Amino acids and virus penetration

By: James V. Kohl | Published on: June 16, 2016

For an example of the ocean of information you must swim through to get to an important fact about virus-driven energy theft and all pathology, see:

The bacteriophage ϕ29 tail possesses a pore-forming loop for cell membrane penetration (June 15, 2016)

They citePrDOS: prediction of disordered protein regions from amino acid sequence” (2007).


We have also developed a system to predict disordered regions from the amino acid sequence. Our system is composed of two predictors, that is, a predictor based on the local amino acid sequence, and one based on template proteins (or homologous proteins for which structural information is available).

The June 15, 2016 article does not mention this fact: “The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.”(2013)

The theft of quantized energy that links the amino acid substitution in the virus to pathology is an important consideration. Without the energy theft, RNA methylation would link hydrogen-atom transfer in DNA base pairs in solution to energy-dependent changes in angstroms that are required for to link energy to healthy longevity in the context of ecosystem complexity and biodiversity that links microbes to humans via the physiology of reproduction.

See also: RNA-mediated degradation of microRNAs: A widespread viral strategy?

Abstract excerpt:

We review what is known about RNA-mediated regulation of miRNA stability and propose 3 potential roles that viral non-coding RNAs might assume to initiate the destruction of a miRNA…

See also: N6-methyladenosine marks primary microRNAs for processing


we have identified m6A as a novel regulator of miRNA processing. Our findings reveal that METTL3 methylates primary inter- and intragenic miRNAs. The  m6A modification facilitates the recognition of pri-miRNA sequences and marks an initiation event in miRNA biogenesis (Fig. 4i) We propose that the m6A mark on transcripts at pri-miRNA sequences initiates a global co-transcriptional program comprising the engagement and processing of primary miRNAs by the microprocessor machinery.The m6A mark thus has an important role in the nucleus—allowing the microprocessor complex to recognize its specific substrates as opposed to unintended secondary structures. Additionally, altered METTL3 expression in various human malignancies may contribute to the aberrant expression of miRNAs seen in cancer.

See also: N6-methyladenosine-dependent RNA structural switches regulate RNA-protein interactions


All these results confirmed that m6A modification can alter its local RNA structure and enhance the accessibility of its base-paired residues or nearby regions to modulate protein binding (Fig. 1f). We term this mechanism that regulates RNA–protein interactions through m6A-dependent RNA structural remodelling ‘the m6A-switch’.

My comment: What are others calling the m6A-switch, which appears to link hydrogen-atom transfer in DNA base pairs in solution from energy-dependent changes in the microRNA/messenger RNA balance to the Structural diversity of supercoiled DNA?

See also: The dynamic N1-methyladenosine methylome in eukaryotic messenger RNA

Reported on February 16, 2016 RNA modification discovery suggests new code for control of gene expression

See also: 2 genes in 2 species (too expensive and too insignificant) March 2015


The ‘m6A-switch’ apppears to link ecological variation to nutrient-dependent RNA-directed DNA methylation, which links RNA-mediated amino acid substitutions to cell type differentiation in all cells of all individuals of all genera via the biophysically constrained chemistry of RNA-mediated protein folding.

See also: Epigenetic switch links MicroRNAs to RNA-protein interactions

See also: UCI Strategic Communication for Journalists  “N6-Methyladenosine” [Wait for it]

See also: CNLM Fellow Tim Bredy discovers “junk DNA” gene that alters brain function

See also: Dynamics of the human and viral m6A RNA methylomes during HIV-1 infection of T cells

Reported as: Newly discovered HIV genome modification may put a twist on vaccine and drug design


“The HIV field has missed this modification in physiological RNA structure and HIV genome for more than 30 years,” Rana said. “I will not be surprised if other viruses with RNA genomes also exploit this m6A modification mechanism to evade immune surveillance and control their replication in human cells. These viruses include, for example, influenza, Hepatitis C, Ebola and Zika, just to name a few.”

See also: m6a RNA Methylation: The Implications for Health and Disease

My comment: Theorists have ignored what serious scientists have detailed in the context of energy-dependent RNA methylation and cell type differentiation that must link learning and memory from ecological variation to ecological adaptation via the conserved molecular mechanisms of protein folding biochemistry that link metabolic networks to genetic networks.  The amount of ignorance is overwhelming, and the theorists are not attempting to inform themselves.

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