Preventing genomic entropy

Transposons—thought to be related to viruses—can copy themselves and insert randomly around the genome. A paper published today (October 15) in Science provides a greater understanding of how cells shut down these rogue jumping genes.

My comment: Shouldn’t someone else be claiming that nutrient-dependent microRNAs prevent the accumulation of viral microRNAs that leads to perturbed protein folding, which links mutations to all pathology in the context of an atoms to ecosystems model?
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Abstract introduction:

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements.

Abstract conclusion:

Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

See also:  “every angstom is dynamic from the 5 prime to the three” in this “cutting edge” musical parody by fun-loving biophysicists who know how to link top-down causation from physics to chemistry and biology via the conserved molecular mechanisms of epigenetic cause and effect.
If you don’t want to attribute the dynamics of every angstom to the epigenetic effects of nutrient energy, are you a neo-Darwinian evolutionary theorist or merely someone else who is equally biologically uninformed?
See also: The decline of human endogenous retroviruses: extinction and survival
Excerpt:

Retroviral replication involves integration into a chromosome of the host cell. Over the last 100 million years (my), retroviruses have repeatedly integrated into germline cells of their host and thus become incorporated into the host genome [1]. Such Endogenous Retroviruses (ERVs) can be grouped into families [2], each one representing the subsequent proliferation of an independent infection of the host genome. Each viral integration is referred to here as a locus, and these loci inevitably accumulate mutations at the host background level, gaining frameshifts and premature stop codons that make them replication-deficient. It is only by the continual copying of loci that the family persists through evolutionary time. There are ~100,000 ERV loci in ~50 families (also called groups) in the human genome [3],[4] making up ~5% of the total sequence (>8% if the other transposable elements called MaLRs are included) [5].

My comment: If the nutrient-dependent epigenetic effects of microRNA-delivered energy did not biophysically constrain the viral microRNAs that perturb the energy-dependent differentiation of all cell types, all individuals of all species would by now have mutated themselves out of existence.  Claims by theorists that species mutated into existence over the last 100 million years seemed to be relatively harmless after neo-Darwinian theory was invented by population geneticists.
Serious scientists can now see how those ridiculous claims will lead to the death of us all by evolutionary theory. The neo-Darwinists have started to include viruses in claims about co-evolution, but they refuse to admit that RNA-mediated events link ecological variation to ecological adaptations that they claim are examples of co-evolution.
Most, if not all, their examples of co-evolution will continue to link microbes to man via the nutrient-dependent pheromone-controlled physiology of reproduction that links the epigenetic landscape to the physical landscape of DNA via metabolic networks and genetic networks with as little as one RNA-mediated amino acid substitution to differentiate all the cell types of all cells in all individuals of all living genera via the requirement to respond to single amino acid substitutions in viruses.
See for example: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution
The authors’ comment is a classic:

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

After they detailed the fact that amino acid substitutions are biophysically constrained in the context of  glucose-dependent ecological adaptation and reported the nutrient-dependent ecological adaptations in viruses, I commented on the article. This published comment was removed and replaced by the authors’ comment:

The idea of biophysical constraints seems antithetical to the idea of nature somehow selecting mutations that cause amino acid substitutions. However, I am not a biophysicist or evolutionary theorist.
The problem may be my focus on nutrient-dependent receptor-mediated amino acid substitutions in species from bacteria to humans (non-viral organisms). Since I am not a virologist or physicist, [Sarcasm alert] I’m not sure that the laws of physics apply to viruses and their replication.
If they do, natural selection for random mutations is not likely to result in amino acid substitutions because the thermodynamics of changes in organism-level thermoregulation preclude such randomness. Stability of protein biosynthesis and degradation that probably depends on protein folding must somehow be controlled. Besides, I don’t know how random mutations in viruses could be naturally selected for inclusion in the human virome (or in the virome of any organism capable of thermoregulating its thermodynamic intercellular signaling).
[Sarcasm alert] If the Second Law of Thermodynamics does not apply to viruses, which means the chemical bonds that enable the amino acid substitutions can form at random and somehow be naturally selected, the details of biophysical constraints in this article seems out of place, since I do not think in terms of constrained random mutations and natural selection in mutation-driven evolution.
Hopefully, someone with a background in biophysics will address my confusion in case others are confused. In addition, I wonder if the consequences of understanding the evolutionary mechanisms that govern viruses extend to consequences important to understanding the evolution of species from bacteria to humans via constrained random mutations and natural selection?

Most teachers know that their students may not understand sarcasm at the time it is used in attempts to make a point. For example, there are times when it can be used to denigrate the works of neo-Darwinists, but most evolutionary theorists will not understand the sarcasm of statements like these:

I’m bringin’ Franklin back. Go ahead and tell the Nobel Winners that.

My comment: Rosalind Elsie Franklin (25 July 1920 – 16 April 1958)^[1] was an English chemist and X-ray crystallographer who made contributions to the understanding of the fine molecular structures of DNA (deoxyribonucleic acid), RNA (ribonucleic acid), viruses, coal, and graphite.^[2] Although her works on coal and viruses were appreciated in her lifetime, her DNA work posthumously achieved profound impact as DNA plays a central role in biology, as it carries the genetic information that is passed from parents to their offspring.
The 2015 Nobel Laureates in Physics, Chemistry, and Physicology and/or Medicine brought Franklin back by linking neutrinos via physics and chemistry to the biological basis of nutrient-dependent RNA-mediated DNA repair that protects all organized genomes from virus-induced genomic entropy. Few teachers understand the role of viruses in cell type differentiation. Light is a virucide; it kills viruses. Viruses prevent cell type differentiation! Most teachers and most students do not understand statements like these: