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All-TigerNet [11056]
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Oculus Spirit [98219]
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IFN dysregulation was noted in natural covid in 5/2020
Apr 30, 2022, 10:41 AM
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Actually before that. This is just another study/article pinning stuff covid already did, on the vaccines.
Actually, if you really want to know, IFN1 suppression is the result of NATURAL covid blocking the expression of the MHC-1 protein on the infected cell surface, which is the very first line of our immune system. When a cell is infected with a virus, it expresses the MHC-1 protein to alert T cells, and interferons, and ultimately antibodies to attack. No MHC-1 expression, NO IMMUNITY. Period. Vaccine, natural, whatever. Side note, IFN suppression (due to MCH suppression) is coded in the ORF8 and ORF1 covid genes, not in the spike.
Prior to omicron IFN suppression was actually how the virus evolved from Wuhan to Delta. By suppressing our innate immune response more and more, viral loads could go higher and higher, increasing both transmission and severity as you have more virus to clear. Immunity with covid is only how well you clear the virus. Period. There is nothing to prevent infection other than a respirator and PPE.
BTW, HIV does this same trick. Airborne AIDS. Kinda. Influenza uses this trick as well, which is why we're on year 1,000+ of the influenza pandemic. I've been saying this since day one. All this "herd immunity" BS is just that. Every article below describes what you just posted, the same process, actually some in much more detail, from BEFORE mRNA vaccines were administered. It's what covid does. We have no answer to it. We have no known biology to address it.
https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1.fullThe ORF8 Protein of SARS-CoV-2 Mediates Immune Evasion through Potently Downregulating MHC-I SARS-CoV-2 infection have caused global pandemic and claimed over 5,000,000 tolls[1][1]–[4][2]. Although the genetic sequences of their etiologic viruses are of high homology, the clinical and pathological characteristics of COVID-19 significantly differ from SARS[5][3],[6][4]. Especially, it seems that SARS-CoV-2 undergoes vast replication in vivo without being effectively monitored by anti-viral immunity[7][5]. Here, we show that the viral protein encoded from open reading frame 8 (ORF8) of SARS-CoV-2, which shares the least homology with SARS-CoV among all the viral proteins, can directly interact with MHC-I molecules and significantly down-regulates their surface expression on various cell types. In contrast, ORF8a and ORF8b of SARS-CoV do not exert this function. In the ORF8-expressing cells, MHC-I molecules are selectively target for lysosomal degradation by an autophagy-dependent mechanism. As a result, CTLs inefficiently eliminate the ORF8-expressing cells. Our results demonstrate that ORF8 protein disrupts antigen presentation and reduces the recognition and the elimination of virus-infected cells by CTLs[8][6]. Therefore, we suggest that the inhibition of ORF8 function could be a strategy to improve the special immune surveillance and accelerate the eradication of SARS-CoV-2 in vivo.
### Competing Interest Statement
The authors have declared no competing interest.
[1]: #ref-1 [2]: #ref-4 [3]: #ref-5 [4]: #ref-6 [5]: #ref-7 [6]: #ref-8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7249038/
https://advancesinrheumatology.biomedcentral.com/articles/10.1186/s42358-020-00151-7Severe COVID-19: what have we learned with the immunopathogenesis? - Advances in Rheumatology The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS-CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.
https://www.medrxiv.org/content/10.1101/2020.03.30.20047852v1.fullEpigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specially, we provide evidence in lupus to suggest hypomethylation and overexpression of ACE2 , which is located on the X chromosome and encodes a functional receptor for the SARS-CoV-2 spike glycoprotein. Oxidative stress induced by viral infections exacerbates the DNA methylation defect in lupus, possibly resulting in further ACE2 hypomethylation and enhanced viremia. In addition, demethylation of interferon-regulated genes, NF?B, and key cytokine genes in lupus patients might exacerbate the immune response to SARS-CoV-2 and increase the likelihood of cytokine storm. These arguments suggest that inherent epigenetic dysregulation in lupus might facilitate viral entry, viremia, and an excessive immune response to SARS-CoV-2. Further, maintaining disease remission in lupus patients is critical to prevent a vicious cycle of demethylation and increased oxidative stress, which will exacerbate susceptibility to SARS-CoV-2 infection during the current pandemic. Epigenetic control of the ACE2 gene might be a target for prevention and therapy in COVID-19.
### Competing Interest Statement
The authors have declared no competing interest.
### Funding Statement
This work was supported by the Lupus Research Alliance and the National Institute of Allergy and Infectious Diseases of the National Institutes of Health grants number U19AI110502 and R01AI097134 to Dr. Sawalha; and the National Natural Science Foundation of China (No. 81830097), the innovation project of Chinese academy of medical sciences (Research Unit, No. 2019-I2M-5-033) and an urgent grant of Hunan Province for fighting against coronavirus disease- 2019 epidemic (2020SK3005 ) to Dr. Lu.
### Author Declarations
All relevant ethical guidelines have been followed; any necessary IRB and/or ethics committee approvals have been obtained and details of the IRB/oversight body are included in the manuscript.
Yes
All necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived.
Yes
I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance).
Yes
I have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable.
Yes
All data are available within the manuscript
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110%er [7361]
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Re: IFN dysregulation was noted in natural covid in 5/2020
May 7, 2022, 9:17 PM
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Tiggity® thank you for spelling out why Covid-19 vaccines won't make much difference as far as prevention of health consequences from Covid-19 infection.
I had read CharlestonTom®'s post as emphasizing the dangers of the Covid-19 vaccine more so than the poor efficacy of the vaccines.
I'll admit: I hadn't yet finished reading the paper itself; only through the first 5 sections. Also, I am neither a molecular biologist nor in the field of infectious disease pathology nor in the field of immunity / immune responses. So it takes me a while to read, conduct brief background work to become marginally comfortable with the contents, and to make sense out of the article.
With that disclaimer, the Abstract, Conclusion, and first 5 sections of the PMS PubCentral article emphasize the dangers of the Covid-19 vaccines and the mechanisms by which both the Pfizer and Moderna mRNA vaccines work to render less effective the body's immune response to numerous abnormal proteins, including those which originate via external factors (i.e., viruses and bacteria) and internal factors (oncogenes).
(*) You clearly know much more than me about protein receptors and epitopes.
If you'd be so kind (because quite frankly I'd rather not spend the time reading the articles that you had linked unless they are significantly focused on immune suppression), would you let me know which (if any) of your links do pertain to immune response / immune suppression.
Thanks in advance for your considerations.
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Oculus Spirit [98219]
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I will point you to the "authors" of the OP "study"
May 9, 2022, 10:01 AM
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Since you tagged me...guess I will respond.
Below are the organizations employing the authors of the study.
https://www.truthforhealth.org/
http://nascoad.com/
https://www.immersionhealthpdx.com/
One of the "authors" of the "study".... (She doesn't work at MIT anymore): https://www.alternet.org/2014/02/meet-controversial-mit-scientist-who-claims-have-discovered-cause-gluten-sensitivty/
Here's the founder of Truth for Health: https://www.prweb.com/releases/healthcare_reform/dr_lee_vliet/prweb3033254.htmFerndale, WA (Vocus) October 15, 2009 -- Elizabeth Lee Vliet, M.D.], a women's health specialist and healthcare reform activist, believes that the healthcare
And this is their "Chief Medical Advisor". A big proponent of HCQ, Ivermectin, and herd immunity. Well, there is no herd immunity so it must now be the vaccine's fault. See how that works.
https://www.bitchute.com/hashtag/petermccullough/
Ok, I think that does it. What I posted was about the virus (every study was on covid immune escape). What the OP posted was about the vaccines. This is another "study", from shady and ultimately political sources, which cites the vaccine as causing something the virus already was shown to cause. The only thing is real scientists know exactly how the virus causes this, and it's not how they say the vaccines cause it, because they're making crap up.
Here's a more recent study from a legitimate scientist which dives deeper into the root causes of IFN dysregulation in covid. They have been studying ORF8 in SARS for 20 years now. This is how the VIRUS does what the OP "study" says the vaccines do. Only one problem, the part of SARS/covid that does what they say the vaccines do, isn't IN THE VACCINE. And neither is aluminum, as they claim.
https://www.biorxiv.org/content/10.1101/2022.05.04.490614v1.fullSARS-CoV-2 variants do not evolve to promote further escape from MHC-I recognition SARS-CoV-2 variants of concern (VOCs) possess mutations that confer resistance to neutralizing antibodies within the Spike protein and are associated with breakthrough infection and reinfection. By contrast, less is known about the escape from CD8+ T cell-mediated immunity by VOC. Here, we demonstrated that VOCs retain similar MHC-I downregulation capacity compared to the ancestral virus. However, VOCs exhibit a greater ability to suppress type I IFN than the ancestral virus. Although VOCs possess unique mutations within the ORF8 gene, which suppresses MHC-I expression, none of these mutations enhanced the ability of ORF8 to suppress MHC-I expression. Notably, MHC-I upregulation was strongly inhibited after the ancestral SARS-CoV-2 infection in vivo . Collectively, our data suggest that the ancestral SARS-CoV-2 already possesses an intrinsically potent MHC-I evasion capacity, and that further adaptation by the variants was not observed.
### Competing Interest Statement
The authors have declared no competing interest.
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