Veren Inc T.VRN

RE:RE:RE:RE:RE:Ex-Pfizer VP Interview

[Dogsbreakfast4U]

We know that the COVID-19 vaccines that we are more or less forced to take have not yet been subjected proper scientific clinical evaluation. Previous clinical studies involving vaccines against respiratory syncytial viruses (such as the common cold) have all failed because of the antibody dependent enhancement (ADE) phenomenon. What is likely happening now, i.e. a resurgence of cases in the middle of summer that is attributed to the so called delta variant, is the fact that the vaccines are exacerbating COVID-19 through ADE. Don't expect our politicians, the media and the medical establishment to admmit this however. They are instead trying to blame the unvaccinated for the problem and suggest "solutions" such as vaccine passports and more vaccines.


Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies - PubMed (nih.gov)

"Antibody-based drugs and vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are being expedited through preclinical and clinical development. Data from the study of SARS-CoV and other respiratory viruses suggest that anti-SARS-CoV-2 antibodies could exacerbate COVID-19 through antibody-dependent enhancement (ADE). Previous respiratory syncytial virus and dengue virus vaccine studies revealed human clinical safety risks related to ADE, resulting in failed vaccine trials. "

A perspective on potential antibody-dependent enhancement of SARS-CoV-2 - PubMed
(nih.gov)

"Antibody-dependent enhancement (ADE) of disease is a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we review observations relevant to the risks of ADE of disease, and their potential implications for SARS-CoV-2 infection. At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies-regardless of what virus is the causative agent-it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward."