Malevolent Designer News - How Creationism's Divine Malevolence Designed The CCHF Virus To Kill Us

CCHF Virus

New study shows how the Crimean-Congo haemorrhagic fever virus enters our cells | Karolinska Institutet

Creationists traditionally have a schizophrenic attitude towards viruses. On the one hand, they blame them all on the biblical myth of 'The Fall', so betraying the fact that creationism is not a science like they claim it to be, but fundamentalist Christianity.

On the other hand, as we saw in the early days of the COVID-19 pandemic, they declared it to be their god's divine punishment for whatever their hobbyhorse was at the time - abortion, same-sex marriage, New Yorkers electing a Democrat, etc., etc., as though their god would inflict a punishment on the whole world for the actions of politicians in America or the way Americans in New York voted. Creationism is nothing if not parochial and ignorant!

Covidiot News - Just Because You Haven't Had COVID-19 Yet, Doesn't Mean You Won't!

The SARS-CoV-2 virus needs to attach to receptors to gain access to our cells.

Kateryna Kon/Shutterstock

Haven't had COVID yet? It could be more than just luck

There are some scary questions for creationists at the end of this article. They follow on naturally from what's being discussed, so creationists should probably avoid reading too far, unless they have a responsible adult with them.

This article from The Conversation is from May 2022, when we were into the second year of the COVID-19 pandemic and most vulnerable people had had the two-step vaccinations and many would have had the spring booster. At that point neither me nor my partner had had COVID-19, which we put down to rigorously following the recommendations regarding mask-wearing, social distancing, hand washing, etc. and had tried to reduce our vulnerability to the sever forms of it by losing about 3 stone in weight and, in my case, getting my blood pressure under control with medication. We also tried to ensure our immune systems were healthy by taking vitamin D3, vitamin C, zinc and iron supplements.

In the early days of the pandemic, even before the official restrictions on social contact, we had observed the basic rules of hygiene and everyone who came into the house used hand-cleanser at the front door. I had even managed to obtain a supply of face-masks and plastic gloves online, which we wore at all times outside the house. Every package that was delivered to the house was left for several hours before we touched it, and all our weekly shopping was delivered or bought with click and collect. Delivered bags were left for four hours before unpacking. And we took weekly tests just in case we had it asymptomatically. All that might seem a little over the top now, but we were vindicated as events were to prove.

We put the fact that we hadn't caught it by mid-2022 down to our preventative measures, not to luck or genetics - a view that was vindicated last year when we both came back from a two-week vacation in France with a mild form of COVID-19, despite having had all the boosters on offer. We probably picked it up in a crowded airport or on the plane, where all the social distancing measures had been forgotten and even face masks were no longer worn. We both felt like we had a mild case of flu for a couple of days and after a week we were testing negative. Had we contracted it in Spring 2020, the outcome would probably have been very different as we had no immunity, and both had three of the risk-factors - overweight, high BP and over 70. In addition, my partner had had a mastectomy and was receiving treatment for breast cancer.

One reason you can't ever be sure that you won't catch COVID-19 is because the virus keeps mutating to produce new variants so, even if you were fortunate enough to have natural or acquired immunity to the variants so far, it is quite possible that the next or subsequent variants will have evolved a way round it. The following chart from the UK NHS, shows the rise and fall of the main variants over the course of the pandemic:

Source: NHS UKHSA Date Dashboard

But still, a few people managed to stay free from the virus. In the following article, reprinted from The Conversation under a Creative Commons license, Lindsay Broadbent, Research Fellow, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, explains why. Her article has been reformatted for stylistic consistency:

Malevolent Designer News - How Creationism's Divine Malevolence Is Adapting The Avian Flu Virus to Kill Marine Mammals

Dead elephant seals line a beach in Argentina in fall 2023.

Photo: Ralph Vanstreels/UC Davis

Avian Influenza Virus Is Adapting to Spread to Marine Mammals | UC Davis

Elephant seals lie dead on a beach in Argentina following an outbreak of avian influenza in the region.

Photo: Maxi Jonas.

As an example of creationist double-think and intellectual bankruptcy, their attitude toward parasites like viruses is a classic:

• "Only God is capable of designing organisms, so "Look at the trees!" and "What about irreducible complexity?"
• "Something else created parasites like bacteria, worms and viruses, because God wouldn't do something like that!"

Simultaneously committing blasphemy and refuting their own argument from teleology!

I wonder then how that rarest of animals, the intellectually honest creationist copes with the news that the creator of the avian flu virus, H5N1, is in the process of adapting it to kill marine mammals such as elephant seals, just as it adapted the SARS-CoV-2 virus from a bat virus to one that could kill humans and cause economic collapse.

Evidence that it is doing so, if you believe viruses are created and don't evolve naturally, which dogma forbids a creationist from believing, comes in the form of a study by scientists from University of California, Davis, and the National Institute of Agricultural Technology (INTA) in Argentina. The study, the first genomic characterization of H5N1 in marine wildlife on the Atlantic shore of South America, is published in the journal Emerging Infectious Diseases and is described in a UC Davis news release:

Covidiot News - How the mRNA Vaccines Give Long-Term Protection Against COVID-19

Long-Term Data Reveals SARS-CoV-2 Infection and Vaccine-Induced Antibody Responses Are Long-Lasting | Mount Sinai - New York

If you listen to antivaxxer covidiots you would believe:

• COVID-19 is no worse than the common cold.
• The SARS-CoV-2 virus which causes COVID-19, is a deadly organism developed by the Chinese for biological warfare.
• COVID-19 was a hoax (which even normally hostile nations had signed up to, apparently).
• God sent the virus to punish America for legalising same-sex marriage (and the rest of the world was collateral damage)
• The vaccines developed against it don't work (regardless of what the clinic trials showed).
• The vaccines contain microchips and special genes to make you become gay and/or subject to satellite control.
• The vaccines contain deadly viruses that can be activated via the 5G phone network.
• Millions of people have died or will die soon because they've been vaccinated.
• [Fill in your own crackpot theory because someone will already have claimed it to be true].

The truth is, however, that millions of people died of COVID-19 in the first year of the pandemic, before a vaccine was generally available and this death rate fell to low levels following the roll out of the first vaccines and subsequent boosters to allow for new variants. Although the virus is still very much with us, people have been able to resume normal activities and the economic and health impact of the virus is now no more than that of seasonal flu, but there were concerns that antibody levels produced in response to the mRNA vaccines were short-lived, giving only temporary protection.

Now a large-scale analysis conducted by leading microbiologists at the Icahn School of Medicine at Mount Sinai has shown that antibody responses induced by COVId-19 vaccines are long-lasting. The results of this analysis are published, open access, in the Cell Press journal, Immunity, and are discussed in a Mount Sinai press release:

The emergence of SARS-CoV-2, the virus that causes COVID-19, in late 2019 sparked the global pandemic that is now in its fifth year. Vaccines that were developed at record speed have saved millions of lives. However, the emergence of SARS-CoV-2 variants and waning immunity have decreased the effectiveness of the vaccines against symptomatic disease. The common perception now is that mRNA-based vaccine-induced immunity wanes quickly. However, this assumption is largely based on data from short-term studies that include a very limited number of data points following peak responses.

The Mount Sinai research team’s analysis of more than 8,000 samples collected over a three-year period in New York City examined how antibody responses to the virus’s spike protein changed after infections, during the primary immunization series, during monovalent and bivalent booster vaccination, and during breakthrough infections.

They found that upon primary immunization, participants with pre-existing immunity (those who had previously been infected with the virus) mounted higher antibody responses faster and achieved higher steady-state antibody titers than individuals who had not been previously infected. The waning of antibody response was characterized by two phases: an initial rapid decay from the strong peak after vaccination, followed by a stabilization phase with very slow decay, suggesting that antibody levels were very long-lasting. Booster vaccination equalized the differences in antibody concentration between participants with and without pre-existing immunity. Breakthrough infections increased antibodies to similar levels as an additional vaccine dose in individuals who had not previously been infected.

This investigation represents one of the most extensive and in-depth assessments of the longevity of SARS-CoV-2 immune responses to date. Its major conclusion is that changes in the virus that allow it to evade immunity, rather than waning immunity, are the major reason for breakthrough infections.

Ours is one of the longest-running COVID-19 studies out there. Following the same group of people monthly over time is rare and powerful because you can compare immune responses on an individual level. SARS-CoV-2 continues to evolve, so this research is important to provide an understanding about the impact of new variants and new vaccine doses on a healthy immune system, and to guide all of us to make the best choices to maintain protection against the virus that continues to circulate in our communities.

Professor Viviana Simon, MD, PhD, lead author
Professor of Microbiology, Medicine and Pathology, Molecular and Cell-Based Medicine
Department of Microbiology
Icahn School of Medicine at Mount Sinai, New York, NY, USA.

This in-depth analysis was made possible through the Protection Associated with Rapid Immunity to SARS-CoV-2 (PARIS) study, an observational, longitudinal cohort of health care workers of the Mount Sinai Health System that was initiated in April 2020. At that time, the densely populated New York metropolitan area was hit with an exponential increase in severe SARS-CoV-2 infections, and essential workers in the health care system were at high risk for infection. In response to the crisis, a team of leading virologists, physician-scientists, and pathologists at Mount Sinai established a specific and sensitive SARS-CoV-2 binding enzyme-linked immunosorbent assay to accurately measure the SARS-CoV-2 antibody titers. This test was used to measure immune responses in the PARIS cohort in order to determine how quickly the antibody defenses were mounted and much these changed over the months and years of follow up.

In addition to showing the impact on a person’s individual antibody response to vaccines based on the type of vaccine received and whether or not they were infected before receiving the first dose, the PARIS study made possible the development of a mathematical model that can be used to predict and characterize antibody responses of both individual people and populations.

People have pandemic fatigue and vaccine uptake has slowed, especially after the vaccines started to be charged to insurance*. We were pleasantly surprised to see that the booster doses promoted a large antibody response regardless of a person’s personal infection history, so we are hopeful that our study findings will encourage people to get their vaccine boosters when eligible and to stay engaged in research. Our work also showcases the impact of viral evolution over time and why it’s critical to keep studies like this going, despite the pandemic fatigue.

Komal Srivastava, MS, Co-first author
Director of Strategy and Operation
Mount Sinai Center for Vaccine Research and Pandemic Preparedness.

According to the research team, the PARIS model has broad applications for studying the kinetics of antibodies produced to different COVID-19 vaccines in diverse populations. They stress much more work remains to analyze side effects, applications of the antibody model and continued research about new vaccines and viral variants.

This study adds an essential piece of data to understand the intricate immune response elicited by SARS-CoV-2 infection and COVID-19 vaccination. In light of the emerging viral variants, which predominantly induce a cross-reactive antibody response against the spike protein, it will be exciting to characterize in depth the role of these antibodies - in particular the non-neutralizing ones - in protection against the most recent circulating viral variants. Likewise, monitoring the induction of variant-specific antibodies after multiple exposures by breakthrough infections and by administration of updated COVID-19 vaccines, such as the XBB.1.5 monovalent booster, will be key to understand the evolution of the antibody response over time.

Assistant Professor Dr Juan Manuel Carreno Quiroz, PhD, Co-first author.
Department of Microbiology
Icahn School of Medicine at Mount Sinai, New York, NY, USA.

*Note: in the UK, vaccines are provided free by the NHS. Other non-US countries will have their own health-care systems which may or may not include charges for the vaccines.

More technical detail and the background to the research is given in the team's paper in Immunology:

Graphical abstract

Highlights

• COVID-19-vaccine-induced immunity wanes but stabilizes at an individual setpoint
• Pre-existing immunity results in rapid antibody responses upon vaccination
• Boosters equalize antibody titers between individuals with and without hybrid immunity
• Antibody kinetics show two phases: an initial rapid decay followed by a steady state

Summary

It is thought that mRNA-based vaccine-induced immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) wanes quickly, based mostly on short-term studies. Here, we analyzed the kinetics and durability of the humoral responses to SARS-CoV-2 infection and vaccination using >8,000 longitudinal samples collected over a 3-year period in New York City. Upon primary immunization, participants with pre-existing immunity mounted higher antibody responses faster and achieved higher steady-state antibody titers than naive individuals. Antibody kinetics were characterized by two phases: an initial rapid decay, followed by a stabilization phase with very slow decay. Booster vaccination equalized the differences in antibody concentration between participants with and without hybrid immunity, but the peak antibody titers decreased with each successive antigen exposure. Breakthrough infections increased antibodies to similar titers as an additional vaccine dose in naive individuals. Our study provides strong evidence that SARS-CoV-2 antibody responses are long lasting, with initial waning followed by stabilization.

Introduction

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in late 2019 sparked the global coronavirus disease 2019 (COVID-19) pandemic that is now in its 4th year. Vaccines to mitigate the impact of the pandemic were developed at record speed and have saved millions of lives. However, the emergence of SARS-CoV-2 variants¹ and waning immunity² have decreased the effectiveness of the vaccines against symptomatic disease.³ These two issues, the emergence of antigenically distinct SARS-CoV-2 variants and waning immunity, are often conflated and used interchangeably but represent two different phenomena.⁴ Most vaccines used in North America and Europe are based on lipid nanoparticles (LNPs) containing messenger RNA (mRNA) produced by Pfizer/BioNTech (BNT162b2) or Moderna (mRNA-1273), and the common perception now is that mRNA-based vaccine-induced immunity wanes quickly.⁵ However, this assumption is mostly based on data from short-term studies that include a very limited number of data points following peak responses.^2,5

In March of 2020, the densely populated New York metropolitan area was hit with an exponential increase of severe SARS-CoV-2 infections, resulting in a staggering number of fatalities and a severely overburdened healthcare system.^6,7,8 Due to shortages of personal protective equipment, essential workers in the health care system were at high risk for infection. In response to this crisis, we established (1) a specific and sensitive SARS-CoV-2 binding enzyme-linked immunosorbent assay (ELISA) to measure humoral immune responses,⁹ and (2) an observational longitudinal cohort of health care workers of the Mount Sinai Health System to determine the kinetics of these humoral responses. This study, named Protection Associated with Rapid Immunity to SARS-CoV-2 (PARIS),¹⁰ aims to capture the dynamics of SARS-CoV-2 antibody responses to infection as well as vaccinations, to determine re-infection rates, and to assess correlates of protection in the context of individual immune histories.

With over 8,000 longitudinal study visits across a single cohort during the first 3 years of the pandemic, our investigation represents one of the most extensive and in-depth assessments of the longevity of SARS-CoV-2 immune responses to date. Using this longitudinal cohort, we determined the kinetics of antibody responses to spike protein after infections, during the primary immunization series, during monovalent and bivalent booster vaccination, as well as during breakthrough infections. Our findings indicate that, in contrast to common perception, COVID-19 mRNA vaccination induces long-lasting antibody responses in humans. The PARIS Study also provides insights into the effect of booster vaccination and breakthrough infections on the stability of antibody responses.

What is clear from this study is that antibody levels remain at protective levels for very much longer that was previously thought and that they continue to give protection against the severe form of the disease. However, as the virus evolves in an environment in which the vast majority of possible victims have already been vaccinated or have had previous infections so have high antibody levels, the variants that can 'escape' this protection will continue to evolve and become the predominant variant.

This diagram from UK data shows how the different variants have evolved and either replaced earlier variants or have reached an equilibrium with them:

Changes in proportions of SARS-CoV-2 variants in UK over time. This diagram is a good illustration of how the proportions of different alleles of a gene change in a species gene pool over time as the species evolves.

Source: National flu and COVID-19 surveillance report: 22 February 2024 (week 8) Ref: GOV-16232

It is essential then that regular boosters, which provide protection against the latest variants, should continue to be given. We are in a long-term struggle with this virus and vaccines keep us ahead of the game.

Creationism in Crisis - How An Ancient Retrovirus Evolved To Create The Vertebrate Brain

A myelinating oligodendrocyte (green)

Credit: Peggy Assinck,
ALTOS Labs-Cambridge Institute Of Science

Ancient retroviruses played a key role in the evolution of vertebrate brains | ScienceDaily

Schematic diagram of a neuron show the myelin sheath as the electrical insulator of the axon.

Wikimedia Commons (CC BY-SA 3.0)

Extinct Late Devonian placoderm Bothriolepis canadensis. Myelin first appeared in these primitive early fish

Credit: Nobumichi Tamura / Stocktrek Images / Getty.

Creationists generally hate endogenous retrovirus (ERV's) because:

1. They are one of the strongest pieces of evidence of common descent appearing in the same locations in the genome of all organisms in a clade, forming nested hierarchies exactly as the Theory of Evolution predicts. The probability of the same viral DNA appearing in the same locus in all species in a clade by chance is, of course, so small it can be dismissed as an explanation.
2. They form a large part of the 'junk' DNA carried by all organisms, which, although a small proportion of it is transcribed into RNA, the RNA doesn't get translated into proteins and most of it doesn't serve any purpose. Some, but by no means all of it may have some regulatory functions.
3. Occasionally, an ancient ERV may have become exapted for some useful purpose unrelated to the original virus, so showing how new genetic information can enter a genome, flatly contradicting creationist's claims that no new information can arise within a genome because the second law of thermodynamics [sic] and Shannon Information Theory somehow forbids it.
4. An ERV serving a useful purpose also contradicts creationist claims that, while their favourite creator god is responsible for all the good stuff, another creator, called 'Sin', is responsible for the harmful stuff like parasites and viruses. Yet in those exapted ERVs we have viruses providing something that is beneficial and therefore, according to creationist dogma, must have been provided by their god!
5. Lastly, the examples of where ancient ERVs have mutated and provided some additional ability or function, such as enabling the formation of the myeline sheath in vertebrates, can't be regarded as detrimental mutations, yet creationist dogma, courtesy of the hapless Micheal J. Behe, is that all mutations are 'devolutionary'[sic].

Unintelligent Design News - A Newly-Discovered Virus-Like Particle That Doesn't Appear to Do Anything Other Than Replicate Itself

Streptococcus sanguinis bacteria, which live in the mouth, may host replicators named obelisks

UK Health Security Agency/
Science Photo Library

Figure 2.

Obelisks encode putatively well-folded proteins
a) Obelisk open reading frame 1 (Oblin-1) is predicted (total mean-pLDDT ± SD = 83.8 ± 13.4, see methods) to fold into a stereotyped N-terminal “globule” formed of a three alpha helix (orange) bundle partially wrapping around an orthogonal four helix bundle, capped with a beta sheet “clasp” (blue, globule mean-pLDDT = 90.1 ± 8.7), joined by an intervening region harbouring the conserved domain-A (magenta) with no predicted tertiary structure, to an arbitrarily placed C-terminal alpha helix. “Globule” emphasised on the right. b) a to-scale (secondary structure) topological representation of Oblin-1 with the “globule” shaded in grey, and the domain-A emphasised with this bit-score sequence logo (see methods). c) Obelisk Oblin-2 is confidently predicted (mean-pLDDT = 97.1 ± 4.6 ) to fold into an alpha helix which appears to be a leucine zipper. Sequence logo of an “i+7” leucine spacing emphasised in red, with hydrophobic “d” position residues emphasised in yellow (expanded in Supplementary Figure 4b). d) homo-multimer predictions of Obelisk-alpha Oblin-2. top: dimer (mean-pLDDT = 94.6 ± 0.6), bottom: trimer (mean-pLDDT = 93.6 ± 0.6). Side-on representations of homomultimers shown with numbers of inter-helix salt-bridges (see Supplementary Figure 5).

A new virus-like entity has just been discovered – ‘obelisks’ explained

At least with most of creationism's putative 'intelligent' designer, there is something that they appear to be for, other than simply reproducing themselves - even if it is, in the case of viruses and bacteria, increasing the suffering in the world by making other organisms sick.

But scientists have just discovered a small particle that seems to be in the edge of life, less so even than a virus, which doesn’t appear to do anything other than replicate, although it seems to need bacteria in which to do this. It’s not clear what harm it does to its bacterial host or even if it has some symbiotic function. But it appears to be almost everywhere, especially in our mouths and gut, where it appears to have speciated into several different forms. The team have named it 'obelisk' because it forms a rod-like shape.

It was discovered by a team of Stanford University researchers led by Andrew Z. Fire, a previous recipient of the 2006 Nobel Prize for Physiology or Medicine who have reported to have 'identified 29,959 Obelisks (clustered at 90% nucleotide identity), with examples from all seven continents and in diverse ecological niches'. Their report has been provided with free access ahead of peer-reviewed publication, in the preprint server, bioRxiv.

The question remains, what do these particles do exactly and are they potentially harmful, or are they beneficial in some way? At least one of their hosts in which they replicate is one of the bacteria responsible for the plaque on our teeth that is responsible for dental caries and gum disease that can result in lost teeth, Streptococcus sanguinis.
Like most viruses, obelisks are a single, circular strand of RNA, but unlike viruses, they don't have a protein coat. They have one and maybe two genes which code for proteins named 'oblins' which are unrelated to any other known proteins. In this respect they differ from other recently (1970) discovered free-living strands of RNA called viroids, which don't have any recognisable genes but are known to cause serious diseases in plants.

In the following article, reprinted from The Conversation under a Creative Commons license, Professor Ed Feil, Professor of Microbial Evolution at The Milner Centre for Evolution, University of Bath, explains the significance of this discovery. His article is reformatted for stylistic consistency:

Unintelligent Design - How A Virus Saved The Unintelligent Designer's Blushes Early In Multicellular History

A virus that infected animals hundreds of millions of years ago has become essential for the development of the embryo

I've remarked before how similar biological systems are to the machines the late William Heath Robinson designed for solving simple, everyday problems. Simple solutions were eschewed for more complicated ones and unlikely items were used in ways they weren't intended for, such as a grandfather clock standing on a piano to support a platform balanced on top. Everything was held together by pieces of knotted string and labour-saving devices took far more people than would have been needed to do the job more simply.

And yet, the whole contraption worked, or at least looked as though it would if were ever made, but take any part away and the whole thing would fail, in an example of what creationists call 'irreducible complexity'.

So, let's pretend that creationism's, 'intelligent'[sic] designer really is behind the design of living organisms and see how closely Heath Robinson unwittingly parodied it:
Just such an example of a Heath Robinson machine in biology was revealed a few days ago in an open access paper published in Science Advances, explaining how a virus which became incorporated in the genome of an early multicellular organism provided a solution to a problem of the designer's own making. The problem it solves was how to overcome the problem created by choosing the same method of cell replication in multicellular organisms that single-celled organisms use, where the entire genome needs to be replicated at each division.

The entire 'point' of multicellularity, and what gave it its success over single-celled organisms is division of labour, in other words, specialisation, so the organisms can be divided into tissues and organs that perform a specialised task. This means that every cell has to have the potential to carry out every function, in the genes it inherits from its parent cell, yet only a few genes are need for its particular specialty.

The process by which this is achieved is the complicated epigenetic system which turns off unneeded genes as the cells differentiate into different cell lines in the developing embryo, and these settings can't normally be reversed.

However, the sperm and egg which then fused to form the zygote from which a new embryo develops, are themselves specialised cells with all the epigenetic settings of their parent cells with an additional few of their own, and these are inherited by the zygote, so to make cell differentiation possible again, the zygote is quickly (within minutes of fertilisation) reset to a state of totipotency.

So, to overcome the epigenetic settings problem that is a problem of the designer's own making, the zygote needs to be epigenetically reprogrammed and this happens in two stages: first to produce a 'totipotent' cell with the potential to produce all the different cells in the embryo as well as the placenta, umbilical cord, and amniotic sack in which the embryo will develop, and then, soon after cell division begins, 'pluripotent' cells from which the different stem cells for the required specialised cell lines will develop.

How this was helped by a virus is the subject of the paper by researchers from the Spanish National Cancer Research Centre (CNIO), Madrid, Spain. First, a little AI background:

Malevolent Designer News - How The SARS-CoV-2 Virus Has Been Redesigned to Have Another Go

The emergence of JN.1 is an evolutionary ‘step change’ in the COVID pandemic. Why is this significant?

To anyone but a reality-denying creationist, the SARS-CoV-2 virus that causes COVID-19, is a classic example of evolution by natural selection, as it continually mutates and those mutations that make it more successful are retained, so it continually improves in its ability to infect and be passed on to another victim, so producing more offspring in the virus gene pool than rival versions.

The latest version to gain predominance, JN.1, currently spreading across the world, is yet another variation on the omicron version, which itself ousted delta as the predominant variety. This new improved version may prove to be so different to omicron that is should be given a new Greek letter designation.

One point that shouldn't go unnoticed is that because, unlike the original, the virus now exists in an environment in which most of its potential victims have a degree of immunity to it, either by vaccination or by previous infection. Because that immunity usually means the ability to produce antibodies to the 'spike' proteins on the surface of the virus, most of the mutations of progressively more successful variants are in the genes that code for those proteins - making it more difficult for antibodies to bind to them.

To a creationist, the SARS-CoV-2 virus, like all the other pathological viruses, presents the paradox of trying to believe their putative designer god is the supreme ruler of and creator of everything in, the universe and is the only entity capable of creating biological organisms, but, because it is omnibenevolent, it would not have designed SARS-CoV-2 and would not be responsible for continually redesigning it to continue making us sick, by evading the immune system it supposedly also designed to protect us from viruses and other pathogens.

Curiously, creationists who continually present what they think is evidence of design as evidence for their magic creator on the grounds that it is the only entity capable of biological design, never use evidence of malevolent design as evidence for the same magic creator. That has to be ascribed to another entity with even greater powers than their supposedly supreme-in-all-things god and with the ability to outwit it, even though that claim is blasphemous within their own religious beliefs. They need to hold those two diametrically opposite views of 'creation' simultaneously to continue to deny the evidence for evolution by natural selection of which the SARS-CoV-2 virus is a perfect example.

And those creationists who do actually believe the religion they purport to believe and who won't contemplate blasphemy, have no recourse but to believe that the SARS-CoV-2 virus was not only designed by their putative designer god but that it also regularly updates it to continue making us sick despite the efforts of biomedical scientists, because the alternative it to accept the unthinkable and ascribe it all the a god-free natural process of evolution by natural selection, just as science claims.

The following article by Suman Majumdar, Associate Professor and Chief Health Officer - COVID and Health Emergencies, Burnet Institute; Brendan Crabb, Director and CEO, Burnet Institute; Emma Pakula, Senior Research and Policy Officer, Burnet Institute; and Stuart Turville, Associate Professor, Immunovirology and Pathogenesis Program, Kirby Institute, University of New South Wales, Australia, explains why the emergence of the JN.1 variant of SARS-CoV-2 is a significant evolutionary step change. It is reprinted from The Conversation under a Creative Commons licence, reformatted for stylistic consistency:

Malevolent Designer News - How To Keep Ahead In The COVID Game Against Creationism's Divine Malevolence - Keep Being Boosted

How long does immunity last after a COVID infection?

Creationists stuck with the evidence of parasites and viruses that appear to be designed for two purposes only - making more copies of themselves and increasing the suffering in the world by making us sick and die - traditionally try to ride two horses. They blame something else, like 'The Fall' or 'Sin' for them, whilst still arguing that their putative designer god is supreme in all things and the only entity capable of creating complex organisms.

They also get in a terrible muddle when asked whether their 'designer' god included an immune system to protect us from these parasites when it designed us before 'The Fall', in which case it was planning for it all along, or whether there was a subsequent upgrade to V.1.2, in which case it couldn't have been omniscient and had to redo its design to account for the unforeseen.

But whatever rationalisation creationists can think up for these mutually contradictory beliefs, we are left with the fact that viruses like the SARS-CoV-2 virus and our immune system are locked in an arms race, in which human medical science has had to get involved because the immune system isn't fit for purpose, and the protection it gives us is only temporary.

Meanwhile, medical scientists, aware of the fact that evolution by natural selection is going to continually produce new variants of the virus and that these viruses may become better at evading our defences, continue to apply that knowledge and develop new vaccines against the latest variants.

The following article by Lara Herrero, Research Leader in Virology and Infectious Disease, and Wesley Freppel, Research Fellow, Institute for Glycomics, both of Griffith University, Australia explains why regular vaccination with boosters to keep out immune system primed for the latest iteration of the arms race with a latest version of the virus. The article is reproduced from The Conversation under a Creative Commons licence, reformatted for stylistic consistency:

Malevolent Designer News - How Does Killing Millions of Seabirds Punish Humans For Adam's & Eve's 'Sin'?

Emperor penguins and southern elephant seals on a South Georgia beach

Emperor penguins and southern elephant seals on South Georgia.
Both species at risk from avian flu.

Avian influenza has killed millions of seabirds around the world: Antarctica could be next

Avian flu is currently devastating flocks of seabirds, wiping out breeding colonies and even spreading to mammalian species such as sea lions and the southern elephant seal, the mass deaths of which are believed to have been caused by the H5N1 strain of the influenza virus.

Creationists claim that pathological parasites like the influenza viruses are the result of Adam's & Eve's sin which their beloved god inflicted on the world without prior warning in a tyrannical act of mass punishment for an arbitrary 'wrong', designated as such without any logical reason and applied to a couple of people who weren't equipped to know right from wrong and who hadn't been made aware of the real consequences.

But how killing millions of seabirds, elephant seals and other species punishes mankind or why the entire creation is being punished for a human 'crime' is never explained, leaving creationists to perform the most contorted mental gymnastics and denial of basic logic to simultaneously ascribe this to their putative designer god and make excuses to absolve it of blame for its criminal behaviour, for fear it'll come after then for not loving it enough.

Enough of the childish superstition and now for the real-world science:

Malevolent Designer News - How Creationism's Favourite Sadist Designed Ebola to Sneak Past Our Defences

Ebola virus proteins (green) are detected in the long tunneling nanotubes connecting cells.

Credit: Texas Biomed

Scientists discover new method Ebola virus uses to infect cells - Texas Biomed

Ebola virus.

Creationism's favourite malevolence is nothing if not sneaky in the way it designs its pathogens to make us sick and die by getting around the immune system it repeatedly designed to protect us from the pathogens it designed to make us sic and die.

For example, as researchers from the Texas Biomedical Research Institute (Texas Biomed) have discovered, the nasty little ebola virus uses a sneaky back-door approach to pass from cell to cell in a way which keeps it hidden from our immune system. Instead, it usurps the system our cells use to pass substances like proteins, nutrients and RNA from one cell to another via a network of nanotubes.

Unintelligent Design - How Creationism's Intelligent [Sic] Designer Stupidly Competes With Itself In An Arms Race.

These microscope images show how interferon in the nucleus raises levels of the protective protein IFI16 (stained green) from low background levels (left) to the higher levels needed to resist herpes infection (right).

Image: HMS MicRoN core imaging facility/
Nicolas Romero Rata

Oral Herpes simplex

How the Immune System Fights to Keep Herpes at Bay | Harvard Medical School

Throughout the Cold War, starting soon after World War II and continuing through most of the second half of the 20th Century, the world's great powers, led by America on one side and Russia on the other, competed in a wasteful arms race where one side tried to outdo the other by building more powerful bombs and better delivery systems while also building better defences capable of preventing successful attack by the other. Money and resources that went into this ultimately pointless arms race could have been used for better, more peaceful projects like better world health care, better education or ending poverty and famine, yet neither side could afford to do the sensible thing because neither side trusted the other to abandon the race and compete with peace instead.

Although we can understand the pressures and insecurities that caused these wasteful arms races, we can also see the ultimate futility of it all and how the costs escalate with every turn of the spiral.

But how much more stupid would it have been if both 'sides' had the same people running them - if both America and Russia had the same political and military leaders? In other words, if the arms race was being run by one side alone, for no better reason than that the leaders had amnesia and didn't know why they built a bigger bomb or a better defence system yesterday and woke up today faced with a threat they had designed yesterday and needed to spend today designing ways to cope with these new threats?

One might be tempted to call into question the sanity of these leaders and wonder about their fitness to lead. What on Earth had allowed them to behave so stupidly? And for what reason? It certainly would have had nothing to do with the health and welfare or safety of the populations of Russia or America, or indeed the rest of the world, so could not be excused as some sort of well-intentioned altruism. An OCD or sheer malevolence, maybe, but not benevolence.

And yet creationists worship what they believe is a supernatural entity who behaves exactly like the amnesiac maniac I've just described. The natural world it reputedly designed, according to creationists, is full of example of these pointless and wasteful arms races for no ultimate long-term benefit to either 'side'.

Malevolent Design - How A Chicken Virus Got More Deadly - Malice Or Evolution?

Ancient DNA reveals how a chicken virus evolved to become more deadly | University of Oxford

Marek's Disease Virus (MDV) is a serious infection in chickens that costs th4e poultry industry over $1 billion annually. Now an international group of virologists and archaeologists led by researchers from Oxford University, Ludwig-Maximilians-Universitat, Munich, Germany, have discovered how it has evolved over time to become more virulent and deadly, or, as creationists insist, has been intelligently redesigned.

The team reached this conclusion from an analysis of the virus in modern and ancient chickens going back over the past 1000 years. The ancient samples were obtained from DNA extracted from chicken bones recovered from 140 archaeological sites in Europe and the Near East. This analysis showed that MDV was widespread in European chickens for at least 1000 year before being first described in 1907.

Creationism in Crisis - A Monster Virus Is A BIG Problem For Creationists

Pithovirus sibericum

Legendre, Matthieu; Bartoli, Julia; Shmakova, Lyubov, et al. (2014)

Pithovirus sibericum

Pithoviruses Are Invaded by Repeats That Contribute to Their Evolution and Divergence from Cedratviruses | Molecular Biology and Evolution | Oxford Academic

Regular readers with very long memories may remember how I wrote about something big and potentially nasty emerging from Siberian permafrost back in 2014.

The 30,000-year-old monster in question was a form of giant virus then unknown to science, now named Pithoviruses sibericus. It came back to life when thawed. Since then, several other related pithoviruses have been discovered in soil and aquatic sources. Fortunately, all those discovered so far are parasitic only on one species of amoeba, Acanthamoeba castellanii and don't pose a threat to humans or multicellular life.

The question was, why are they so large, or more particularly, why do they have such a massive genome, including some genes normally found in complex cells. the Pithovirus species so far discovered have a genome of between 460 to 686 kb. Their genome, moreover, is similar to that of bacteria and archaea, in that it is DNA-based and forms a single circular 'chromosome'.

But it's not the fact that the first one was found in permafrost dating back 20,000 before 'Creation Week', difficult though that little inconvenience is for creationists; it is the account of how they acquired this massive genome that is the thing of nightmares for any creationists who understand the biology.

They acquired it by processes that give the lie to their basic dogma that new genetic information can't arise in a genome without 'God magic'.

A team of researchers have shown that they acquired new genetic information and such a massive genome by:

1. Horizontal gene transfer (5% -7 %)
2. Gene duplication (14% - 28%)
3. Massive inversions of repeated sequences of DNA.

All these are familiar mutations in which the genome size is increased, and by which 'spare' copies of genes and novel sequences are free to mutate and give rise to new genes and new functions.

And this gives the lie to the ludicrous creationist dogma that no new information can arise by mutation because all mutations are deleterious. There is nothing deleterious in having a spare copy of a gene, nor in mutations in that spare copy, least of all if it gives a new function that increases fitness.

The researchers, from the Institut de Microbiologie de la Méditerranée, FR3479), IM2B, IOM, Aix–Marseille University, Centre National de la Recherche Scientifique, Marseille, France were led by Matthieu Legendre. Their findings are published, open access, in Molecular Biology and Evolution:

Evolution in Progress - How The Different SARS-CoV-2 Variants Rise and Fall In The Population

I came across this the other day while perusing NHS information sources about COVID-19, which is now declining again in UK, having had a brief revival a few weeks ago. It's a chart showing how new variant rise to dominance in the viral population, to be replaced in their turn by newer variants.

Screen clip of page 16 of the National Influenza and COVID-19 surveillance report Week 45

This diagram only covers a year since November 2022.

This, in miniature, is exactly how new gene variants can rise in the species gene pool, depending on how advantageous they are compared to other variants. Some will increase rapidly to become the predominant form and may even stage something of a rally when in competition with a new variant. Some will linger on for a long time as a small proportion of the total, while others will become extinct, or very nearly extinct as newer variants enter the fray. What allows the new variants to increase as a proportion of the total is, of course, that it produces more copies of itself than its rivals do.

Creationism in Crisis - Scientists Create Evolutionary Arms Races In a Laboratory

In laboratory flasks containing just two teaspoons of media, scientists document how rapid adaptation between bacteria and viruses produce complex ecological networks.

Credit: Josh Borin,
UC San Diego

A typical E. coli phage virus.

Bacteria-Virus Arms Race Provides Rare Window into Rapid and Complex Evolution

Creationists hate evolutionary arms races because they can't be sensibly explained in terms of intelligent design by a single omnipotent, omniscient designer and for a creationist, any other sort of designer(s) would be a serious blasphemy that would see them swiftly ejected from their cult and cast into outer darkness, socially speaking.

And yet evolutionary arms races are an integral part of evolution, probably accounting for more biodiversity than sex selection and environmental change. Evolutionary arms races are the inevitable result of the fact that living things eat other living things, either as parasite or as predators, so there are two ways an organism in a parasite-host or predator-prey relationship can gain an advantage over others of its species: it can either be a more successful parasite/predator or it can be better at avoiding being parasitised or eaten. Either scenario will lead to more offspring carrying the genes for greater success so they will increase in the species gene pool and the whole population will evolve in that direction, creating selection pressure on the other member of the relationship to respond appropriately.

This is all the result of natural selection at works, with no plan and no sentience needed.

It should not be beyond the wit of an average 10-year-old to comprehend that unless childhood brainwashing and theophobic psychosis has prevented rational thinking.

of course, in a natural setting, this all happens relatively slowly in small increments over time, so the evolutionary changes might not be observable for several generations.

So, a group of researchers from UC San Diego, Georgia Institute of Technology and Maryland University, have found a way to speed up the process in laboratory flasks by using small quantities of bacteria and the bacterial parasites, bacteriophage viruses, usually simply called phage viruses.

The news release from UC San Diego explains the research and its significance:

Malevolent Designer News - How HIV Research is Trying to Overcome the "Designer's" Devilish Malevolence

Human Immunodeficiency Virus (HIV)

Human Immunodeficiency Virus (HIV)

Pinpointing HIV immune response

The traditional creationist double-think response, when presented with evidence of malevolent design in the form of parasites such as pathological viruses, bacteria, protozoa or worms, etc., is to blame something called 'Sin' for their creation, absolving their proclaimed intelligent [sic] designer of any culpability, while maintaining that everything living must be attributed to their god because it is the only entity capable of designing living organisms.

However, in the case of HIV, the virus that causes Acquired Immune Deficiency Syndrome (AIDS) in humans, they greeted it with barely concealed jubilation in their caring Christian way, declaring it to be a 'Gay Plague' sent by their god to punish homosexuals, so they now can't blame Satan or 'Sin' for its creation. A case of being hoist by their own petard.

And to add to creationists' embarrassment, they also believe the human immune system that HIV evades then suppresses, was designed by their, allegedly perfect, omniscient designer to protect us from the parasites it created to harm or kill us, in which case, HIV, like so many other pathogens, is a testament to its incompetence.

HIV is one of a group of RNA retroviruses that can hide from our immune system by inserting a DNA version of their RNA into our DNA using the enzyme reverse transcriptase that they bring with them. Once inserted, the virus looks for all the world like just another chunk of junk DNA. Indeed, like most species, our DNA contains lots of mutated and harmless relics of these retrovirus from our evolutionary history.

Now though, medical science, in trying to do what seems beyond the capability of creationism's putative omnipotent intelligent [sic] designer is closing in on just how HIV manages to evade and suppress our immune system, and how our immune system responds to it.

In a paper just published open access in the journal Science Communications a team of scientists led by Ruy M. Ribeiro, a theoretical biologist at Los Alamos National Laboratory, Los Alamos, NM, USA has shown, using experiments on Macaque monkeys and mathematical modelling, that, although the body's immune system does succeed in suppressing virus production and in killing infected cells, the response only last for a very short time at the start of infection.

Unintelligent Design - How Viruses Are Needed To Promote Mammalian Cell Growth

Illustration of bacteriophages infecting a bacterium.

Fig 1. Uptake of T4 phage by mammalian cells does not trigger a pro-inflammatory immune response [modified].

(A) A549 cells and (B) MDCK-I cells incubated with T4 phages for 2 hours. Images were taken with a confocal microscope; the plasma membrane is shown in magenta, T4 phage DNA in green, and the cell nucleus in blue.

Bichet MC, Adderley J, Avellaneda-Franco L, Magnin-Bougma I, Torriero-Smith N, Gearing LJ, et al. (2023)

Mammalian cells internalize bacteriophages and use them as a resource to enhance cellular growth and survival | PLOS Biology

Imagine you're a designer charged with designing a mammalian cell so it grows and multiplies efficiently. You've already designed DNA and genes to make the right proteins to stimulate cell growth, but it isn't working as well as it should.

What do you do?

An intelligent designer, especially an omnipotent, omniscient designer, wouldn't have designed it sub-optimally in the first place, but if it had, it would simply redesign it and make sure all the right genes were provided because, being omnipotent, nothing would be impossible.

But whatever designed the mammalian cell didn't do the intelligent thing.

Instead it opted for an unnecessarily complex solution - it used the bacteriophage viruses that it had designed to infect and kill the bacteria it had designed earlier, to infect mammalian cells and give them the missing genes to correct its mistake. It then modified the process it had designed to protect the cells from infection, so these viruses don't trigger an immune response and get destroyed.

No going for the simple solution like a normal intelligent designer would, when a much more complex solution is available, eh?

This is what you need to believe to be an intelligent [sic] design creationist, to explain the findings of a group of researchers led by Jeremy J. Barr of the School of Biological Sciences, Monash University, Clayton, Australia. They have discovered that phage viruses, which proliferate in our gut where they normally parasitise and kill bacteria, are taken in by mammalian cells where they accumulate and activate metabolic pathways that promote cell metabolism and growth and prolong the cell cycle.

The findings of the team are published open access in PLOS Biology:

Malevolent Designer News - Is Creationism's Divine Malevolence Planning the Next Pandemic?

News - Bird flu is undergoing changes that could increase the risk of widespread human transmission - University of Nottingham

On top of a couple of recent papers showing creationist dogma to be false and that, if there were such a thing as an intelligent designer of living things, that designer can only be regarded as a malevolent monster, we have another paper which, if we believe creationist dogma, again shows their divine creator to be an obsessive, sadistic psychopath.

It is the news that scientists at Nottingham University, UK., and China have discovered how the variant of the H3N8 avian flu virus which is endemic in Chinese poultry farms, is mutating in a way which could make it more likely to cross the species barrier into humans and become the next pandemic.

What is the H3N8 Avian influenza virus and what threat does it pose to humanity?

H3N8 Avian influenza, also known as avian flu or bird flu, is a subtype of the influenza A virus that primarily affects birds, especially waterfowl and shorebirds. It is one of several subtypes of avian influenza viruses, each identified by specific combinations of surface proteins: hemagglutinin (H) and neuraminidase (N). In the case of H3N8, it refers to the third type of hemagglutinin (H3) and the eighth type of neuraminidase (N8) found on the virus's surface.

While H3N8 avian influenza primarily affects birds, it has the potential to pose a threat to humans under certain circumstances. Here are some key points to consider regarding its potential threat to humanity:

1. Zoonotic Transmission: Avian influenza viruses, including H3N8, are zoonotic, which means they can infect humans when they come into close contact with infected birds or contaminated environments. Most human cases of avian influenza have resulted from direct or indirect exposure to infected poultry.
2. Limited Human Infections: H3N8 avian influenza has not been as widely reported in human infections as some other avian influenza subtypes, such as H5N1 and H7N9. However, there have been occasional cases of H3N8 avian influenza infection in humans, often associated with direct contact with infected birds.
3. Potential for Adaptation: Avian influenza viruses have the ability to mutate and potentially adapt to human hosts. If a strain of H3N8 were to acquire the ability for efficient human-to-human transmission, it could lead to a more widespread outbreak or even a pandemic. This is a significant concern with avian influenza viruses in general.
4. Influenza Pandemic Preparedness: Due to the risk of avian influenza strains causing pandemics, public health organizations and governments worldwide monitor and study these viruses closely. Preparedness plans and strategies are in place to respond quickly to potential outbreaks, including the development of vaccines and antiviral medications.
5. Importance of Surveillance: Surveillance of avian influenza in both bird populations and humans is crucial to detect any changes in the virus's behavior or its potential to infect humans more easily. Timely identification and containment of outbreaks are essential to minimize the risk to public health.

In summary, H3N8 avian influenza is primarily a bird virus, but it can infect humans in rare cases. The main threat it poses to humanity lies in its potential to evolve and adapt to human-to-human transmission, potentially leading to a wider outbreak or pandemic. Vigilant surveillance, early detection, and preparedness are key components in mitigating this threat and preventing a significant public health crisis.

As explained in a Nottingham University news release, the evidence comes from an isolate of the H3N8 avian influenza virus (AIV) recovered from a human patient:

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: