/* */ Rosa Rubicondior: Malevolent Designer News - Three More Examples of Malevolent Design

Tuesday, 29 June 2021

Malevolent Designer News - Three More Examples of Malevolent Design

The virus that causes COVID-19 normally gets inside cells by attaching to a protein called ACE2. Researchers at Washington University School of Medicine in St. Louis have found that a single mutation confers the ability to enter cells through another route, which may threaten the effectiveness of COVID-19 vaccines and therapeutics designed to block the standard route of entry.
Image: Getty images
Virus that causes COVID-19 can find alternate route to infect cells – Washington University School of Medicine in St. Louis

Creationist mode:


Creationists who believe only their special magic friend designs living organisms because nothing can evolve naturally and the only intelligent [sic] designer clever enough is their special magic invisible friend, must be thrilled at the recent news of its brilliance, especially with its design of the SARS-CoV-2 virus that is currently killing people by the tens of thousands, ruining economies and making hundreds of millions more sick.

But, it's not just the SARS-Cov-2 virus which is the result of its special efforts to make us sick: it has been hard at work with its attempt to get round human medical science's success with anti-biotics with its resistant strains such as MRSA, and has come up with a particularly nasty form of Streptococcus pneumoniae, which it has designed to take advantage of an infection with any one of the many strains of influenza virus, to do even more damage to our lungs. First, the news that the SARS-CoV-2 virus may have found an alternative way to enter our cells to begin making more viruses and destroying our cells in the process. And this has special relevance to medical science's attempts to control the pandemic with vaccines, because most of these vaccines are designed to reduce the viruses ability to enter our cells using its 'spike' proteins.

These 'spike' proteins bind to proteins on the cell surface known as ACE2 and then force an opening through which it injects its RNA into the cell. The vaccines target these 'spike' proteins so rendering them non-functional. However, researches at Washington University School of Medicine, St Louis, MO, USA, have discovered a simple, single amino acid mutation at position 484 that means the virus may be able to bypass the ACE2 binding sites. Position 484 seems to be particularly prone to mutation so there is plenty of opportunity for experimentation, given the high incidence of COVID-19 in the world population which means countless trillions of replications every day.

However, the researchers found no evidence that the virus has yet hit upon this way around the growing herd immunity due to vaccinations and natural immunity from infections.

Given the determination of Creationism's intelligent [sic] designer to do as much damage as possible with this virus, it should not be beyond its wit to come up with just the right mutation er... redesign soon.

As a society we are witnessing first-hand the powerful impact that vaccination can have on curbing the spread of infection. However, on the backdrop of the COVID-19 epidemic we must not lose sight of the fact that we are also waging war on a more subtle epidemic of antimicrobial resistant infection, which is potentially equally deadly.

In this study we have identified a mechanism by which a protein made by the bacterium – known as Staphylococcal Protein A (SpA) – attacks and rapidly kills white blood cells. This protein has been widely studied for its immune evasion capacity and has a well-documented role in rendering antibodies raised against the bacterium non-functional.

Here we uncover a previously undocumented strategy by which SpA forms immune complexes through its interaction with host antibodies, that in turn exert toxic effects on multiple white blood cell types. This discovery highlights how important it will be for effective vaccines to be capable of disarming the effects of protein A.

Rachel McLoughlin, Co-first author
Professor in Immunology
School of Biochemistry and Immunology and the Biomedical Sciences Institute
Trinity College, Dublin, Ireland.
The second piece of news is that researchers from Trinity College, Dublin, Ireland, have discovered that the intelligent [sic] designer appears to have made its multi-resistant Streptococcus aureus (MRSA) bacterium even more robust by giving it a special trick - it produces a toxin which attacks our white blood cells which prevents them doing their job - fighting infections. So, not content with finding a way around the success of medical science with antibiotics, the intelligent [sic] designer is now stripping us of our natural defences - the defences it allegedly designed to help us fight off infections by, for instance, S. aureus. And, with a trick it has pulled off many times before - by making our own immune response work against us. That is, the immune response it allegedly created to protect us...

The Trinity College News release explains:
New research has uncovered a novel trick employed by the bacterium Staphylococcus aureus to thwart the immune response, raising hopes that a vaccine that prevents deadly MRSA infections is a little closer on the horizon.

Immunologists from Trinity, working with scientists at GSK – one of the world’s largest vaccine manufacturers – discovered the new trick of the troublesome Staphylococcus aureus, which is the causative agent of the infamous “superbug” MRSA.

They found that the bacterium interferes with the host immune response by causing toxic effects on white blood cells, which prevents them from engaging in their infection-fighting jobs...

MRSA – a global killer

An estimated 700,000 deaths occur annually due to infections against which antibiotics are no longer effective. If this is allowed to continue, modern medicine as we know it will cease to exist; a common childhood infection or routine surgical procedure could become fatal, with the threat of AMR infection likened to that of climate change in some circles.

Immediate and significant action is required to turn the tide of AMR and the development of novel vaccines to prevent these types of infection in the first place, are an attractive and potentially very effective option.
The bad news for devoted followers of this malevolence designer is that the researchers believe this makes MRSA vulnerable to a vaccine which targets this protein, using the same technology as was used to develop the anti-COVID-19 vaccines.

Proposed mechanism of action for SpA-induced toxicity. (A) In the presence of murine IgG, SpA forms limited immune complexes; these smaller complexes cross-link the BCR on murine VH3+ B cells, leading to clonal expansion and eventual collapse via apoptosis of these cells. (B) In contrast, in the presence of full-length human IgG, SpA forms large immune complexes; these complexes then interact with VH3+ B cells, leading to rapid necrosis of these cells. (C) The presence of murine anti-SpA sera prevents the formation of large immune complexes and thus acts to limit SpA-mediated toxicity.
Their research was published open access recently in the ASM journal mBio:
ABSTRACT

One of the defining features of Staphylococcus aureus is its ability to evade and impair the human immune response through expression of staphylococcal protein A (SpA). Herein, we describe a previously unknown mechanism by which SpA can form toxic immune complexes when in the presence of human serum, which leads to the loss of human leukocytes. Further, we demonstrate that these toxic complexes are formed specifically through SpA’s interaction with intact human IgG and that, in the presence of purified IgG Fab and Fc fragments, SpA shows no such toxicity. The mechanism of action of this toxicity appears to be one mediated by necrosis and not by apoptosis, as previously hypothesized, with up to 90% of human B cells rapidly becoming necrotic following stimulation with SpA-IgG complexes. This phenomenon depends on the immunoglobulin binding capacity of SpA, as a nonbinding mutant of SpA did not induce necrosis. Importantly, immune sera raised against SpA had the capacity to significantly reduce the observed toxicity. An unprecedented toxic effect of SpA-IgG complexes on monocytes was also observed, suggesting the existence of a novel mechanism independent from the interaction of SpA with the B cell receptor. Together, these data implicate SpA in inducing indiscriminate leukocyte toxicity upon formation of complexes with IgG and highlight the requirement for vaccination strategies to inhibit this mechanism.

IMPORTANCE Staphylococcus aureus is one of the largest health care threats faced by humankind, with a reported mortality rate within the United States greater than that of HIV/AIDS, tuberculosis, and viral hepatitis combined. One of the defining features of S. aureus as a human pathogen is its ability to evade and impair the human immune response through expression of staphylococcal protein A. Herein, we show that SpA induces necrosis in various immune cells by complexing with human immunoglobulins. Vaccination of mice with a nontoxigenic SpA mutant induced sera capable of inhibiting this mechanism. These observations shed new light on the toxic mechanisms of this key staphylococcal virulence factor and on protective modalities of SpA-based vaccination.

This novel virulence trait, which increases severity of S. pneumoniae superinfection, involves pneumococcal surface protein A, now identified as an adhesin.
The third example of the intelligent [sic] designer's brilliant malevolence is the discovery by a team from the University of Alabama at Birmingham (UAB), USA. They have discovered that the bacterium Streptococcus pneumoniae has been designed with a surface protein that enables it to stick to the surface of dead and dying lung cells and so take advantage of the damage done by the influenza viruses, to finish off the job they started and kill the victim, or at least make them very sick.

The UAB News release explains:
The research, published in the journal Cell Reports, was led by Carlos Orihuela, Ph.D., and David Briles, Ph.D., professor and professor emeritus in the University of Alabama at Birmingham Department of Microbiology. Orihuela and Briles say their findings provide further explanation for how an infection by influenza A flu virus — followed by S. pneumoniae superinfection — causes severe pneumonia and a high death rate. The mechanism also points to possible improvements for disease treatment and vaccination.

A historical example of the deadly synergy of flu infection followed by S. pneumoniae superinfection is found in banked lung samples from the 1918 Spanish influenza pandemic that killed 40 million to 50 million people — the vast majority of these samples showed co-infection or secondary infection with S. pneumonia.
The teams research was published open access in Cell Reports recently:
Highlights
  • Pneumococcal surface protein A (PspA) functions as an adhesin
  • PspA binds host GAPDH, present on the surface of dying host cells
  • PspA influences localization of Streptococcus pneumoniae in the airway
  • PspA effects are exacerbated by damage caused by influenza A virus infection

Summary

Streptococcus pneumoniae (Spn) alone and during co-infection with influenza A virus (IAV) can result in severe pneumonia with mortality. Pneumococcal surface protein A (PspA) is an established virulence factor required for Spn evasion of lactoferricin and C-reactive protein-activated complement-mediated killing. Herein, we show that PspA functions as an adhesin to dying host cells. We demonstrate that PspA binds to host-derived glyceraldehyde-3-phosphate dehydrogenase (GAPDH) bound to outward-flipped phosphatidylserine residues on dying host cells. PspA-mediated adhesion was to apoptotic, pyroptotic, and necroptotic cells, but not healthy lung cells. Using isogenic mutants of Spn, we show that PspA-GAPDH-mediated binding to lung cells increases pneumococcal localization in the lower airway, and this is enhanced as a result of pneumolysin exposure or co-infection with IAV. PspA-mediated binding to GAPDH requires amino acids 230–281 in its α-helical domain with intratracheal inoculation of this PspA fragment alongside the bacteria reducing disease severity in an IAV/Spn pneumonia model.

There then we have three more examples of the lengths Creationism's putative intelligent [sic] designer is going to in its determination to make as many humans sick and die as possible. Not content with developing antibiotic resistance it has given MRSA an additional trick to use against us; not content with designing the SARS-CoV-2 virus to kill people in the tens of thousands, it is developing a work-around for the vaccines medical science has developed to fight it with, and not content with the harm the influenza virus does it has designed S. pneumonae to come in and finish the job.

Creationist mode:


It takes a special sort of malevolence to so obsessively keep designing new and ever-more exotic ways to make people sick and it takes a special sort of malevolence to regard an entity capable of doing so as something worthy of worhip and adoration. And yet, despite their professed adoration of this sadistic monster, Creationists insist it gets the credit for all this evil and suffering rather than give the credit to a perfectly well understood natural process.

I often wonder what, in the remote possibility that this magic designer is real, it would think of Creationists who insist it is the only explanation for parasites and the suffering they cause.

Thank you for sharing!









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