Virulence and your UTI

By: James V. Kohl | Published on: March 23, 2017

Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. — Kalevi Kull


Take on the role of a virus competing to infect a host cell and replicate your viral components!

If you have played this game, you probably know more about virulence than the researchers and journalists who report on it.

Bacterial virulence phenotypes of Escherichia coli and host susceptibility determine risk for urinary tract infections

…our findings suggest that UTI risk and outcome may be determined by complex interactions between host susceptibility and the urovirulence potential of diverse bacterial strains.

Reported as: Urinary tract infections reveal the importance of interactions between host susceptibility and bacterial gene expression

…infection depends on both the host environment and gene expression levels in the bacteria.

The epigenetically-effected host environment biophysically constrains viral latency in all living genera. Viral latency exemplifies how ecological variation must be linked to nutrient energy-dependent pheromone-controlled ecological adaptations and gene expression in E. coli, which prevent virus-driven genomic entropy in all living genera.

They reveal the importance of energy-dependent pheromone-controlled quorum sensing, which links virus-driven energy theft to messenger RNA degradation and all pathology via what is known about bacteria in the light organ of the bobtail squid and the microRNAome of all mammals. 

  …sperm have been reported to carry both RNA and microRNA to the fertilized zygote [17], [18]. MicroRNA (miRNA) are important regulators in translation, and their altered expression often leads to disease or cancer.

Telling us about UTIs does nothing to reveal the importance of biophysically constrained energy-dependent viral latency to the understanding of all pathology.

For example, if you were taught that antibiotic resistance is due to mutations in bacteria such as E.coli, which causes most UTIs, you may never learn that bacteriophages drive the nutrient-dependent pheromone-controlled ecological adaptations in the bacteria and viral latency is the key to healthy longevity in all living genera. UTI risk is predicted by differences in the microRNA/messenger RNA balance that link amino acid substitutions in the host to protection from amino acid substitutions in viruses that cause virulence.

Ask yourself where the terms virus and virulence came from — if not from what was suspected or what is known about virus-driven energy theft.

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