Malevolent Designer News - More Evidence of Sheer Nastiness with SARS-CoV-2

New findings show that a Covid-19 infections can provoke an auto-immune response to give long-term health problems.

Many patients with COVID-19 produce immune responses against their body's own tissues or organs, finds study

The more we find out about the effects of the SARS-CoV-2 virus, currently responsible for the Covid-19 pandemic, the more it looks like Creationism's intelligent [sic] designer went to great lengths of sheer nastiness when it designed this virus - If you believe that tosh, that is!

In an open access paper published a few days ago in the journal Clinical & Experimental Immunology, a group of researchers led by Professor Alex Richter, of the University of Birmingham, show that some patients infected with the virus go on to produce antibodies against their own body tissues and so develop systemic symptoms not directly related to the virus itself:

The antibodies we identified are similar to those that cause a number of skin, muscle and heart autoimmune diseases.

We don’t yet know whether these autoantibodies are definitely causing symptoms in patients and whether this is a common phenomenon after lots of infections or just following COVID-19. These questions will be addressed in the next part of our study.

Professor Alex Richter, First author
Clinical Immunology Service,
Institute for Immunology and Immunotherapy,
University of Birmingham, Birmingham, UK

Abstract

COVID-19 has been associated with both transient and persistent systemic symptoms that do not appear to be a direct consequence of viral infection. The generation of autoantibodies has been proposed as a mechanism to explain these symptoms. To understand the prevalence of autoantibodies associated with SARS-CoV-2 infection, we investigated the frequency and specificity of clinically relevant autoantibodies in 84 individuals previously infected with SARS-CoV-2, suffering from COVID-19 of varying severity in both the acute and convalescent setting. These were compared with results from 32 individuals who were on ITU for non-COVID reasons. We demonstrate a higher frequency of autoantibodies in the COVID-19 ITU group compared with non-COVID-19 ITU disease control patients and that autoantibodies were also found in the serum 3-5 months post COVID-19 infection. Non-COVID patients displayed a diverse pattern of autoantibodies; in contrast, the COVID-19 groups had a more restricted panel of autoantibodies including skin, skeletal muscle and cardiac antibodies. Our results demonstrate that respiratory viral infection with SARS-CoV-2 is associated with the detection of a limited profile of tissue-specific autoantibodies, detectable using routine clinical immunology assays. Further studies are required to determine whether these autoantibodies are specific to SARS-CoV-2 or a phenomenon arising from severe viral infections and to determine the clinical significance of these autoantibodies.

Richter, A.G., Shields, A.M., Karim, A., Birch, D., Faustini, S.E., Steadman, L., Ward, K., Plant, T., Reynolds, G., Veenith, T., Cunningham, A.F., Drayson, M.T. and Wraith, D.C. (2021),
Establishing the prevalence of common tissue-specific autoantibodies following SARS CoV-2 infection.
Clin Exp Immunol. (Accepted Author Manuscript.) DOI: 10.1111/cei.13623

Copyright: © 2021 T|he authors. Published by John Wiley & Sons, Inc.
Open access Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

In this detailed study of a range of different tissues, we showed for the first time that COVID-19 infection is linked to production of selective autoantibodies. More work is needed to define whether these antibodies contribute to the long-term consequences of SARS-CoV-2 infection and hence could be targeted for treatment.

Professor David Wraith

The team examined three groups of patients with mild to severe symptoms of Covid-29 infection and a fourth, control, group of 32 patients treated in intensive care for non-Covid-19 related conditions. According to the Birmingham University news release, they found:

• Group one: 32 individuals sampled during their stay in intensive care for reasons other than COVID-19. 41% of individuals had autoantibodies. In this group, there were many different causes of their illness (over half was pneumonia) and autoantibodies were found against nearly all of the different autoantigens examined, indicating a more random distribution.
This is an interesting study that reveals new insights into a potential autoimmune component to the effects of COVID-19. Research like this has been made possible by the huge collaborative efforts made by those that are a part of the UK Coronavirus Immunology Consortium. This study is another important step towards delivering real improvements in prevention, diagnosis, and treatment of COVID-19 to patients.


Professor Paul Moss,
Principal Investigator of the UK Coronavirus Immunology Consortium
Professor of Haematology,
University of Birmingham
• Group two: 25 individuals who were sampled during their stay in intensive care following a diagnosis of severe COVID-19. 60% had autoantibodies. Of those who tested positive for autoantibodies, 41% had epidermal (skin) antibodies, while 17% had skeletal antibodies.
• Group three: 35 individuals who had been admitted to intensive care with COVID-19, survived and were sampled three to six months later during routine outpatient follow up. 77% of individuals had autoantibodies. Of those who tested positive for autoantibodies, 19% had epidermal (skin) antibodies, 19% had skeletal antibodies, 28% had cardiac muscle antibodies; and 31% had smooth muscle antibodies.
• Group four: 24 healthcare workers sampled one to three months after mild to moderate COVID-19 that did not require hospitalisation. 54% of individuals had autoantibodies. In those who tested positive for autoantibodies, it was against only four autoantigens: 25% had epidermal (skin) antibodies; 17% had smooth muscle antibodies; 8% had anti-neutrophil cytoplasm (ANCA) antibodies that target a type of human white blood cells; and 4% had gastric parietal antibodies which are associated with autoimmune gastritis and anaemia.

As the first author, >Professor Alex Richter, pointed out, more work is needed to ascertain whether this is a unique aspect of infection by the SARS-CoV-2 virus or of virus infections in general. Whichever it turns out to be, creationists are obliged by dogma to ascribe it to the deliberate intent of their supposedly omniscient, omnipotent designer god.

It probably goes without saying, but if this thing really had been designed by an intelligent entity with the powers to make chemistry and physics do something they couldn't do without it, and had not evolved by a natural process, like Creationist insist, then we could only regard that entity as malevolent in the extreme, responsible as it would be for indiscriminate suffering in the world, not just for the human species but for every other species subject to the predation of parasitic organism like this virus and the myriad of other parasites that live on and in them. That includes just about every living organism and even some of the predators have predators predating on them!

And why would an intelligent entity capable of such creation, intend it's creation to suffer so horribly, unless it enjoys watching it suffer and created it just for that pleasure?

Curiously, no creationist ever engages with that inescapable conclusion from their belief that intelligent [sic] design is a better explanation for the origins and diversity of life on earth than a purely utilitarian, unthinking and so amoral creative natural process which can be fully explained by science. and almost without exception, they will insist that this designer is an omnibenevolent god worthy of worship and adoration.

It's almost as though they're too embarrassed by the facts or too ashamed of their creator god to talk about what, if it were real and does what they believe, would be a deeply repugnant aspect of its personality.

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