One of creationism's putative major success in the last 100 years, has been its new (as of 2019) coronavirus, SARS-CoV-2 (Severe Acute Respiratory Syndrome – Corona Virus - 2.
According to the WHO, as of 11 August 2024, there have been 775,917,102, cases worldwide (increasing at about 40,000 new cases per week) with 7,058,381 deaths (increasing at about 900 per week), despite the fact that 13.64 billion doses of COVID vaccine have been administered.
What information do you have on the evolutionary history of SARS-CoV-2 since the initial wave in 2019-2020? The evolutionary history of SARS-CoV-2, the virus responsible for COVID-19, has been marked by the emergence of several variants with distinct genetic changes since the initial outbreak in late 2019. Here’s a detailed overview of the virus’s evolution:And, despite the fantastic efforts of medical scientists, the virus keeps on mutating to evade any immunity we have, either acquired by infection or received via vaccination.
Conclusion
- Initial Strain (Wuhan-Hu-1)
- Emergence: SARS-CoV-2 was first identified in Wuhan, China, in late 2019. The original strain, often referred to as the "Wuhan strain" or "Wuhan-Hu-1," rapidly spread worldwide, leading to the COVID-19 pandemic.
- Characteristics: This initial strain had a relatively stable genetic profile with a low mutation rate compared to other RNA viruses.
- Early Variants (2020)
- D614G Mutation: One of the first significant mutations was the D614G mutation in the spike protein. By mid-2020, this variant had become the dominant strain globally. The D614G mutation was associated with increased infectivity, though it didn’t appear to cause more severe disease.
- Other early variants: Several other minor variants circulated, but none had a significant impact on the course of the pandemic at this stage.
- Alpha Variant (B.1.1.7) - Late 2020
- Emergence: First identified in the UK in September 2020, the Alpha variant spread rapidly and became dominant in many countries by early 2021.
- Key Mutations: It had multiple mutations, including N501Y in the spike protein, which increased its transmissibility.
- Impact: The Alpha variant was more transmissible than previous strains, leading to larger outbreaks and increased pressure on healthcare systems.
- Beta (B.1.351) and Gamma (P.1) Variants - Late 2020 to Early 2021
- Beta Variant: First identified in South Africa, this variant contained the E484K mutation, which allowed it to partially evade immunity from previous infection or vaccination.
- Gamma Variant: Identified in Brazil, it shared several mutations with Beta, including E484K, and was associated with reinfections.
- Delta Variant (B.1.617.2) - Mid 2021
- Emergence: Detected in India in late 2020, the Delta variant became globally dominant by mid-2021.
- Key Characteristics: Delta was more transmissible than Alpha and was associated with increased severity of illness. It also showed some immune evasion, reducing the effectiveness of vaccines, although they remained effective at preventing severe disease and death.
- Impact: Delta led to significant surges in cases and hospitalizations worldwide.
- Omicron Variant (B.1.1.529) - Late 2021 to Present
- Emergence: First identified in South Africa and Botswana in November 2021, Omicron quickly spread globally, becoming the dominant strain by early 2022.
- Key Mutations: Omicron has an unusually high number of mutations, particularly in the spike protein. These mutations allow for significant immune evasion, reducing the effectiveness of prior immunity from infection or vaccination.
- Sublineages: Omicron has diversified into numerous sublineages, including BA.1, BA.2, BA.4, BA.5, and more recently, variants such as XBB.1.5 and EG.5. These sublineages have shown varying degrees of immune evasion and transmissibility.
- Impact: Omicron and its subvariants have caused multiple waves of infection, although they are generally associated with less severe disease compared to Delta, particularly in vaccinated individuals.
- Current Trends (2023-2024)
- Ongoing Evolution: SARS-CoV-2 continues to evolve, with new variants and subvariants emerging. The virus’s genetic diversity is increasing, with ongoing surveillance needed to monitor the emergence of potentially more transmissible or immune-evasive variants.
- Immune Evasion: Newer Omicron subvariants continue to show immune evasion capabilities, leading to breakthrough infections even in fully vaccinated individuals, although vaccines still provide significant protection against severe disease.
- Long-Term Evolutionary Trends
- Antigenic Drift: Similar to influenza, SARS-CoV-2 is expected to continue evolving through antigenic drift, with periodic updates to vaccines likely required to maintain immunity in the population.
- Endemicity: SARS-CoV-2 is likely transitioning to an endemic virus, with seasonal surges influenced by factors such as population immunity, variant characteristics, and public health measures.
The evolutionary history of SARS-CoV-2 highlights the virus’s capacity for rapid mutation and adaptation. Each significant variant has had distinct impacts on transmissibility, immune evasion, and disease severity, shaping the global response to the pandemic. Ongoing monitoring and adaptation of public health strategies will be crucial as the virus continues to evolve.
There is also a nasty little sting in the tail of infection because, built into the design' is the ability to cause 'long COVID', i.e., debilitating symptoms that persist for months or longer after recovery from the initial infection, and it is in regards to this aspect of the virus' ability that a research team at Northwestern University and the University of Illinois-Chicago have just announced a breakthrough.
They have discovered that a deletion in the spike protein on the surface of the virus is what enables it to penetrate brain cells! Creationists might like to ponder on that discovery because it contravenes what they insist is a basic principle of genetics that all mutations are invariably deleterious and yet here we have an advantageous mutation from the point of view of the virus that involves a reduction in genetic information!
And that introduces another problem for creationists because these mutations, which in every case have made the virus more successful, can't honestly be waved aside as 'devolution' caused by 'genetic entropy', because something that improves on what preceded it can't logically be described as less perfect or the nonsensical term 'devolved'. In biology, of course, there is not, and never was, perfection.
The result of evolution is only ever something better in the environment in which there are natural selectors. A perfect organism would not be able to evolve of change in any way since there could never be any variations for natural selection to work on.
And that leaves intelligent [sic] design creationists the task of explaining why a supposedly omnibenevolent creator god is working to design ever better viruses for making us sick, rather than have us accept that this is the result of a natural evolutionary process in which no god-magic was involved.
The UK Office for National Statistics has estimated that 1.9 million people in the UK were suffering from self-reported 'long COVID'.
1. Main points
- An estimated 1.9 million people living in private households in the UK (2.9% of the population) were experiencing self-reported long COVID (symptoms continuing for more than four weeks after the first confirmed or suspected coronavirus (COVID-19) infection that were not explained by something else) as of 5 March 2023 (see Figure 1).
- Of people with self-reported long COVID, 83,000 (4%) first had (or suspected they had) COVID-19 less than 12 weeks previously, 1.7 million people (92%) at least 12 weeks previously, 1.3 million (69%) at least one year previously and 762,000 (41%) at least two years previously.
- Of people with self-reported long COVID, 545,000 (29%) first had (or suspected they had) COVID-19 before Alpha became the main variant; this figure was 247,000 (13%) in the Alpha period, 327,000 (17%) in the Delta period and 698,000 (37%) in the Omicron period.
- Long COVID symptoms adversely affected the day-to-day activities of 1.5 million people (79% of those with self-reported long COVID), with 381,000 (20%) reporting that their ability to undertake their day-to-day activities had been “limited a lot”.
- Fatigue continued to be the most common symptom reported as part of individuals’ experience of long COVID (72% of those with self-reported long COVID), followed by difficulty concentrating (51%), muscle ache (49%) and shortness of breath (48%).
- As a proportion of the UK population, the prevalence of self-reported long COVID was greatest in people aged 35 to 69 years, females, people living in more deprived areas, those working in social care, those aged 16 years and over who were not working and not looking for work, and those with another activity-limiting health condition or disability.
Source: UK ONS
The research team have just published their findings in Nature Microbiology and announced them in a Northwestern University press release:
Spike mutations help SARS-CoV-2 infect the brain
‘This could help us understand neurological symptoms of COVID-19’
Scientists have discovered a mutation in SARS-CoV-2, the virus that causes COVID-19, that plays a key role in its ability to infect the central nervous system. The findings may help scientists understand its neurological symptoms and the mystery of “long COVID,” and they could one day even lead to specific treatments to protect and clear the virus from the brain.
- Still unknown what causes neurological complications of COVID-19 including ‘long COVID,’ ‘brain fog’ and loss of taste and smell
- Viruses with a deletion in the spike protein are better able to infect the brains of mice
- ‘These findings suggest there might be treatments that could work better to clear the virus from the brain’
The new collaborative study between scientists at Northwestern University and the University of Illinois-Chicago uncovered a series of mutations in the SARS-CoV-2 spike protein (the outer part of the virus that helps it penetrate cells) that enhanced the virus’ ability to infect the brains of mice.
Looking at the genomes of viruses found in the brain compared to the lung, we found that viruses with a specific deletion in spike were much better at infecting the brains of these animals. This was completely unexpected, but very exciting.
Assistant Professor Judd F. Hultquist, co-corresponding author
Assistant professor of medicine (infectious diseases) and microbiology-immunology
Feinberg School of Medicine.
Northwestern University.
The study was published Aug. 23 in Nature Microbiology.
Changes in spike help the virus infect different cells in the body
In this study, researchers infected mice with SARS-CoV-2 and sequenced the genomes of viruses that replicated in the brain versus the lung. In the lung, the spike protein looked very similar to the virus used to infect the mice. In the brain, however, most viruses had a deletion or mutation in a critical region of spike that dictates how it enters a cell. When viruses with this deletion were used to directly infect the brains of mice, it was largely repaired when it traveled to the lungs.
In order for the virus to traffic from the lung to the brain, it required changes in the spike protein that are already known to dictate how the virus gets into different types of cells. We think this region of spike is a critical regulator of whether or not the virus gets into the brain, and it could have large implications for the treatment and management of neurological symptoms reported by COVID-19 patients.
Assistant Professor Judd F. Hultquist.
SARS-CoV-2 has long been associated with various neurological symptoms, such as the loss of smell and taste, “brain fog” and “long COVID.”
It’s still not known if long COVID is caused by direct infection of cells in the brain or due to some adverse immune response that persists beyond the infection. If it is caused by infection of cells in the central nervous system, our study suggests there may be specific treatments that could work better than others in clearing the virus from this compartment.
Assistant Professor Judd F. Hultquist.
The generation of new variants in the brain could produce new variants of concern in the population, said co-corresponding author Justin Richner, assistant professor of microbiology and immunology at UIC.
It could be that the virus is using these different tissue sites to evolve into new, different variants, and then those can traffic back into the respiratory tract and then spread throughout the population. Potentially this could be a source of novel variants of concern that emerge in the population.
Justin M. Richner, co-corresponding author Department of Microbiology and Immunology
College of Medicine
University of Illinois Chicago, Chicago, IL, USA.
Other Northwestern authors on the study include Lacy M. Simons, Tanushree Dangi, Egon A. Ozer, Pablo Penaloza-MacMaster and Ramon Lorenzo-Redon.
AbstractSo, a couple of points for creationists to ignore here:
Severe coronavirus disease 2019 and post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are associated with neurological complications that may be linked to direct infection of the central nervous system (CNS), but the selective pressures ruling neuroinvasion are poorly defined. Here we assessed SARS-CoV-2 evolution in the lung versus CNS of infected mice. Higher levels of viral divergence were observed in the CNS than the lung after intranasal challenge with a high frequency of mutations in the spike furin cleavage site (FCS). Deletion of the FCS significantly attenuated virulence after intranasal challenge, with lower viral titres and decreased morbidity compared with the wild-type virus. Intracranial inoculation of the FCS-deleted virus, however, was sufficient to restore virulence. After intracranial inoculation, both viruses established infection in the lung, but dissemination from the CNS to the lung required the intact FCS. Cumulatively, these data suggest a critical role for the FCS in determining SARS-CoV-2 tropism and compartmentalization.
Class, J., Simons, L.M., Lorenzo-Redondo, R. et al.
Evolution of SARS-CoV-2 in the murine central nervous system drives viral diversification. Nat Microbiol (2024). https://doi.org/10.1038/s41564-024-01786-8
© 2024 Springer Nature Ltd.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.
- Firstly the evidence of evolution by loss of genetic information.
- Secondly, the evidence of malevolence in the design of a virus to evade our immunity and still cause suffering even after we've recovered from the acute phase of the illness it causes - if you subscribe to the intelligent [sic] design notion, that is.
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.
Illustrated by Catherine Webber-Hounslow.
Available in Hardcover, Paperback or ebook for Kindle
Illustrated by Catherine Webber-Hounslow.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
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.
Available in Hardcover, Paperback or ebook for Kindle
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