Immune escape is an unlikely explanation for PR-2B emergence as both PR-1 and PR-2B belong to the Asian/American genotype. Furthermore, prM and E amino acid sequence analysis showed weak bootstrap values (fig. S2), indicating low levels of antigenic differences between the clades. Instead, PR-2B emergence and subsequent replacement of PR-1 viruses could be due to differences in epidemiological fitness.
My comment: The journal article indicates that the fitness of the virus is biophysically constrained and RNA-mediated via the balance of viral microRNAs to nutrient-dependent microRNAS and amino acid substitutions in the context of the chemistry of protein folding. Epidemiological fitness is a function of nutrient-dependent RNA-mediated organism-level thermoregulation via amino acid substitutions, not mutations and evolution.
The article was reported as:
This study highlights the critical and oft forgotten role played by non-coding RNAs in the battle between viruses and their human hosts…
My comment: The critical role of non-coding RNAs has not been forgotten by any serious scientist. However, I don’t know any evolutionary theorist or theoretical physicist who understands anything currently known to serious scientists about the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding via amino acid substitutions. The substitutions links viral microRNAs from entropic elasticity to the anti-entropic epigenetic effects of nutrient-dependent microRNAs. The nutrient-dependent microRNAs lead to proper cell type differentiation and healthy longevity. The accumulation of viral microRNAs typically perturbs protein folding and leads to pathology.
The article was reported as:
Species biodiversity at any given site can be revealed in a single drop of soup. It’s a technique that shaves weeks, months, years off traditional ecological methods, saves money and spares the need for tons of taxonomic expertise.
Mitogenomics link nutritional epigenetics to pharmocogenomic testing via the nutrient-dependent metabolic networks and genetic networks of all living genera. The networks are perturbed by viruses via the effects of viral microRNAs on RNA-mediated amino acid substitutions and protein folding.
The first author of High-throughput monitoring of wild bee diversity and abundance via mitogenomics is a co-author of Phylogenomics resolves the timing and pattern of insect evolution
Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relationships.
See also: Evolution of MicroRNA Research Over the Past Decade More than 20,000 microRNA-Focused Publications Were Assessed as a Means to Characterize the Field
My comment: The claim about the “…oft forgotten role played by non-coding RNAs in the battle between viruses and their human hosts…” is ridiculous. Portraying the results of the research cited above in the context of subgenomic RNA and/or evolution is equally ridiculous.
Epidemiological fitness is a function of nutrient-dependent RNA-mediated organism-level thermoregulation via amino acid substitutions, not mutations and evolution. Thermodynamic cycles of protein biosynthesis and degradation link amino acid sustitutions to RNA-mediated organism-level thermoregulation in all genera via what is known about virus-driven cell type differentiation, which is controlled by nutrient-dependent microRNAs in the context of the physiology of reproduction.
See also: Hazelnut farmers use pheromones to confuse moths, save orchards and reduce pesticide use
To disrupt the mating, the farmer floods the orchard air with female pheromone so that the male moth is confused and loses the scent of the target female.
My comment: Viruses disrupt the physiology of reproduction by altering the nutrient-dependent production of species-specific pheromones in species from microbes to man. Think twice, will the viruses kill us all — along with the honeybees — or will it be evolutionary theory. Evolutionary theorists do not seem to understand the fact that the honeybee is not a model of evolution. It is a model organism that links ecological variation to ecological adaptation via RNA-mediated cell type differentiation, which is controlled by the balance of viral microRNAs and nutrient-dependent microRNAs.
See: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
Excerpt 1) The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, and diseases of the X chromosome (Honeybee Genome Sequencing Consortium, 2006). Included among these different aspects of eusocial species survival are learning and memory, as well as conditioned responses to sensory stimuli (Maleszka, 2008; Menzel, 1983).
Excerpt 2) The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects.