Malevolent Designer News - How Creationism's Divine Malevolence is Trying to Increase Suffering With its Monkeypox Virus

Monkeypox mutations cause virus to spread rapidly, evade drugs and vaccines, MU study finds // University of Missouri

Monkey pox virus particles

Creationists insist that all organisms are the work of their beloved creator god, without whom nothing exists and without whom nothing can evolve because changes in the genome require its intervention. Being omniscient, of course, Creationism's creator knows exactly what its modifications to organisms such as viruses will do, and creates them for that purpose.

So, what creationists would have us believe is that their beloved creator, or divine malevolence, as it should be called, based on its long history of creating pathogens and other parasites designed to make its creation suffer – if you believe Creationists - is that, fresh from its stunning success with the SARS-CoV-2 virus that caused the COVID-19 pandemic still raging across the world, it modified another nasty little virus to increase the suffering still further.

The virus in question is the Orthopox virus that caused the outbreak of Monkeypox, currently giving cause for concern to medical authorities throughout the world.

Orthopox viruses are a family of double-stranded DNA viruses which include variola (smallpox), cowpox and vaccinia. However, it is not ancestral to nor a descendant of variola. Until recently, following its identification as a disease of West African monkeys in 1965, it had been a low-level disease in humans, endemic to West Africa and the Congo Basin, with symptoms similar to, but not as severe as, smallpox. Then is suddenly mutated, broke out of its enclave in West Africa and has now infected more than 77,000 people in more than 100 countries worldwide.

A team of researchers at the University of Missouri have identified the specific mutations in the monkeypox virus that contribute to its continued infectiousness. Or as a Creationist must believe, the specific modifications their divine malevolence made to it to make it more infectious and better able to evade antiviral drugs and vaccinations, so more people would suffer from it.

The University of Missouri news release explains the discovery and how the team made them:

Our focus is on looking at the specific genes involved in copying the virus genome, and monkeypox is a huge virus with approximately 200,000 DNA bases in the genome. The DNA genome for monkeypox is converted into nearly 200 proteins, so it comes with all the ‘armor’ it needs to replicate, divide and continue to infect others. Viruses will make billions of copies of itself and only the fittest will survive, as the mutations help them adapt and continue to spread.

When they sent me the data, I saw that the mutations were occurring at critical points impacting DNA genome binding, as well as where drugs and vaccine-induced antibodies are supposed to bind. These factors are surely contributing to the virus’ increased infectivity. This work is important because the first step toward solving a problem is identifying where the problem is specifically occurring in the first place, and it is a team effort.

One hypothesis is when patients were being treated for HIV and herpes with these drugs, they may have also been infected with monkeypox without knowing, and the monkeypox virus got smarter and mutated to evade the drugs. Another hypothesis is the monkeypox virus may be hijacking proteins we have in our bodies and using them to become more infectious and pathogenic.

Professor Kamlendra Singh. corresponding author
Bond Life Sciences Center
And Department of Veterinary Pathobiology
University of Missouri, Columbia, MO, USA

Kamlendra Singh, a professor in the MU College of Veterinary Medicine and Christopher S. Bond Life Sciences Center principal investigator, collaborated with Shrikesh Sachdev, Shree Lekha Kandasamy and Hickman High School student Saathvik Kannan, to analyze the DNA sequences of more 200 strains of monkeypox virus spanning multiple decades, from 1965, when the virus first started spreading, to outbreaks in the early 2000s and again in 2022.

By doing a temporal analysis, we were able to see how the virus has evolved over time, and a key finding was the virus is now accumulating mutations specifically where drugs and antibodies from vaccines are supposed to bind. So, the virus is getting smarter, it is able to avoid being targeted by drugs or antibodies from our body’s immune response and continue to spread to more people.

Shrikesh Sachdev, co-author
Bond Life Sciences Center
University of Missouri, Columbia, MO, USA

Needles in a haystack

Singh has been studying virology and DNA genome replication for nearly 30 years. He said the homology, or structure, of the monkeypox virus is very similar to the vaccinia virus, which has been used as a vaccine to treat smallpox. This enabled Singh and his collaborators to create an accurate, 3D computer model of the monkeypox virus proteins and identify both where the specific mutations are located and what their functions are in contributing to the virus becoming so infectious recently.

Kannan and Kandasamy examined five specific proteins while analyzing the monkeypox virus strains: DNA polymerase, DNA helicase, bridging protein A22R, DNA glycosylase and G9R. The evolution of viruses Researchers continue to question how the monkeypox virus has evolved over time. The efficacy of current CDC-approved drugs to treat monkeypox have been suboptimal, likely because they were originally developed to treat HIV and herpes but have since received emergency use authorization in an attempt to control the recent monkeypox outbreak.

The team found that over time, 10 mutations had occurred since the reference year (1965). Four of them affected proteins which enable it to bind to the host, or improved DNA replication, three of which all emerged some time during 2022 and one in 2018. Of the remaining 6, they all appear to have reverted back to their 1965 form. Presumably, Creationists would claim the creator changed his mind and tried some new mutations.

Although behind a paywall, the full paper can be read in the Journal of Autoimmunity:

Highlights

• L108F in MPXV DNA polymerase emerged in the 2022 outbreak.
• L108F can enhance DNA binding affinity, processivity and drug sensitivity of F8L.
• Mutation L108F can change the fidelity and sensitivity to nucleoside inhibitors.
• G9R mutations that emerged in 2022, are likely to affect interaction of G9R with E4R.

Abstract

Attributes contributing to the current monkeypox virus (MPXV) outbreak remain unknown. It has been established that mutations in viral proteins may alter phenotype and pathogenicity. To assess if mutations in the MPXV DNA replication complex (RC) contribute to the outbreak, we conducted a temporal analysis of available MPXV sequences to identify mutations, generated a DNA replication complex (RC) using structures of related viral and eukaryotic proteins, and structure prediction method AlphaFold. Ten mutations within the RC were identified and mapped onto the RC to infer role of mutations. Two mutations in F8L (RC catalytic subunit), and two in G9R (a processivity factor) were ∼100% prevalent in the 2022 sequences. F8L mutation L108F emerged in 2022, whereas W411L emerged in 2018, and persisted in 2022. L108 is topologically located to enhance DNA binding affinity of F8L. Therefore, mutation L108F can change the fidelity, sensitivity to nucleoside inhibitors, and processivity of F8L. Surface exposed W411L likely affects the binding of regulatory factor(s). G9R mutations S30L and D88 N in G9R emerged in 2022, and may impact the interaction of G9R with E4R (uracil DNA glycosylase). The remaining six mutations that appeared in 2001, reverted to the first (1965 Rotterdam) isolate. Two nucleoside inhibitors brincidofovir and cidofovir have been approved for MPXV treatment. Cidofovir resistance in vaccinia virus is achieved by A314T and A684V mutations. Both A314 and A684 are conserved in MPXV. Therefore, resistance to these drugs in MPXV may arise through similar mechanisms.

Kannan, Saathvik R.; Sachdev, Shrikesh; Reddy, Athreya S.; Kandasamy, Shree Lekha; Byrareddy, Siddappa N.; Lorson, Christian L.; Singh, Kamal
Mutations in the monkeypox virus replication complex: Potential contributing factors to the 2022 outbreak
Journal of Autoimmunity (2022); 133, 102928. DOI: 10.1016/j.jaut.2022.102928

© 2022 Elsevier B.V..
Reprinted under the terms of the Copyright, Designs and Patents Act 1988, s60.

Of course, what the team found is that the virus is evolving under selection pressure, especially in the parts of its DNA that are the targets of vaccines and antiviral drugs. Antibodies and antiviral drugs are the environmental factors that select for those mutants which can ignore them. This is bog standard evolution at work.
Sadly for Creationists though, they are obliged by dogma to deny evolution as the cause of these mutations and so of the growing problem of monkeypox, and give all the credit to their imaginary creator friend, with all the connotations that carries.

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