Antigenic change due to a single amino acid

By: James V. Kohl | Published on: November 22, 2013

Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

Björn F. Koel et al.

“The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

The relevance to evolutionary theory and to the biology of behavior is that a single amino acid substitution also enabled adaptation to the sensory environment during the past ~30K years in a human population in central China. Their adaptability is exemplified across species via the conserved molecular mechanisms that appear to be responsible for evolution in viruses. Debate about whether viruses are alive and whether they exhibit behaviors can now include evidence of the conserved molecular mechanisms of physics, chemistry, and biology in species of living and non-living organisms. The origins of human behavior in viruses adds new dimensions for consideration in the context of theories that suggest random mutations cause things to somehow happen that appear to defy the basic principles of biology and levels of biological organization that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of all living organisms via molecular mechanisms of organization in viruses.
My comment to the Science Magazine cite was submitted on Thu, 11/21/2013 – 22:04 and approved on Fri, 11/22/2013 – 05:44
The idea of biophysical constraints seems antithetical to the idea of nature
somehow selecting mutations that cause amino acid substitutions. However, I
am not a biophysicist or evolutionary theorist.
The problem may be my focus on nutrient-dependent receptor-mediated amino
acid substitutions in species from bacteria to humans (non-viral organisms).
Since I am not a virologist or physicist,I’m not sure that the laws of
physics apply to viruses and their replication.
If they do, natural selection for random mutations is not likely to result in
amino acid substitutions because the thermodynamics of changes in
organism-level thermoregulation preclude such randomness. Stability of
protein biosynthesis and degradation that probably depends on protein folding
must somehow be controlled. Besides, I don’t know how random mutations in
viruses could be naturally selected for inclusion in the human virome (or in
the virome of any organism capable of thermoregulating its thermodynamic
intercellular signaling).
If the Second Law of Thermodynamics does not apply to viruses, which means
the chemical bonds that enable the amino acid substitutions can form at
random and somehow be naturally selected, the details of biophysical
constraints in this article seems out of place, since I do not think in terms
of constrained random mutations and natural selection in mutation-driven
evolution.
Hopefully, someone with a background in biophysics will address my confusion
in case others are confused. In addition, I wonder if the consequences of
understanding the evolutionary mechanisms that govern viruses extend to
consequences important to understanding the evolution of species from
bacteria to humans via constrained random mutations and natural selection?


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