Is there anyone who is still touting neo-Darwinian pseudoscientific nonsense who understands how the transgenerational epigenetic inheritance of Zika virus damage must be linked to all energy-dependent RNA-mediated cell type differentiation or from the virus-driven degradation of messenger RNA to all pathology?

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See for comparison:

Direct radiocarbon dating and genetic analyses on the purported Neanderthal mandible from the Monti Lessini (Italy)


If materials from sites excavated long ago (e.g. Riparo Mezzena) are to be used to provide additional data on these complex phases of our evolutionary history, then it should only be done using the whole suite of state-of-the-art methods at our disposal.

My comment: The state-of-the-art methods at everyone’s disposal link energy-dependent RNA methylation to all biodiversity.  All state-of-the-art methods at your disposal link virus-driven energy theft to all pathology via what is known to serious scientists about biophysically constrained protein folding chemistry and the physiology of reproduction.

What is currently known about the epigenetics of gene expression has replaced ridiculous theories that were based on pseudoscientific nonsense. For example, no serious scientist believes that de Vries 1902 definition of “mutation” can be linked to assumptions about how many accumulated mutations it might take to cause one species to evolve into another. Why would anyone try to cast doubts on facts about energy theft and cell type differentiation?

Researchers Cast Doubt on CRISPR-Like System in Giant Viruses


“MIMIVIRE is not analogous to the CRISPR-Cas system, does not function via a nucleic acid recognition system, and is unlikely to possess all the attributes of a bona fide adaptive immune system,” Claverie and Abergel wrote in their paper.

My comment: The problem for neo-Darwinists is the fact that RNA-mediated amino acid substitutions have already been linked to virulence by one substitution in the influenza virus and energy-dependent ecological adaptation has been linked to substitutions in all hosts.

The failed attempt to portray viruses-in-viruses as if they could replicate outside the context of energy-dependent links from angstroms to ecosystems may be one of the final failures of theorists who do not recognize any aspect of how cell type differentiation occurs.

If all cell types in all cells of all living genera are protected from viruses by an innate immune system that has not been found in viruses, these reported results attest to the claims of young earth creationists and Paul M. Lieberman, who wrote:

“…viral latency is responsible for life-long pathogenesis and mortality risk…” — Epigenetics and Genetics of Viral Latency

See also: Viral Genome Junk Is Bunk


…the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6″

2/29/16 MIMIVIRE is a defense system in mimivirus that confers resistance to virophage

Reported as: Giant Virus Has CRISPR-like Immune Defense

6/19/16 CRISPR-Cas-like system in giant viruses: why MIMIVIRE is not likely to be an adaptive immune system

Reported as: Researchers Cast Doubt on CRISPR-Like System in Giant Viruses

5/18/16 N (6)-Methyladenosine (m(6)A) Methylation in mRNA with A Dynamic and Reversible Epigenetic Modification

The report from 5/18/16 does not seem to have been reported in any science news outlet

2/10/16 The dynamic N1-methyladenosine methylome in eukaryotic messenger RNA

Reported as: RNA modification discovery suggests new code for control of gene expression

See also: In an attempt to discuss what is known to serious scientists about biophysically constrained RNA-mediated protein folding chemistry and how RNA-mediated amino acid substitutions are linked to supercoiled DNA, which protects all organized genomes from virus-driven entropy, I commented on this news:

Breakthrough in understanding how stem cells become specialized (discussion)


Sebastian Aguiar Brunemeier What kind of experiment would you design that would prove your hypothesis true? That being “virus-driven energy theft as the cause of all pathology.”

That’s quite a claim, “all pathology.” Surely you mean “more than we believe today” but as far as aging goes, there are plenty of other primary causes as described in The Hallmarks of Aging.


A Post Doc who threatened me with litigation wrote:

We house our animal mouse models in pathogen free environments (aside from transponson). They still age and die with pathological features. Sorry

He failed to consider the role that endogenous retroviruses play. They prevent the light-activated assembly of the microRNA-RNA-peptide nanocomplex link from endogenous substrates to biophysically constrained viral latency.

Addendum:  What’s the Water at the Church Lab? A Conversation Between George Church and Jorge Conde

The link from the Virus-mediated archaeal hecatomb in the deep seafloor to what’s in the water at the Church Lab established the fact that all pathology is caused by the virus-driven degradation of messenger RNA, which links mutations to diseases — not to the evolution of new species via food energy pheromone-controlled sympatric speciation in organisms from microbes to humans.

See also: Systems of Connected and Aggregated Enzyme Reactions

Reported on 8/6/16 as: Systems of Connected and Aggregated Enzyme Reactions

It is often explicitly, or implicitly, considered that an enzyme reaction occurring under steady state conditions is a system that collects connected states of the enzyme that appear during the reaction. Moreover, there is little doubt that many enzymes in vivo are aggregated as multienzyme complexes in such a way that one can wonder whether the corresponding enzyme reactions are not aggregated to form a functional structure that connects and associates the elementary reactions as to form a coherent whole. The rate equation of the global system of Figure 3 becomes more complex than the individual equations of the enzymes E1 and E2 in isolation. However, one can notice that the global system is dependent upon antagonistic effects exerted by system 1. A first effect is a tendency to drift towards thermodynamic equilibrium. This tendency is exerted through the rate constants of substrate binding and release.

Why do people like Sebastian Aguiar Brunemeier – who claims to be a Fulbright Research Fellow on the molecular biology of aging — and the post doc fellow who supposedly is paid to do research on aging  — ask about experimental design or comment on their pathogen-free environments?

All aspects of biophysically constrained protein folding chemistry are energy-dependent and RNA-mediated in the context of the physiology of reproduction, which links the innate immune system to supercoiled DNA. The anti-entropic virucidal energy of ultraviolet light from the sun is the only known link to thermodynamic cycles of protein biosynthesis and degradation in the context of healthy longevity, and virus-driven energy theft is the only known link to all pathology.

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