weakened versions of the pathogen. They had a high risk associated with mistakes in the killing/weakening process that sometimes caused people to become infected. e.g. the Cutter incident. Gen 2 vaccines take the part of the pathogen the body reacts to and puts it on something that isn't dangerous, such as another virus. These are slow to create and carry allergy risks. Gen 3 vaccines are the mRNA platform. There's no allergy risk. There's no risk of live pathogen causing infection. They're faster to create, faster to produce, and theoretically can be much cheaper once the manufacturing becomes more common.
"I think the risk of taking the vaccine vastly outweighs the risks of contracting the Chinese Bioweapon."
What specific risk, exactly? The only components in the mRNA vaccines are a lipid (fat) shell, which disappears when it encounters a cell or will be broken down over the course of a few days, and the messenger RNA inside. The mRNA can only interact with a ribosome and the only thing that does is cause the ribosome to build the surface glycoprotein for SARS-CoV-2. It's harmless by itself, but the immune system recognizes it as foreign and the resulting response is what builds lasting immunity. That mRNA breaks down naturally within the cells within hours or days.
In less than a week, there's nothing left of the vaccine in your body. The only way you'd ever know somebody had the thing is by checking for antibodies, and that testing wouldn't be able to distinguish between having the vaccine or having COVID-19. So what risks - specifically - are we talking about here? Testing? Just between the US and the UK, Pfizer and Moderna have spent months testing their respective vaccines on over 100,000 closely monitored volunteers. The Phase 1, Phase 2, and Phase 3 clinical trials done are exactly the same trials done for EVERY drug and vaccine.
Why are we suddenly to believe that the testing we do for everything on the market is suddenly insufficient? Why are we suddenly supposed to buy into fear with zero basis? I don't live in fear; I study facts and make informed decisions. The risks here are a headache and a fever for the vaccine or a 3% chance of landing in the ICU and 0.65% chance of death for the virus. I'll take the headache and fever, please.
Do we have any mRNA based vaccines on the market currently?
Yes we do, for VEEV: https://www.mdpi.com/2076-393X/8/2/273/htm
Further, we have two vaccines just out of testing about to enter the market. That would be the Pfizer and Moderna COVID-19 vaccines. Both have completed all the normal Phase 1, Phase 2, and Phase 3 clinical trials. Both have been proven safe and effective with over 100,000 closely monitored volunteers between the US and the UK.
No one knows if antibody-dependent enhancement (ADE) or enhanced respiratory disease (ERD) will occur in patients in the future, when challenged with a new viral variation. In other words, a worsening of disease possibly resulting in death. An adjuvant is being included in the vaccine to, hopefully, minimize the possibility, but the risk is unclear. One thing known for sure: The dead lab animal victims in earlier studies have no opinion on this.
Sorry, which conspiracy ridden drek website published this particular nonsense?
I especially like the use of “No one knows”! Ooooo SPOOKY! Yes, no one knows if drinking a cup of tea will cause your eyes to explode. Probably not, but hey “NO ONE KNOOOOWWWWWWSSSS”. Throw in some scary sounding medical terms and you’ve got yourself a winner!
Where it falls down is when it says “An adjuvant is being included in the vaccine”. Whoops! The Pfizer and Moderna vaccines include no adjuvants. Almost had it!
But wait, there’s more! “The dead lab animal victims in earlier studies...” Whoops! Neither the animals in the clinical studies nor any of the human participants in the Phase 1, Phase 2, or Phase 3 human trials died. None.
I always prefer my fantasy writing to include space ships and other fun far-away things. I think if you’re going to write pure fiction, at least make it entertaining.
Your writing borders on hypomanic if not manic. A little defensive, are you?
Sample references (first 61 from 2020 Nature article).
“Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies
Wen Shi Lee, Adam K. Wheatley, […]Brandon J. DeKosky
Nature Microbiology volume 5, pages1185–1191(2020)”
References
1.
Zhou, Y. et al. Network-based drug repurposing for novel coronavirus 2019-nCoV/SARS-CoV-2. Cell Discov. 6, 14 (2020).
CAS
PubMed
PubMed Central
Google Scholar
2.
Lu, R. et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet 395, 565–574 (2020).
CAS
PubMed
PubMed Central
Google Scholar
3.
Lam, T. T. et al. Identifying SARS-CoV-2 related coronaviruses in Malayan pangolins. Nature 583, 282–285 (2020).
CAS
PubMed
Google Scholar
4.
Hoffmann, M. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 181, 271–280 (2020).
CAS
PubMed
PubMed Central
Google Scholar
5.
Yan, R. et al. Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2. Science 367, 1444–1448 (2020).
CAS
PubMed
PubMed Central
Google Scholar
6.
Daly, J. L. et al. Neuropilin-1 is a host factor for SARS-CoV-2 infection. Preprint at https://www.biorxiv.org/content/10.1101/2020.06.05.134114v1 (2020).
7.
Cantuti-Castelvetri, L. et al. Neuropilin-1 facilitates SARS-CoV-2 cell entry and provides a possible pathway into the central nervous system. Preprint at https://www.biorxiv.org/content/10.1101/2020.06.07.137802v1 (2020).
8.
Wrapp, D. et al. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Science 367, 1260–1263 (2020).
CAS
PubMed
PubMed Central
Google Scholar
9.
Kim, H. W. et al. Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine. Am. J. Epidemiol. 89, 422–434 (1969).
CAS
PubMed
Google Scholar
10.
Graham, B. S. Vaccines against respiratory syncytial virus: the time has finally come. Vaccine 34, 3535–3541 (2016).
PubMed
PubMed Central
Google Scholar
11.
Nader, P. R., Horwitz, M. S. & Rousseau, J. Atypical exanthem following exposure to natural measles: eleven cases in children previously inoculated with killed vaccine. J. Pediatr. 72, 22–28 (1968).
Google Scholar
12.
Polack, F. P. Atypical measles and enhanced respiratory syncytial virus disease (ERD) made simple. Pediatr. Res. 62, 111–115 (2007).
PubMed
Google Scholar
13.
Dejnirattisai, W. et al. Cross-reacting antibodies enhance dengue virus infection in humans. Science 328, 745–748 (2010).
CAS
PubMed
Google Scholar
14.
Sridhar, S. et al. Effect of dengue serostatus on dengue vaccine safety and efficacy. N. Engl. J. Med. 379, 327–340 (2018).
PubMed
Google Scholar
15.
Hohdatsu, T. et al. Antibody-dependent enhancement of feline infectious peritonitis virus infection in feline alveolar macrophages and human monocyte cell line U937 by serum of cats experimentally or naturally infected with feline coronavirus. J. Vet. Med. Sci. 60, 49–55 (1998).
CAS
PubMed
Google Scholar
16.
Halstead, S. B. & O’Rourke, E. J. Dengue viruses and mononuclear phagocytes. I. Infection enhancement by non-neutralizing antibody. J. Exp. Med. 146, 201–217 (1977).
CAS
PubMed
PubMed Central
Google Scholar
17.
Vennema, H. et al. Early death after feline infectious peritonitis virus challenge due to recombinant vaccinia virus immunization. J. Virol. 64, 1407–1409 (1990).
CAS
PubMed
PubMed Central
Google Scholar
18.
Hohdatsu, T., Nakamura, M., Ishizuka, Y., Yamada, H. & Koyama, H. A study on the mechanism of antibody-dependent enhancement of feline infectious peritonitis virus infection in feline macrophages by monoclonal antibodies. Arch. Virol. 120, 207–217 (1991).
CAS
PubMed
PubMed Central
Google Scholar
19.
Weiss, R. C. & Scott, F. W. Antibody-mediated enhancement of disease in feline infectious peritonitis: comparisons with dengue hemorrhagic fever. Comp. Immunol. Microbiol. Infect. Dis. 4, 175–189 (1981).
CAS
PubMed
PubMed Central
Google Scholar
20.
Ye, Z. W. et al. Antibody-dependent cell-mediated cytotoxicity epitopes on the hemagglutinin head region of pandemic H1N1 influenza virus play detrimental roles in H1N1-infected mice. Front. Immunol. 8, 317 (2017).
PubMed
PubMed Central
Google Scholar
21.
Winarski, K. L. et al. Antibody-dependent enhancement of influenza disease promoted by increase in hemagglutinin stem flexibility and virus fusion kinetics. Proc. Natl Acad. Sci. USA 116, 15194–15199 (2019).
CAS
PubMed
Google Scholar
22.
Polack, F. P. et al. A role for immune complexes in enhanced respiratory syncytial virus disease. J. Exp. Med. 196, 859–865 (2002).
CAS
PubMed
PubMed Central
Google Scholar
23.
Polack, F. P., Hoffman, S. J., Crujeiras, G. & Griffin, D. E. A role for nonprotective complement-fixing antibodies with low avidity for measles virus in atypical measles. Nat. Med. 9, 1209–1213 (2003).
CAS
PubMed
Google Scholar
24.
Gao, T. et al. Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation. Preprint at https://www.medrxiv.org/content/10.1101/2020.03.29.20041962v3 (2020).
25.
Gralinski, L. E. et al. Complement activation contributes to severe acute respiratory syndrome coronavirus pathogenesis. mBio 9, e01753-18 (2018).
PubMed
PubMed Central
Google Scholar
26.
Larsen, M. D. et al. Afucosylated immunoglobulin G responses are a hallmark of enveloped virus infections and show an exacerbated phenotype in COVID-19. Preprint at https://www.biorxiv.org/content/10.1101/2020.05.18.099507v1 (2020).
27.
Chakraborty, S. et al. Symptomatic SARS-CoV-2 infections display specific IgG Fc structures. Preprint at https://www.medrxiv.org/content/10.1101/2020.05.15.20103341v1 (2020).
28.
Hiatt, A. et al. Glycan variants of a respiratory syncytial virus antibody with enhanced effector function and in vivo efficacy. Proc. Natl Acad. Sci. USA 111, 5992–5997 (2014).
CAS
PubMed
Google Scholar
29.
Zeitlin, L. et al. Enhanced potency of a fucose-free monoclonal antibody being developed as an Ebola virus immunoprotectant. Proc. Natl Acad. Sci. USA 108, 20690–20694 (2011).
CAS
PubMed
Google Scholar
30.
Wang, T. T. et al. IgG antibodies to dengue enhanced for FcγRIIIA binding determine disease severity. Science 355, 395–398 (2017).
CAS
PubMed
PubMed Central
Google Scholar
31.
Hui, K. P. Y. et al. Tropism, replication competence, and innate immune responses of the coronavirus SARS-CoV-2 in human respiratory tract and conjunctiva: an analysis in ex-vivo and in-vitro cultures. Lancet Respir. Med. 8, 687–695 (2020).
CAS
PubMed
PubMed Central
Google Scholar
32.
Yip, M. S. et al. Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus. Virol. J. 11, 82 (2014).
PubMed
PubMed Central
Google Scholar
33.
Robinson, W. E. Jr, Montefiori, D. C. & Mitchell, W. M. Antibody-dependent enhancement of human immunodeficiency virus type 1 infection. Lancet 1, 790–794 (1988).
PubMed
Google Scholar
34.
Robinson, W. E. Jr et al. Antibody-dependent enhancement of human immunodeficiency virus type 1 (HIV-1) infection in vitro by serum from HIV-1-infected and passively immunized chimpanzees. Proc. Natl Acad. Sci. USA 86, 4710–4714 (1989).
PubMed
Google Scholar
35.
Takada, A., Watanabe, S., Okazaki, K., Kida, H. & Kawaoka, Y. Infectivity-enhancing antibodies to Ebola virus glycoprotein. J. Virol. 75, 2324–2330 (2001).
CAS
PubMed
PubMed Central
Google Scholar
36.
Takada, A., Feldmann, H., Ksiazek, T. G. & Kawaoka, Y. Antibody-dependent enhancement of Ebola virus infection. J. Virol. 77, 7539–7544 (2003).
CAS
PubMed
PubMed Central
Google Scholar
37.
Ochiai, H. et al. Infection enhancement of influenza A NWS virus in primary murine macrophages by anti-hemagglutinin monoclonal antibody. J. Med. Virol. 36, 217–221 (1992).
CAS
PubMed
Google Scholar
38.
Sariol, C. A., Nogueira, M. L. & Vasilakis, N. A tale of two viruses: does heterologous flavivirus immunity enhance Zika disease? Trends Microbiol. 26, 186–190 (2018).
CAS
PubMed
Google Scholar
39.
Wan, Y. et al. Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J. Virol. 94, e02015-19 (2020).
PubMed
PubMed Central
Google Scholar
40.
Jaume, M. et al. Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway. J. Virol. 85, 10582–10597 (2011).
CAS
PubMed
PubMed Central
Google Scholar
41.
Cheung, C. Y. et al. Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis. J. Virol. 79, 7819–7826 (2005).
CAS
PubMed
PubMed Central
Google Scholar
42.
Yip, M. S. et al. Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS. Hong Kong Med. J. 22, 25–31 (2016).
CAS
PubMed
Google Scholar
43.
Ana-Sosa-Batiz, F. et al. Influenza-specific antibody-dependent phagocytosis. PLoS ONE 11, e0154461 (2016).
PubMed
PubMed Central
Google Scholar
44.
Yasui, F. et al. Phagocytic cells contribute to the antibody-mediated elimination of pulmonary-infected SARS coronavirus. Virology 454–455, 157–168 (2014).
PubMed
Google Scholar
45.
Zhou, J. et al. Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis. J. Infect. Dis. 209, 1331–1342 (2014).
CAS
PubMed
Google Scholar
46.
Ho, M. S. et al. Neutralizing antibody response and SARS severity. Emerg. Infect. Dis. 11, 1730–1737 (2005).
CAS
PubMed
PubMed Central
Google Scholar
47.
Zhao, J. et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019. Clin. Infect. Dis. https://doi.org/10.1093/cid/ciaa344 (2020).
48.
Liu, Y. et al. Viral dynamics in mild and severe cases of COVID-19. Lancet Infect. Dis. 20, 656–657 (2020).
CAS
PubMed
PubMed Central
Google Scholar
49.
Zheng, S. et al. Viral load dynamics and disease severity in patients infected with SARS-CoV-2 in Zhejiang province, China, January–March 2020: retrospective cohort study. BMJ 369, m1443 (2020).
PubMed
PubMed Central
Google Scholar
50.
Long, Q. X. et al. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nat. Med. 26, 1200–1204 (2020).
CAS
PubMed
Google Scholar
51.
Sekine, T. et al. Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19. Cell https://doi.org/10.1016/j.cell.2020.08.017 (2020).
52.
Mathew, D., Giles, J. R., Baxter, A. E., Oldridge, D. A. & Greenplate, A. R. Deep immune profiling of COVID-19 patients reveals distinct immunotypes with therapeutic implications. Science https://doi.org/10.1126/science.abc8511 (2020).
53.
Tetro, J. A. Is COVID-19 receiving ADE from other coronaviruses? Microbes Infect. 22, 72–73 (2020).
CAS
PubMed
PubMed Central
Google Scholar
54.
Khan, S. et al. Analysis of serologic cross-reactivity between common human coronaviruses and SARS-CoV-2 using coronavirus antigen microarray. Preprint at https://www.biorxiv.org/content/10.1101/2020.03.24.006544v1 (2020).
55.
Tseng, C. T. et al. Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus. PLoS ONE 7, e35421 (2012).
CAS
PubMed
PubMed Central
Google Scholar
56.
Deming, D. et al. Vaccine efficacy in senescent mice challenged with recombinant SARS-CoV bearing epidemic and zoonotic spike variants. PLoS Med. 3, e525 (2006).
PubMed
PubMed Central
Google Scholar
57.
Bolles, M. et al. A double-inactivated severe acute respiratory syndrome coronavirus vaccine provides incomplete protection in mice and induces increased eosinophilic proinflammatory pulmonary response upon challenge. J. Virol. 85, 12201–12215 (2011).
CAS
PubMed
PubMed Central
Google Scholar
58.
Yasui, F. et al. Prior immunization with severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein causes severe pneumonia in mice infected with SARS-CoV. J. Immunol. 181, 6337–6348 (2008).
CAS
PubMed
Google Scholar
59.
Agrawal, A. S. et al. Immunization with inactivated Middle East respiratory syndrome coronavirus vaccine leads to lung immunopathology on challenge with live virus. Hum. Vaccin. Immunother. 12, 2351–2356 (2016).
PubMed
PubMed Central
Google Scholar
60.
Weingartl, H. et al. Immunization with modified vaccinia virus Ankara-based recombinant vaccine against severe acute respiratory syndrome is associated with enhanced hepatitis in ferrets. J. Virol. 78, 12672–12676 (2004).
CAS
PubMed
PubMed Central
Google Scholar
61.
Czub, M., Weingartl, H., Czub, S., He, R. & Cao, J. Evaluation of modified vaccinia virus Ankara based recombinant SARS vaccine in ferrets. Vaccine 23, 2273–2279 (2005).
There’s no difference between the antibodies created by your body for the glycoprotein produced by the vaccine vs the glycoprotein produced by the virus. The reason we know that is because the exact same RNA producing the glycoprotein for the virus is used in the mRNA vaccine. So it’s literally, fundamentally, biologically impossible to tell the difference.
So the argument being made is we shouldn’t vaccinate against a disease that’s killing people because it’s possible that at some point in the future, having antibodies to this disease (which you’ll also have if you contract the actual disease) could complicate some future, unknown pathogenic infection?
Yeah, I’m going to laugh at that. It’s ridiculous. The vaccines cause headaches, body aches, and a fever. The disease being vaccinated against causes 5% of people to be hospitalized, 3% to end up in the ICU, and 0.65% to die.
I’ll take the headache.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.