Researchers link host glucose metabolism with severity of influenza infection. By Abby Olena | December 15, 2013
Excerpt: Vast amounts of time and research dollars go into studying how the quickly mutating influenza virus works, anticipating which strains will be most active each year, and changing the flu vaccine accordingly.
My comment: Evolutionary theorists seem to have convinced most people to believe in mutation-driven evolution. Indeed, Haldane’s idea shows up even in reports about viruses, like this one. Few people seem interested in examining biological facts. Those who do would see that bio-physical constraints on beneficial mutations enable adaptations. These bio-physical constraints prevent mutations from being fixed in the DNA of the organized genome in any species from microbes to man.
If mutations are not fixed in the genome, natural selection cannot “select” them. People can make up stories about how natural selection “selects” but there is no experimental evidence to support their stories. I think the lack of experimental evidence has something to do with the fact that mathematical models are not constrained by the reality of molecular mechanisms. That would explain two things: 1) why theorists seem to think mathematical models show that biophysical constraints on beneficial mutations need not be considered, and 2) why no one has commented on my repeated assertions that adaptations occur via amino acid substitutions in all species, sans mutations.
See for review: Antigenic change due to a single amino acid
For example, in some human seasonal influenza viruses: “The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.” Nutrient-dependent amino acid substitutions have been linked to species diversity in every other species on this planet that has been studied. Thus, the finding of a link between the concentration of glucose in cells and viral infection suggests to me that the viruses thrive via amino acid substitutions when they can acquire enough “food.”
Food appears to provides the energy they need to thrive. It also makes sense that viruses, react to starvation via seemingly futile thermodynamic cycles that result in amino acid substitutions that enable the molecular stability required for their organism-level thermoregulation. As it is in every other species, their survival is based on the biophysical constraints of nutrient-dependent / energy-controlled reproduction. Even when the complexity of protein folding is not involved in the formation of variant alleles, it’s hard to deny that biophysical constraints on the thermodynamics of hydrogen bonds must be considered. Biophysical constraints are not just there to limit your reproduction, they limit reproduction in every organism.
I think that’s why we see evidence that there are biophysical constraints on the amino acid substitutions that differentiate all cell types, individuals, and all species. If I’m right, it’s because the amino acid substitutions also help to optimize organism-level thermoregulation in the context of nutrient availability. Too little food, or too much of it, throws off the finely-tuned balance between the thermodynamics of intercellular signalling and organism level thermoregulation.
A battle is waged between the ability of viruses to reproduce and the ability of their host to survive the attack on their immune system. This is not a battle of which organism can mutate more quickly. Mutations cause diseases and disorders via perturbed protein folding. Winning the battle for survival depends on organism-level thermoregulation. In living organisms, survival is nutrient-dependent and pheromone-controlled. But that fact simply attests to the origins of life and of organismal complexity in the context of biophysical constraints on adaptations in viruses. It tells us nothing about mutation-driven evolution, and neither does anything else that is based on biological facts.