Virus-driven death by evolutionary theory

Distinct lineages of Ebola virus in Guinea during the 2014 West African epidemic


The data presented here indicates EBOV is able to generate and fix nucleotide and amino acid variation within co-circulating viral lineages on the time-scale of individual outbreaks, including the presence of country-specific lineages, and which may ultimately produce variants with important fitness differences.

Reported as: Three Ebola virus variants identified in Guinea.

Excerpt 1)
The Ebola epidemic has been ongoing in West Africa for over a year, with 27,341 reported cases, of which 11,184 have been fatal[1].

Excerpt 2):

Each variant is defined by a combination of mutations affecting different viral proteins, in particular the VP35 protein, which may be a virulence factor; the virus envelope glycoprotein, which may alter the immune system’s perception of the virus; or the polymerase, which is usually a more conserved viral region.

My comment: Each variant arises via fixation of amino acid substitutions that differentiate the cell types of all genera. The link from viral microRNAs to entropic elasticity and the anti-entropic epigenetic effects of nutrient-dependent fixation of amino acid substitutions also links DNA repair to thermodynamic cycles of protein biosynthesis and degradation. The cycles enable nutrient-dependent fixation of the variants in the viruses and organism-level thermoregulation in living organisms.
Theorists who do not know the difference between an amino acid substitution and a mutation may lead to the death of us all before serious scientists and science journalists begin to report on how RNA-mediated cell type differentiation occurs. Currently, most people seem to believe that mutations cause cell type differentiation because they believe in ridiculous theories.
See also: Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak and Identifying Recent Adaptations in Large-Scale Genomic Data
Excerpt 1):

As natural selection can only act on mutations that drive phenotypic variation…

The ridiculous claim that natural selection can only act on mutations that drive phenotypic variation has been repeated often enough to automatically be included in articles that clearly attest to biophysically constrained RNA-mediated links from the epigenetic landscape to the physical landscape of DNA in all genera.  See also:
Excerpt 2)

TLR5 is a well-described Toll-like receptor that plays a crucial role in the immunological clearance of bacterial pathogens. Its ligand, flagellin, is the principal component of the bacterial flagellum and is one of the most abundantly expressed proteins in nearly all flagellated bacteria.

The claim that the bacterial flagellum of one species re-evolved over-the-weekend can be placed into the context of virus-driven ecological adaptations that are nutrient-dependent and pheromone-controlled in species from microbes to man via the conserved molecular mechanisms of RNA-mediated cell type differentiation that have been detailed since the time of our 1996 review: From Fertilization to Adult Sexual Behavior
See also my comments on: Evolution is unpredictable and irreversible, biologists show.
Summary: RNA-mediated cell type differentiation is perfectly predictable. It leads to ecological adaptation or extinction of populations and species.
See also: Scientists pinpoint mutations responsible for ineffective 2014-2015 flu vaccine

Our studies show that flu viruses recently acquired mutations in critical regions that are recognized by our immune system,” Hensley said. “These new mutations likely contributed to the ineffectiveness of flu vaccines during the 2014-2015 flu season.”

See also: Amino Acid Changes in Hemagglutinin Contribute to the Replication of Oseltamivir-Resistant H1N1 Influenza Viruses 
Mutations perturb protein folding, which is why they are not fixed in the organized genomes of any living species. Amino acid substitutions stabilize the organized genomes of species from microbes to man via nutrient-dependent microRNAs that prevent the genomic entropy caused by viral microRNAs. The amino acid substitutions are fixed in the context of the physiology of reproduction in living organisms and in the context of nutrient-dependent replication in viruses.
That fact links viruses to pathology and nutrients to RNA-mediated health via the biophysically constrained chemistry of nutrient-dependent protein folding in all genera.
Think about that the next time you learn that someone died from a viral infection.
Evolutionary theory killed them as surely as the theorists claim it was a virus that mutated.
See also: Europe’s first humans: what scientists do and don’t know

No one knows why Neanderthals went extinct soon after humans arrived in Europe. Bar-Yosef, like many scientists, sees humans as an invasive force that occupied Europe’s prime land, pushing Neanderthals into more marginal regions such as the Iberian Peninsula. But researchers have blamed the demise of Neanderthals on climate, disease and even domestic dogs.

My comments: Serious scientists know that modern human populations are among the other populations of ecologically adapted organisms. They know that viral microRNAs wiped out the Neanderthals who could not acquire the nutrient-dependent microRNAs that link entropic elasticity to the anti-entropic effects of nutrients on the biophysically constrained chemistry of protein folding in all genera via the physiology of their reproduction.
See also: How to build a Neanderthal

Epigenetic maps help to explain how archaic humans differed from modern ones despite having very similar DNA sequences.

My comment: RNA-mediated events link the epigenetic landscape to nutrient-dependent amino acid substitutions; organism-level thermoregulation; and to species survival via thermodynamic cycles of biophysically constrained protein biosynthesis and degradation.

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