Malevolent Designer News - Why Creationism's Favourite Sadist Gave Some People Protection From COVID-19 - If You Believe That Superstitious Nonsense

Gene Mutation May Explain Why Some Don’t Get Sick from COVID-19 | UC San Francisco

The thing about being a follower of the intelligent [sic] design cult is that you have to believe whatever the 'design' is, that was precisely what your putative intelligent [sic] designer intended to design because, although you should never say so, your designer god is one and the same god that fundamentalist Christians and Moslems believe in, i.e., it is omniscient, omnipotent and inerrant so is incapable of making a mistake.

So, what the cult now has to explain is why their favorite sadist gave some people a gene which protects then against symptomatic COVID-19, but not everyone, if, as the normal excuse for these parasites is valid - i.e., it wasn't God, it was something called 'sin' which creates viruses (and apparently the supreme, omniscient ruler of the universe is powerless to stop it or uncaring enough to not bother, or maybe even unaware of it).

In which case, why create the protective gene?

Of course, a ready explanation which fits in with the intelligent [sic] design superstition is that it wanted a few people to catch COVID-19 but not know they has=d it, so they could spread it around - the infectious but asymptomatic cases that are believed to have been responsible for a great deal of the pandemic's success.

So, creationists need to explain whether their intelligent [sic] designer deliberately created these super-spreaders to infect as many people as possible and if not, what did it create them for and how come it didn't know what the outcome would be? The discovery of this gene was made by a group led by researchers from the University of California San Francisco, who have just published their findings, open access, in Nature. As the UC San Francisco news release explains:

People who contract COVID-19 but never develop symptoms – the so-called super dodgers – may have a genetic ace up their sleeve. They’re more than twice as likely as those who become symptomatic to carry a specific gene variation that helps them obliterate the virus, according to a new study led by UC San Francisco researchers.

The paper published July 19, 2023 in Nature, offers the first evidence that there is a genetic basis for asymptomatic SARS-CoV-2. The research helps to solve the mystery of why some people can be infected without ever getting sick from COVID-19.

If you have an army that’s able to recognize the enemy early, that’s a huge advantage. It’s like having soldiers that are prepared for battle and already know what to look for, and that these are the bad guys.>/p>

Professor Jill Hollenbach, PhD, MPH., Study co-supervisor
Weill Institute for Neurosciences
Department of Neurology,
University of California, San Francisco, CA, USA

The secret lies with the human leukocyte antigen (HLA), or protein markers that signal the immune system. A mutation in one of the genes coding for HLA appears to help virus-killing T cells identify SARS-CoV-2 and launch a lighting attack. The T cells of some people who carry this variant can identify the novel coronavirus, even if they have never encountered it before, thanks to its resemblance to the seasonal cold viruses they already know. The discovery points to new targets for drugs and vaccines.

The mutation – HLA-B*15:01 – is quite common, carried by about 10% of the study’s population. It doesn’t prevent the virus from infecting cells but, rather, prevents people from developing any symptoms. That includes a runny nose or even a barely noticeable sore throat.

UCSF researchers found that 20% of people in the study who remained asymptomatic after infection carried at least one copy of the HLA-B*15:01 variant, compared to 9% of those who reported symptoms. Those who carried two copies of the variant were far more likely – more than eight times – to avoid feeling sick.

Leveraging a national marrow donor database

Researchers suspected early on that HLA was involved, and fortunately a national registry existed that contained the data they were looking for. The National Marrow Donor Program/Be The Match, the largest registry of HLA-typed volunteer donors in the U.S., matches donors with people who need bone marrow transplants.

But they still needed to know how the donors fared against COVID-19. So, they turned to a mobile app developed at UCSF, called the COVID-19 Citizen Science Study. They recruited nearly 30,000 people who were also in the bone marrow registry and tracked through the first year of the pandemic. At that time, vaccines were not yet available, and many people were undergoing routine COVID testing for work or whenever they were potentially exposed.

We did not set out to study genetics, but we were thrilled to see this result come from our multidisciplinary collaboration with Dr. Hollenbach and the National Marrow Donor Program.

Professor Mark J. Pletcher, MD, MPH, co-author Department of Epidemiology and Biostatistics
University of California, San Francisco, CA, USA

The primary study group was limited to those who self-identified as white because the final set of study respondents did not have enough people in it from other ethnic and racial groups to analyze.

Researchers identified 1,428 unvaccinated donors who tested positive between February 2020 and the end of April 2021, before the vaccines were widely available and when it still took many days to get back test results.

Of these, 136 individuals remained asymptomatic for at least two weeks before and after testing positive. Only one of the HLA variants – HLA-B*15:01 – had a strong association with asymptomatic COVID-19 infection, and this was reproduced in two independent cohorts. Risk factors for severe COVID-19, like being older, overweight and having chronic diseases like diabetes did not appear to play a role in who remained asymptomatic.

We are proud to partner on research that has the potential to leverage a long-term public investment in building the national registry to help cure diseases and improve our ability to avoid future pandemics.

Martin Maiers Center for International Blood and Marrow Transplant Research (CIBMTR)
National Marrow Donor Program/Be The Match, Minneapolis, MN, USA

To figure out how HLA-B*15:01 managed to quash the virus, Hollenbach’s team collaborated with researchers from La Trobe University in Australia. They homed in on the concept of T-cell memory, which is how the immune system remembers previous infections.

The researchers looked at T cells from people who carried HLA-B*15:01 but had never been exposed to the SARS-CoV-2 virus, and found these cells still responded to a part of the novel coronavirus called the NQK-Q8 peptide. They concluded that exposure to some seasonal coronaviruses, which have a very similar peptide, called NQK-A8, enabled T cells in these individuals to quickly recognize SARS-CoV-2 and mount a faster, more effective immune response.

By studying their immune response, this might enable us to identify new ways of promoting immune protection against SARS-CoV-2 that could be used in future development of vaccines or drugs.

Professor Stephanie Gras, project co-supervisor
Department of Biochemistry and Chemistry
La Trobe Institute for Molecular Science,
La Trobe University, Bundoora, Victoria, Australia.

Co-authors: Additional authors at UCSF include Mark J. Pletcher, MD, MPH; Jeffrey E. Olgin, MD; Gregory M. Marcus, MD, MAS; Sulggi Lee, MD, PhD; Jeffrey N. Martin, MD, PhD; J. Daniel Kelly, MD, PhD, MPH; Sarah A. Goldberg, MAS; Scott Lu, MD; Michelle Davidson, MD, MPH; Steven G. Deeks, MD; Timothy J. Henrich, MD; Michael J. Peluso, MD; Kara Lynch, PhD; Danillo G. Augusto, PhD; Joseph J. Sabatino, Jr., MD, PhD; Tasneem Yusufali, MS; Noah D. Peyser, PhD; Gurjot Gill; Fiona Beltran; Cassandra Yun; Rebecca Hoh; Xochitl Butcher; Kerry Kizer; Karoline Guthrie; Victoria Murray; Vivian Pae; Sannidhi Sarvadhavabhatla.

Technical detail is given in the team's paper in Nature

Abstract

Studies have demonstrated that at least 20% of individuals infected with SARS-CoV-2 remain asymptomatic^1,2,3,4. Although most global efforts have focused on severe illness in COVID-19, examining asymptomatic infection provides a unique opportunity to consider early immunological features that promote rapid viral clearance. Here, postulating that variation in the human leukocyte antigen (HLA) loci may underly processes mediating asymptomatic infection, we enrolled 29,947 individuals, for whom high-resolution HLA genotyping data were available, in a smartphone-based study designed to track COVID-19 symptoms and outcomes. Our discovery cohort (n = 1,428) comprised unvaccinated individuals who reported a positive test result for SARS-CoV-2. We tested for association of five HLA loci with disease course and identified a strong association between HLA-B*15:01 and asymptomatic infection, observed in two independent cohorts. Suggesting that this genetic association is due to pre-existing T cell immunity, we show that T cells from pre-pandemic samples from individuals carrying HLA-B*15:01 were reactive to the immunodominant SARS-CoV-2 S-derived peptide NQKLIANQF. The majority of the reactive T cells displayed a memory phenotype, were highly polyfunctional and were cross-reactive to a peptide derived from seasonal coronaviruses. The crystal structure of HLA-B*15:01–peptide complexes demonstrates that the peptides NQKLIANQF and NQKLIANAF (from OC43-CoV and HKU1-CoV) share a similar ability to be stabilized and presented by HLA-B*15:01. Finally, we show that the structural similarity of the peptides underpins T cell cross-reactivity of high-affinity public T cell receptors, providing the molecular basis for HLA-B*15:01-mediated pre-existing immunity.

Augusto, D.G., Murdolo, L.D., Chatzileontiadou, D.S.M. et al.
A common allele of HLA is associated with asymptomatic SARS-CoV-2 infection.
Nature (2023). https://doi.org/10.1038/s41586-023-06331-x

Copyright: © 2023 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Reading this piece of research, there is clearly a triple whammy for creationists.

1. Not only do they need to explain why their putative designer gave 20% of people a gene which makes them immune to the effects of the SARS-CoV-2 virus or whether this was so they could catch COVID-19 asymptomatically, and pass it on to others without even realising it, since that is the result of the mutant gene.
2. If the intention was to protect some people, why didn't it give everyone the same mutant gene?
3. Why, if what Michael J. Behe would have them believe, all mutations are deleterious and therefore 'devolutionary' [sic], a mutation that give immunity to the effects of SARS-CoV-2 infection should be regarded as deleterious?

As always, the comments section below is open to any creationists who wish to make a reasoned attempt to answer these questions, but experience has taught me not to expect anything other than abuse, diversions, deflections and the babble of people with the mind of a slow nine year-old who won't have read beyond the title.

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Thank you for sharing!

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