The rapid tests detect C-reactive protein (CRP), a marker of infections caused by bacteria, in patients’ blood. A low level of CRP is suggestive of viral infection and therefore antibiotic treatment is not required.
My comment: The level of one protein differentiates between a viral and a bacterial infection. That fact attests to claims that one RNA-mediated amino acid substitution in a virus increases its virulence.
Major antigenic changes are less likely to occur when the nutrient energy-dependent stability of the host microbiome already exemplifies ecological adaptation to the virus. Ecological adaptation occurs via the pheromone-controlled physiology of reproduction in species from microbes to humans.
Pseudoscientists may still hope to publish in “Science” or in “Nature” until even the top supporters of the evolution industry are forced to withdraw their support.
For example, see these two citations from: Tempo and mode of genome evolution in a 50,000-generation experiment, in which ‘adaptation’ is mentioned 10 times in the body of the text.
Wichman, HA, et. al, (1999) Different trajectories of parallel evolution during viral adaptation. Science 285, 422–424.
Kvitek, DJ & Sherlock, G. (2013) Whole genome, whole population sequencing reveals that loss of signaling networks is the major adaptive strategy in a constant environment. PLoS Genet. 9, e1003972 (2013).
My comment: Ecological variation must link the adaptations to viruses via energy-dependent RNA-mediated amino acid substitutions. Do authors who make claims about parallel genome evolution in the context of mutations but place them into the context of population-wide adaptations know that? The two citations suggest that these authors do not know enough about energy-dependent RNA-mediated cell type differentiation.
Olivier Tenaillon, Jeffrey E. Barrick, Noah Ribeck, Daniel E. Deatherage, Jeffrey L. Blanchard, Aurko Dasgupta, Gabriel C. Wu, Sébastien Wielgoss, Stéphane Cruveiller, Claudine Médigue, Dominique Schneider & Richard E. Lenski
Alternatively, they may be deliberately misrepresenting what is known to all serious scientists about energy-dependent biophysically constrained RNA-mediated protein folding chemistry by linking their results to genome evolution in Lenski’s long term evolution experiment (LTEE).
See for comparison: Changing Folding and Binding Stability in a Viral Coat Protein: A Comparison between Substitutions Accessible through Mutation and Those Fixed by Natural Selection (2014)
Bloom and collaborators presented a thermodynamic framework to predict the probability that a protein retains its structure after one or more random amino acid substitutions, and highly simplified models of proteins were used to support their prediction that the substitutions tend to be destabilizing , , , , , .
We find that there are unexpected differences between accessible and observed substitutions. Observed substitutions tend to have smaller effects on stability than expected by chance. Substitutions observed in high temperature adaptations tend to stabilize folding but slightly destabilize binding. Finally their cumulative stability effects in lab adaptations can be considerably greater than individual effects suggesting that selection is acting on local aspects of protein stability.
My comment: Holly A. Wichman, who is the first author of the 1999 article about parallel evolution during viral adaptation is a co-author of the 2014 article about fixed substitutions, which are referred to as mutations. With news that C-Reactive Protein (CRP) is suggestive of viral infection, claims about fixed amino acid substitutions and mutations can be placed into their proper perspective.
For example, mutations may be fixed in a virus during replication, but only energy-dependent RNA-mediated amino acid substitutions can be fixed in the organized genomes of species from microbes to humans via the physiology of reproduction. Nutrient energy-dependent microRNAs allow fixation of RNA-mediated amino acid substitutions in C-Reactive Protein, which stabilizes the organization of the human genome.
The role of CRP as both a risk factor and a biomarker warrants investigation of its regulation by other molecular factors. We have discovered a posttranscriptional mechanism by which the RBP HuR and the miRNA miR-637 modulate CRP expression downstream of IL-6 signaling. We have identified HuR and miR-637 as new factors that may play an integral role in the development of the inflammatory state and may represent new valuable targets in the diagnosis, treatment, or prevention of inflammation and diseases with a major inflammatory component.
My comment: This suggests all virus-driven energy theft, which is linked to all pathology in all living genera, can be treated in the context of nutrient energy-dependent microRNA flanking sequences. The flanking sequences link hydrogen-atom transfer in DNA base pairs in solution from RNA methylation to cell type differentiation via RNA-mediated amino acid substitutions, the innate immune system, and the physiology of reproduction. The physiology of energy-dependent reproduction links fixation of the nutrient-dependent amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
See also: New Perspectives on Ebola Virus Evolution also with Holly A. Wichman
We tested for positive selection and considered the placement of adaptive amino acid substitutions along the phylogeny and within the protein structure of GP1,2. We conclude that: 1) the common practice of rooting the phylogeny of EBOV between the first known outbreak in 1976 and the next outbreak in 1995 provides a misleading view of EBOV evolution that ignores the fact that there is a non-human EBOV host between outbreaks; 2) the N-terminus of GP1 may be constrained from evolving in response to the host immune system by the highly expressed, secreted glycoprotein, which is encoded by the same region of the GP gene; 3) although the mucin-like domain of GP1 is essential for EBOV in vivo, it evolves rapidly without losing its twin functions: providing O-linked glycosylation sites and a flexible surface.
My comment: They linked virus-driven energy theft to amino acid substitutions in the EBOV lineage between outbreaks. They link changes in the virus from a non-human host to the ability of human hosts to protect themselves via nutrient energy-dependent glycosalation sites and receptor-mediated behaviors that link glycobiology from energy-dependent RNA methylation to supercoiled DNA. But they also link virus-driven energy theft in the human host to all pathology via this report.
…viral latency is responsible for life-long pathogenesis and mortality risk…
My comment: Rarely do researchers see the amount of confusion about biologically-based cause and effect that is exemplified in two articles published on the same day, albeit in different journals. However, in this case, the conclusions in Tempo and mode of genome evolution in a 50,000-generation experiment will make no sense to serious scientists who understand the claims in New Perspectives on Ebola Virus Evolution.
For example, the 50,000-generation experiment cannot be linked from energy-dependent amino acid substitutions in the virus carried by mosquitoes to mutations in the Ebola virus in humans. However, nutrient-dependent RNA-amino acid substitutions can be linked to prevention of Ebola virus-driven energy theft and the prevention of all virus-driven human pathology via what is known about the biophysically constrained chemistry of RNA-mediated protein folding in all living genera.