Transcriptome plasticity is an evolutionary surrogate in humans and serves to counter the profound threats imposed by continuously evolving infectious diseases, chemical exposures, and a changing environment. The race to adapt between infections agents and host cells pits very high genome plasticity of viruses and efficient horizontal gene transfer of bacteria against human cell transcriptome plasticity. The human alternate exon use as a “plug and play” strategy creating real time transcriptome plasticity represents a differentiating feature from bacteria and most viruses. Biology always seems to find a way and our resilient transcriptome plasticity can be hacked by infectious agents as they can influence alternate exon use in their host cells as part of their remarkable ability to manipulate their host.
Evolution operates through natural selection. In the case of infectious disease, the human host responds to defend against the infection, most frequently by an immune response. The response imposes natural selection on the infectious pathogen that evolves to evade the host response. Infectious pathogens are at a significant evolutionary advantage due to their relatively short replication interval. If a single-stranded RNA virus is capable of doubling every 10 min then entirely new populations can arise to evade selection pressure in an hour. If bacteria can double every 60 min then an entirely new bacterial population can arise to evade selection pressure within an average workday. Human evolution is much slower such that a generation time of 20 years means a human population can arise to evade selection pressure only after a 100 years or more. An evolutionary competition between humans and their infectious pathogens favors the infectious pathogen and numerous pandemics support this observation.
KeywordsSplice-site affinity Nuclear receptors Transcription factors Small nuclear ribonucleoproteins Resilient metabolism Placebo effect Aromatherapy
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