Although the ultimate origins of RNA viruses are uncertain, it seems reasonable to assume that these infectious agents have a long evolutionary history, appearing with, or perhaps before, the first cellular life-forms (38).
The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis…
Perhaps the evolutionists have placed the cart before the horse on this issue, as proposed by several creationist scientists.4,6 In fact, in an ironic twist, the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6
We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.
My comment: Watch Larry Young link the works of Luis P. Villarreal from the evolution of viruses to the evolution of love here: Also, read how Larry Young explains the development of heterosexual preferences for the size of women’s breasts: This new theory finally explains why men love breasts.
If you accept this pseudosceintific nonsense about viruses and evolved sex differences and somatic differences in cell type differentiation and responses to the differences, read no further.
Only those who are interested in facts about biologically-based cause and effect are encouraged to proceed.
…anywhere from 30 percent to 90 percent of people have already been exposed to AAVs—which are not pathogenic—and have developed immunity to them…
My comment: The development of the immunity is genetically predisposed and nutrient-dependent. It requires RNA-mediated gene duplication and RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera via fixation of amino acid substitutions in the context of the physiology of reproduction.
Fixation of the substitutions during life history transitions determines the cell types of all cells in all individuals of all living genera, because it protects cell types from virus-driven perturbations in protein folding that are clearly linked to pathology. For contrast: These virus-driven pathologies are placed into the context of evolution by theorists who seem to know nothing about how cell type differentiation occurs. For example, see:
Adeno-associated viruses (AAVs) have shown promise as gene-therapy delivery vehicles in clinical trials evaluating treatments for hemophilia and a genetic form of blindness.
My comment: When you see researchers link the biophysically constrained nutrient-dependent chemistry of RNA-mediated protein folding to diseases and to evolution, ask them how they differentiate the role viruses play in genomic entropy from the role they claim viruses play in the “viral evolutionary lineage.”
You might be amazed to learn that the entirety of the neo-Darwinian evolutionary perspective on RNA-mediated cell type differentiation has been placed into the context of drug development or the development of other therapies by serious scientists who think they are combating disease when they should be joining others who are Combating Evolution to Fight Disease. The serious scientists who are combating evolution are among those who continue to examine how cell type differentiation typically occurs and compare it to virus-perturbed cell type differentiation in attempts to help prevent diseases by using what is known about RNA-mediated events to determine which viruses are causing them, and how are immune system protects us from those that are not causing perturbed protein folding. Obviously, our immune system protects us from pathology.
That suggests an obvious link from the immune system to the development of sexual preferences that include sexual orientation.
Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).
People like Larry Young may help others understand how RNA-mediated cell type differentiation occurs when funding for research on viruses linked to mutations is limited. It must be limited to exclude those who are trying to link mutations to evolution of love via the hormone-organized and hormone-activated behaviors that link insects to mammals. Insects and mammals are linked via food odors and pheromones that epigenetically effect thermodynamic cycles of protein biosynthesis and degradation in species from microbes to man. See for example:
Feedback loops link odor and pheromone signaling with reproduction
Biosynthesis of amino acids – Macaca mulatta (rhesus monkey)
Question: How many other amino acids are linked to the creation of achiral glycine
Olfactory Receptor Patterning in a Higher Primate
Question: How many olfactory receptor genes can be linked from the nutrient-dependent pheromone-controlled physiology of reproduction in yeasts to the substitution of achiral glycine in the gonadotropin releasing hormone (GnRH) decapeptide, which is conserved in all vertebrates?
See also: Starvation effects handed down for generations
Whatever the epigenetic control turns out to be, it is clearly handed down across generations.
In my 2013 review Nutrient-dependent/pheromone-controlled adaptive evolution: a model, I cited the work that linked ecological speciation in nematodes from grazers to predators with teeth.
Differences in the behavior of nematodes are determined by nutrient-dependent rewiring of their primitive nervous system (Bumbarger et al., 2013). Species incompatibilities in nematodes are associated with cysteine-to-alanine substitutions (Wilson et al., 2011), which may alter nutrient-dependent pheromone production.
The epigenetic control of morphological and behavioral phenotypes is obviously nutrient-dependent and RNA-mediated in the context of their physiology of reproduction and ecological speciation.
This was reported as: The neurobiological consequence of predating or grazing
“The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans“, Ralf Sommer concludes. A clear-cut result like that was not what he had necessarily expected.