Malevolent Designer News - Creationism's Divine Malevolence Is Still Victimising Frogs

Foothill yellow-legged frog, Rana boylii

Photo Credit: Brome McCreary

Foothill yellow-legged frog, Rana boylii

Photo: Rebecca Fabbri/USFWS

Scientists assemble a richer picture of the plight and resilience of the foothill yellow-legged frog | The Current

Almost unnoticed by the general public and noticed only by biologists and wildlife conservationists, is a pandemic far more deadly than the Covid-19 pandemic, or even the Medieval Black Death.

It kills a very high percentage of its victims, has already exterminated whole populations of frogs and other amphibians, and has contributed significantly to the global mass extinction currently underway.

It is, of course, the chytrid fungus Batrachochytrium dendrobatidis, which, along with a closely-related fungus, B. salamandrivorans, causes the fatal disease, chytridiomycosis, in frogs and other amphibians.

As an example of the work of creationism's divine malevolence, it takes some beating for its sheer malevolent nastiness. It infects the skin of these amphibians, through which they breath, and causes it to thicken and fail as a respiratory organ, leading to suffocation, multiple organ failure and death. Here is how I described it in my illustrated book, The Malevolent Designer: Why Nature's God is not Good:

Exterminating Frogs with a Fungus.

Most of the examples I’ve talked about so far have been organisms and viruses that affect humans, but we are far from being the only species that Creationism’s putative intelligent designer seems to have taken an intense dislike to. For example, the world’s frogs and other amphibians are currently being decimated by chytridiomycosis, caused by a couple of related Chytrid fungi, Batrachochytrium dendrobatidis and B. salamandrivorans. It has been estimated that over 500 different species have been severely reduced in number by this fungal plague, with over 90 extinctions.

These fungi seem to have originated in an area of Southeast Asia by modification of a common, harmless, soil fungus. In that part of the world, the local population of amphibians seems to be resistant to the pathogenic forms of the fungi, suggesting that these fungi frequently become pathogenic and the local population have built up resistance to it.

According to research carried out by a team from the Fenner School of Environment and Society, Australian National University, ACT, Australia, it was resistance in the local population which probably kept the disease from spreading more widely, until human agency intervened to change the environment. They have related the increased trade in amphibian species to the spread of the fungi all over the world where they found species with no evolved resistance (42).

Figure 5 Frog Victims of Chytrid Fungus

Illustration: Catherine Webber-Hounslow

Recently, another team found that one of the factors that could have made these fungi so successful is that the frog’s immune response seems to have worked against it. Researchers from the University of Central Florida and the Smithsonian Conservation Biology Institute (SCBI) found that, in the frog Rana yavapaiensis, a species known to vary in its ability to survive attack by these fungi, those which showed an elevated immune response had a worse outcome that those with a lower response (43). Somehow, the frog’s ‘designed’ immune system was working against it and the fungi had been ‘designed’ to exploit this.

ID advocates would have us believe that, for reasons unknown, their putative intelligent designer has deliberately redesigned a soil fungus so it can overcome the immune system it designed to protect frogs from infections, and so exterminate over 90 species of amphibians that it designed earlier and severely endanger some 500 species in what has been described as the biggest single loss of biodiversity, albeit, aided and abetted by humans in this endeavour. Creationism’s intelligent designer must really hate the frogs it designed. Maybe a private definition of the word ‘intelligent’ is being employed here.

Now a team of researchers from multiple American wildlife and conservation agencies have looked in detail at the spread of this fungus in one particular frog which has declined so rapidly it is now an endangered species - the foothill yellow-legged frog, Rana boylii. This small frog's range once extended from Oregon to Baja California.

They have shown that human agency is implicated in the spread of this fungus by not only spreading it around the world in trade, as the earlier Australian study found (42), but with regard to the foothill yellow-legged frog specifically, by global warming, climate change and habitat destruction as more land is converted to agriculture. They have published their work, open access, in Royal Society Open Science. It is also explained in a University of California Santa Barbara, news release:

Up to only a few inches in length, with a lemon-hued belly, the foothill yellow-legged frog may seem unassuming. But its range once stretched from central Oregon to Baja California. In 2023, it was listed under the federal Endangered Species Act. Its rapidly decreasing range is due in part to a fungal pathogen called Batrachochytrium dendrobatidis, or Bd, that has devastated amphibians around the world.

A team of researchers, including UC Santa Barbara’s Andrea Adams, has conducted the most comprehensive study to date of disease dynamics in foothill yellow-legged frogs. The team’s data — sourced from both wild frogs and specimens in museum collections — enabled them to track patterns of infection across a large geographic range. In a study published in Royal Society Open Science, the researchers reveal that drought, rising temperatures and the increasing conversion of land for agriculture appear to be the largest factors driving Bd infection in this species.

The researchers aimed to assemble as much data as they could, both in space and time. They surveyed in the creeks and rivers of California and Oregon, where they swabbed wild yellow-legged frogs for the presence of Bd. It also led them into fluorescent-lit museum collections to sample specimens from as far back as the 1890s.

The team leveraged a large network of people and institutions to amass this wealth of samples.

Many foothill yellow-legged frog field researchers had data that they weren’t actively analyzing, and so we were able to bring all of this data together and get it into a usable format that we could use to paint a much bigger picture of what is, and was, going on with Bd in this species.

Andrea J. Adams, co-author.
Earth Research Institute
University of California, Santa Barbara, CA, USA.

The researchers swabbed each frog’s skin to determine if the animal was infected. To test for Bd, they used a PCR test, similar to some tests for COVID. By searching for Bd DNA from thousands of samples, the researchers were able to identify infection rates and severity. Co-lead author Ryan Peek ran this information through statistical models, which accounted for climatic, geographic, biologic and land use variables. This enabled the team to track disease patterns across a large geographic range over roughly 120 years.

The team discovered that disease patterns of Bd aligned with historical frog declines. The pathogen began to spread in the 1940s from the southern coast of California, moving northward and eventually affecting nearly the entire region. The biggest factors driving infection seem to be drought, increasing temperatures and the use of ever more land for agriculture.

Bd is a fungus that is spread through spores in the water, but that spread may occur differently in foothill yellow-legged frogs in different regions and climates, the researchers found. In some places, drought increased infection, while in others, it did not, possibly because of the presence or absence of other species that can carry Bd and share the same water, such as American bullfrogs, a species introduced from eastern North America.
“

If you combine the fact that there are bullfrogs building up the number of spores that these frogs are exposed to, and then they’re all kind of stuck in these small pools together, that explains why drought matters. They are suddenly getting hit with a really large number of spores and getting sick and dying.

These findings open more questions about what was stopping transmission and what allowed it to happen later.

Dr. Anat M. Belasen, co-first author
Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA
And Department of Ecology and Evolutionary Biology,
Cornell University, Ithaca, NY, USA.

What’s more, foothill yellow-legged frogs live exclusively in streams and rivers, not ponds and lakes. So the species is already stressed when these waterways shrink into isolated pools.

The progression of Bd in the foothill yellow-legged frog also differed from its course in other western amphibians. In many other species, the disease radiated from urban centers, rather than this clear south-to-north trend. What’s more, the disease showed up later in the foothill yellow-legged frog than in other species in its range.

Frogs switch from herbivores as tadpoles to carnivores as adults, which means they connect different nutrient cycles together in the food web. Their position at the center of the food chain also influences the ecosystem.

When you remove frogs from an ecosystem, what you get is less control of insects, things that the frogs would eat. There is also less food for things that eat the frogs, like snakes, birds and small mammals. It really throws things off and makes the ecosystem less stable and less functional.

“There are areas that have wet soils that would be alongside suitable habitat. In areas where more of those lands have been converted to agriculture, we see a higher risk of frogs being infected with the fungus.

Dr. Anat M. Belasen.

Co-author Jamie Bettaso swabs a wild foothill yellow-legged frog to test for fungal infection.

Photo Credit: Jamie Bettaso

The conversion of land for agriculture was another major factor influencing the spread of Bd. for these frogs.

In addition to disease hotspots, the team also identified a number of cold spots — areas where the pathogen is present but less influential. The existence of so many cold spots in different areas is a good sign, as it may mean that many areas have conditions suitable for keeping disease rates low, even as climate change increases temperatures and patterns of drought.

The authors are curious what might explain this clustering, especially when cold spots appear in unexpected locations: for example, places with similar habitat, land-use and climatic impacts as hotspots. It suggests there may be some genetic basis for the differences, whether on the pathogen side or the host side. Adams is currently researching the feasibility of reintroducing foothill yellow-legged frogs to Southern California.

The results of this paper shed a lot of light on the dynamics of where Bd occurs, what drives its spread and how the pathogen and frog may interact in the future.

We took a big snapshot of this species’ disease relationship through time. Earlier studies provided the researchers with glimpses into disease patterns in smaller geographic regions, “but now we have a much larger dataset that further confirms many of these patterns, and expands on them.

Andrea J. Adams.

More detail is given in the team's open access paper in Royal Society Open Science:

Abstract

Species with extensive geographical ranges pose special challenges to assessing drivers of wildlife disease, necessitating collaborative and large-scale analyses. The imperilled foothill yellow-legged frog (Rana boylii) inhabits a wide geographical range and variable conditions in rivers of California and Oregon (USA), and is considered threatened by the pathogen Batrachochytrium dendrobatidis (Bd). To assess drivers of Bd infections over time and space, we compiled over 2000 datapoints from R. boylii museum specimens (collected 1897–2005) and field samples (2005–2021) spanning 9° of latitude. We observed a south-to-north spread of Bd detections beginning in the 1940s and increase in prevalence from the 1940s to 1970s, coinciding with extirpation from southern latitudes. We detected eight high-prevalence geographical clusters through time that span the species' geographical range. Field-sampled male R. boylii exhibited the highest prevalence, and juveniles sampled in autumn exhibited the highest loads. Bd infection risk was highest in lower elevation rain-dominated watersheds, and with cool temperatures and low stream-flow conditions at the end of the dry season. Through a holistic assessment of relationships between infection risk, geographical context and time, we identify the locations and time periods where Bd mitigation and monitoring will be critical for conservation of this imperilled species.

1. Introduction

Threatened species with large geographical ranges often require unique, regional conservation strategies to combat stressors such as infectious disease. Pathogen surveys and reporting have become standard for North American wildlife diseases [1,2]; however, relative risk across a landscape and among populations within species remains difficult to anticipate, especially when data are collected by separate research groups [3]. Central reporting databases [4], synthetic analyses and retrospective surveys can help assess disease threats and identify high-risk populations.

Among the most significant wildlife diseases, amphibian chytridiomycosis caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd) has contributed to declines of hundreds of species worldwide [5]; but see [6]. In North America, notable Bd-associated declines have occurred across the west including the southern Rocky Mountains [7,8], Arizona and New Mexico [9,10], Nevada [11] and California [12–14]. In several of these cases, infection outcomes varied widely among populations due to host-related and environmental factors including genetics, prior Bd exposure and abiotic conditions [15–17].

For the stream-dwelling foothill yellow-legged frog, Rana boylii, Bd's role in the species' changing abundance across its endemic range (California and Oregon, USA) is not well-understood. The species has declined for at least the last half-century, with extirpations reported from xeric lower latitudes [18], at the wetter northern range limit [19] and downstream of large dams range-wide [20]. A mix of abiotic and biotic factors influence Bd infection risk and disease dynamics in many systems, including elevation, latitude, climate, habitat quality and host characteristics [21]. The relative importance of these factors remains unclear in rivers with winter flood/summer drought flow regimes typical across R. boylii's geographical range. Bd is considered a significant potential threat to R. boylii [22] because it is implicated in the species' disappearance from rivers of California's South Coast [23] and in recent autumn die-offs of R. boylii in Central Coast streams [24,25]. A large-scale assessment of Bd infections is needed to clarify how infections relate to historical declines in some regions' rivers and persistence in others, identify clusters of increased infection risk across the species’ range, and evaluate how infection incidence and severity changes with the seasonality of the Mediterranean climate and across the diverse ecoregions that R. boylii occupies.

Here, we leverage data from over 2000 field and museum samples covering 124 years to synthesize knowledge and evaluate patterns of Bd infections in R. boylii. We use a combination of modelling approaches and spatial scan statistics to ask: (i) how are Bd detections in R. boylii are distributed over space and time, (ii) whether watersheds with high versus low Bd infection risk clustered historically and today, and (iii) how Bd infections are related to biotic and abiotic factors. Our results highlight priority populations for Bd mitigation, regions that are data-deficient and warrant further sampling and monitoring, and remaining gaps in our knowledge about Bd susceptibility in R. boylii. Our study serves as a resource for wildlife managers implementing disease mitigation and species recovery projects, such as re-introductions, and as an example of collaborative research to address conservation challenges in wide-ranging imperilled species.

Figure 1.
Distribution of R. boylii samples assayed for Bd infection. Diamonds show museum samples (collected 1897–2005), circles show field samples (2005–2021). Filled symbols indicate Bd-positive samples. (a) Sampling locations across California and Oregon, USA. Symbols overlap in some localities; see inset barplots for sample sizes. Rana boylii clades are outlined and labelled, with California Endangered Species Act status abbreviated in parentheses: SSC = Species of Special Concern, TH = Threatened, EN = Endangered. (b) Spatio-temporal spread of Bd detections. Symbol size indicates sample size at the HUC-12 (sub-watershed) level. Generalized additive model (GAM) of latitude∼capture year + sample size in Bd-positive samples is shown with black curved line (R² = 0.133).

Photo of R. boylii in Napa County, CA by Marina De León.

Belasen A. M., Peek R. A., Adams A. J., Russell I. D., De León M. E., Adams M. J., Bettaso J., Breedveld K. G. H., Catenazzi A., Dillingham C. P., Grear D. A., Halstead B. J., Johnson P. G., Kleeman P. M., Koo M. S., Koppl C. W., Lauder J. D., Padgett-Flohr G., Piovia-Scott J., Pope K. L., Vredenburg V., Westphal M., Wiseman K. and Kupferberg S. J. (2024)
Chytrid infections exhibit historical spread and contemporary seasonality in a declining stream-breeding frog
R. Soc. Open Sci.11. 231270. 231270 DOI: 10.1098/rsos.231270

Copyright: © 2024 The authors.
Published by The Royal Society. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

It must be thrilling for devotees of the putative divine malevolence to see the stunning success it is having exterminating so many species of frog, but one can't help but wonder what the ancestral frog did to incur this wrath. Did it maybe eat a forbidden mosquito or spawn out of wedlock?

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ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

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Creationism in Crisis - Biological Chirality Explained - And Another Favourite Creationist Gap Slams Shut With No God(s) Found

How molecular “handedness” emerged in early biology | Scripps Research

Back in the 1980's when I first encountered (mostly) American creationists on the emerging Internet, one of their arguments from personal incredulity was that 'no-one can explain' why amino acids occur naturally in two stereo forms, yet only one is found in nature (therefore God did it!).

This 'problem' for evolutionary biologist now seems to have dropped out of favour with creationists, probably because, as more and more former creationists realise they've been fooled, only the lower tail-end of the IQ bell curve remain, and this phenomenon, known as chirality, is a little difficult to understand and requires a modicum of understanding of chemistry.

Basically, at the heart of an amino acid is a carbon atom with four different atoms of groups attached. This structure can be thought of as a pyramid with a triangular base (known as a tetrahedron) with the carbon atom in the centre and each of the four atoms or groups at each point of the tetrahedron. These groups can be attached to the carbon in two separate ways so that one is a mirror image of the other. These are known as chiral forms or stereo-isomers. No matter how you rotate one, it can never be the same as its opposite chiral form.

These chiral forms have the same chemical properties and the same physical properties apart from one - the way they interact with polarised light. One form causes the plane of polarity of polarised light to rotate in one direction, the other in the other direction; so they are also known as optical isomers.

The chiral forms of amino acids are prefixed with 'D' or 'L' (upper case; Dextro and Laevo (right and left)) according to the physical structure, or 'd' and 'l' (lower case) according to which direction they rotate the plane of polarity of polarized light.

ChatGPT explains it more succinctly:

Creationism in Crisis - Evolution By Loss Of Complexity - How A Mutation Cost Our Ancestors Their Tails

A mutation cost our simian ancestors their tails

Photo: Getty / Steve Adams

Change in Genetic Code May Explain How Human Ancestors Lost Tails | NYU Langone News

In that distant, pre-'Creation Week' history of Life On Earth, 25 million years before creationists think Earth was created out of nothing, and all living things on it were magicked into existence without ancestors, a 'jumping gene' inserted a short length of DNA termed AluY, into the gene which controls tail length in monkeys, and the resulting tailless monkeys went on to diversify into the apes - gibbons, siamangs, orangutans, gorillas, chimpanzees, bonobos, and the hominins which were to evolve into the Australopithecines and the Homo genus, including Homo sapiens, all of which still possess that short insertion in the TBXT gene, which otherwise is identical to one of the gene which grow the tail of the simians.

As an example of design, it is one of the least intelligent, since, instead of removing all the genes required to grow a tail, the 'designer' simply broke an essential gene and left all the others to do nothing apart from having to be replicated in every cell in every ape that ever lived, as an example of the massive waste and unnecessary complexity that characterises an evolved process and gives the lie to any notion of any intelligence being involved.

By inserting the AluY snippet into a mouse BBXT gene the researchers found a variety of tail effects, including mice born without tails. They also showed that there was a small increase in the incidence on neural tube defects (spina bifida) in mice.

Quite why tailless would have been selected for during the evolution of these ancestors of the modern apes is a matter for speculation; maybe a tail was becoming an encumbrance for a brachiating mode of locomotion as opposed to running along the top of branches and jumping from branch to branch, which the smaller monkeys used, where a tail was an important balance organ. For a heavier ape hanging beneath the branches by its arms, there would have been less need for a balance organ and a tail would have been liable to damage and infection.

How this was discovered by a team led by researchers at New York University Grossman School of Medicine, is the subject of an open access paper in Nature and a NYU Langone Health 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 - What Life Was Like 3.5 Billion Years Before 'Creation Week'

Rocks of the Pilbara Craton exposed on the surface: grey barite rock at the bottom, reddish stromatolites due to oxidation at the top

Photo: Jan-Peter Duda

Barite quarry in the “Dresser Formation” of the Pilbara Craton. These rocks are around 3.5 billion years old and contain evidence of microbial life.

Photo: Jan-Peter Duda

Information for the Media - Georg-August-Universität Göttingen

Long, long ago, in that dim distant past when Earth was young, and fully 3.5 billion years before creationism's god decided to create a small flat planet with a dome over it centred on the Middle East, thermophile organisms, probably bacteria or archaea were living in a lake in a volcanic caldera in what is now the Pilbara Craton in Western Australia.

This is the conclusion of a research team led by the University of Göttingen wo have just published their work, open access, in the journal, Precambrian Research. Their work is also the subject of a brief news release by the University of Göttingen.

Malevolent Designer News - How Creationism's Favourite Sadist May Use Climate Change To Increase The Suffering In The World

Nematode movement

Parasitic worms cause huge economic loss to farmers and can infest humans too.

Temperature, humidity may drive future transmission of parasitic worm infections | Penn State University

Creationists who believe nothing happens unless their invisible magic god wants it to have to have all manner of intellectual gymnastics to avoid giving it credit for all the nasty things to be found in nature, such as parasitic worms.

Their favourite strategy is the old trick of believing two mutually exclusive ideas simultaneously - that only their god is capable of designing living systems, so anything too complex for them to understand must have been created by it, whilst simultaneously believing that all pathogens are created by another entity, called 'Sin', no matter how complex or difficult to understand they may be.

And of course, they are forbidden by dogma to believe in more than one creator and must believe, also by dogma, that that creator is omni-everything - omnibenevolent, omniscient and omnipotent - so they have to believe that whatever its designs do, they were designed to do it, and whatever the future may bring, they were aware of that whilst designing their creations.

What percentage of the surface of Earth is habitable to humans without special equipment? Approximately 29% of the Earth's surface is comprised of land, which is habitable to humans without special equipment. The remaining 71% is covered by water, primarily in the form of oceans, which generally require specialized equipment for prolonged habitation. Therefore, without considering other factors such as climate, terrain, and resources, roughly 29% of Earth's surface is habitable to humans without special equipment.

That means, creationists have no choice but to accept that the results of climate change were part of their designer creator's plan, as was the response of their creations to it. And one of those responses to climate change may be an increase in parasitic worms in parts of the world they have not been prevalent in before.

Many of these worms are, or have been, confined to the tropics and sub-tropical zones, and the northern and southern part of the world, where most advanced economies are based, have been relatively free from them. But, as Earth gets warmer, the 'habitable zone' for parasitic worms expands to incorporate more of the advanced economies, but the habitable zone for humans shrinks even further.

This is the prediction of a team of researchers from the Center for Infectious Disease Dynamics and Department of Biology, The Pennsylvania State University (PennState), Pennsylvania, USA, and Dipartimento di Elettronica, Informazione e Bioingegneria, Politecnico di Milano, Milano, Italy, led by Professor Isabella Cattadori and Dr. Chiara Vanalli of PennState, who have just published their findings, open access, in the journal Ecology Letters. Their work is explained in a PennState news release:

Unintelligent Design - How The Same Function Evolved Twice - Once in Vertebrates And Again in Insects

Sunset over University of California - Irvine

Diagram of an insect compound eye.

Credit: Bugboy52.40 via Wikipedia (CC BY-SA 3.0 Deed)

UC Irvine study shows similarities and differences in human and insect vision formation – UCI News

Regardless of the different structures in the compound eyes of insects and the eyes of vertebrates, at the heart of them both is a light-sensitive molecule, 11-cis-retinal, also known as 'visual Chromophore', but these are produced in two different ways from the same starting compound - β-carotene - which in humans is obtained from eating plants like carrots which are rich in Vitamin A from which β-carotene is derived.

This is one of those examples which are so common in biology, of where, had it been intelligent, the same designer could have used a process it had designed earlier but did not, instead it designed an even more complex way of doing the same thing, giving the lie to claims that the same 'intelligent' designer designed living things, insects and vertebrates have two different ways to achieve the same product - 11-cis-retinal; the second being the more complicated of the two.


Although the earliest vertebrates appeared about 518 million years ago, so predating the first insects by about 130 million years, the creationists dogma of omniscience which they traditionally ascribe to their putative designer god, would mean this alleged designer was already aware of the less complex way to make 11-cis-retinal, when if supposedly designed the vertebrate method.

Besides, creationist dogma also says they were all created on the same day - 10,000 years ago.

Trumpanzee News - How QAnon Lured Gullible People Into The Trumpanzee Cult

How people get sucked into misinformation rabbit holes – and how to get them out

From our perspective in Europe, it seems almost incomprehensible how the political situation in the USA has degenerated to such an extent that Donald Trump may be elected as POTUS again, despite the incompetence, buffoonery and criminality that characterised his earlier term.

What was once the 'shining beacon on the hill', which set the rest of the world an example (albeit more than a little idealised) of how democracy operated to produce a prosperous, egalitarian society where aspiration and enterprise were rewarded and the economy worked for all, has degenerated to warring factions, full of mutual hate and fueled by the most ludicrous and lurid conspiracy theories.

A significant number of adult Americans now believe there is a 'deep state' run by senior Democrats, that operates as a Satanic paedophile cult and that the serial adulterer, insurrectionist and crook, Donald Trump, was personally appointed by God as their saviour, because God obviously takes a keen interest in US politics and would pick someone with a narcissistic personality disorder to do his work for him. This god also promised to ensure Trump was reelected 2020, so the fact that he was kicked out of office must have been due to the same deep state/Democrat conspiracy to steal the election - and then hide the evidence where even God can't guide Trump's supporters to it.

And of course, the serious criminal charges Trump is now facing in a number of different US courts, are all part of that conspiracy, as are the judges, prosecutors and prosecution witnesses, so the more damming the evidence and the more charges he faces are evidence of the conspiracy, not evidence of Trump's guilt and unsuitability to hold elected office, let alone be in charge of a nuclear arsenal and the US public finances, and able to appoint senior members of the judiciary.

The only real conspiracy in the USA is that run by the shadowy and rabidly far-right, pro-Trump QAnon, so how did the QAnon cult lure so many people down their particular paranoid rabbit hole to the extent that they are prepared to take up arms against their fellow countrymen and stage an attempted coup d'etat in the name of patriotism?

Creationism in Crisis - What Made Snakes Able To Evolve So Quickly 100 Million Years Before 'Creation Week'?

Lialis burtonis. Not a snake, but a legless gecko.

Image credit: Pascal Title, University of Michigan/Stony Brook University.

A false boa, Pseudoboa nigra, eating a lava lizard, Tropidurus hispidus.

Image credit: Ivan Prates, University of Michigan.

Snakes do it faster, better: How a group of scaly, legless lizards hit the evolutionary jackpot | University of Michigan News

100 million years ago the ancestral snake was just another lizard but then suddenly (on the evolutionary timescale) something happened that enables snakes to diversify into thousands of different species while the other lizards plodded along slowly, diversifying at a much slower rate than the snakes.

But what was it that allowed this sudden radiation into so many species and why did it give the snakes the edge over their cousins the lizards? It was an event that an international team led by University of Michigan biologists have called an evolutionary singularity, in an analogy with whatever was at the start of the Big Bang.

The team has estimated that snakes have evolved up to three times faster than lizard, an ability that was facilitated by three things - an elongated body and loss of legs; enhanced sensory detection enabling them to find and track prey, and a flexible skull that enabled them to swallow large prey.

In an attempt to understand this, the team assembled a large database of lizard and snake diets from examining the stomach contents of tens of thousands of museum specimens. They also sequenced the partial genomes of almost 1,000 species from which they were able to construct the evolutionary trees of lizards and snakes.

Their findings are the subject of a paper in Science and of a news release from the University of Michigan:

Abiogenesis News - Closing Creationism's Favourite Gap On Their Ever-Shrinking Little God

Hot Springs in Yellowstone National Park

Credit: iStock / tomolson54

Hot Spring in Yellowstone National Park.

Credit: iStock / tomolson54

Compound vital for all life likely played a role in life’s origin | UCL News - UCL – University College London

Abiogenesis is the gap creationists prefer to shoehorn their ever-shrinking little god into because they feel safer placing it there, believing that they have an unarguable claim that 'you can't get life from non-life'. Hilariously, you can sow confusion in their smug certainty in two simple ways:

1. Ask them to define 'life' and state whether it is a substance, a process or something else, because it only takes a moment's thought to realise 'life' is what we call the metabolic processes that organic molecules perform, so is simply the laws of chemistry and physics in operation. There is no magic ingredient needed.
2. Ask them what happens when the non-living food they eat becomes living tissues during the processes of digestion and assimilation if it is 'impossible'?

Their claim is nonsense of course; it's simply slogan delivered in response to trigger words which creationists no more understand than a parrot understands the meaning of the words it squawks.

There is nothing in the laws of chemistry or physics that makes abiogenesis impossible; given the right conditions there is no reason the inorganic chemicals present on the early Earth couldn't build more complex molecules or why those molecules couldn't perform the necessary processes to grow, repair and replicate. And once replication is possible, then selection would have been inevitable, and with selection, the processes which performed best would inevitably produce more copies.

Of course this can't be replicated easily in a laboratory because what no laboratory process can replicate is the long period of time, possibly millions of years, the process had on the early Earth, but what scientists can do is show that essential molecules to kick-start the processes could have arisen on the early Earth in the conditions that pertained then.

This is exactly what a team from University College London have shown in respect of a molecule which is the functional unit of one of the basic enzymes involved - Coenzyme A. The molecule is pantetheine. In earlier studies, pantetheine failed to be produced leading some to think that it would not have formed on early Earth and would therefore be absent and unable to play its essential role in metabolism.

Molecular structure of pantetheine

Creationism in Crisis - Evolution Of The Carnivores 315-251 Million Years Before 'Creation Week'

Inostrancevia, a more advanced predatory synapsid and one of the first sabertoothed carnivores, from the late Permian (~259-252 Million years ago). (Display at the Royal Ontario Museum, Canada)

Credit: Suresh A. Singh

Dimetrodon, an early predatory synapsid from the early Permian (~298-272 Million years ago). (Display at the Royal Tyrell Museum, Canada).

Credit: Suresh A. Singh

February : Killer instinct drove evolution of mammals’ predatory ancestors | News and features | University of Bristol

The ancestors of all modern mammals, the synapsids, first appeared in the fossil record long before the dinosaurs. Some were vegetarian while others were the top land predators for 60 million years before being replaced by the dinosaurs. Their evolution followed the same pattern of an arms race with their prey species in which the carnivores had to get better at killing to survive.

This gives the lie to the claim of any involvement of a single intelligent designer in their evolution since no intelligent designer worthy of the name would compete with itself in an arms race in which there are no winners or losers while all the time additional complexity is needed to keep up.

Tell me all about the synapsids, please. Synapsids are a group of vertebrates that includes mammals and their extinct relatives. They are characterized by several key features, including a single temporal opening behind the eye socket, teeth set in sockets, and a more erect posture compared to earlier reptiles. Synapsids first appeared during the late Carboniferous period, about 315 million years ago, and they were a dominant group throughout much of the Permian and Triassic periods. Here are some key points about synapsids:

1. Evolutionary History: Synapsids evolved from reptilian ancestors, specifically from a group called the pelycosaurs. One of the most famous pelycosaurs is Dimetrodon, which lived during the early Permian period and is often mistakenly identified as a dinosaur. Synapsids evolved further into two main groups: the therapsids and the cynodonts.
2. Therapsids: This group includes the most mammal-like synapsids. They had more advanced jaw structures, with larger temporal fenestrae (openings behind the eye socket) and specialized teeth. Therapsids diversified during the Permian period, with some species evolving into large herbivores like the iconic sail-backed Dimetrodon, while others were carnivorous predators. Towards the end of the Permian, some therapsids gave rise to the first true mammals.
3. Cynodonts: Cynodonts were a subgroup of therapsids that emerged during the late Permian and diversified extensively during the Triassic period. They exhibited several mammalian characteristics, including a more upright posture, specialized teeth, and possibly hair-like structures. Some cynodonts were quite small and likely had a lifestyle similar to modern mammals, while others were larger predators.
4. Mammalian Evolution: The transition from cynodonts to true mammals occurred during the Triassic period. Early mammals retained many reptilian features but also displayed characteristics that are distinctly mammalian, such as lactation and specialized jaw joints. By the end of the Triassic period, mammals had become more diverse and widespread.
5. Impact on Evolutionary History: Synapsids, particularly therapsids and cynodonts, played a crucial role in evolutionary history. They were among the dominant land vertebrates during the Permian and Triassic periods, occupying various ecological niches as herbivores, carnivores, and omnivores. The extinction of many synapsid groups at the end of the Permian, possibly due to environmental changes and the effects of the Permian-Triassic mass extinction event, paved the way for the rise of dinosaurs as the dominant land vertebrates during the Mesozoic Era.
6. Modern Descendants: The only surviving descendants of synapsids are mammals, which have diversified into a vast array of species occupying nearly every terrestrial and aquatic habitat on Earth. From tiny shrews to massive whales, modern mammals exhibit remarkable diversity in terms of size, shape, behavior, and ecological adaptations.

Overall, synapsids are a fascinating group of vertebrates that played a significant role in the evolutionary history of life on Earth, ultimately giving rise to the diverse and successful lineage of mammals that we see today.

Now a team of researchers from Bristol University, together with a colleague from the Open University, Milton Keynes, have traced the evolution of the carnivorous synapsid jaw and body size and discovered a major change in the jaw about 270 million years ago which would have been associated with a shift in the behaviour of these carnivores as they became better at killing their prey more quickly, so reducing the risk of injury.
Their findings are the subject of an open access paper in Communications Biology and is the subject of a Bristol University news release: