by Alan MacDonald MD, FCAP
July 12, 2016
Borrelia spirochetes – both burgdorferi group (sl) and Miyamotoi – do not give genes per se, but are endowed with Open Reading Frames ( ORFs).
Each ORF codes for a specific protein.There are ORFs on the chromosome and on each of the plasmids. Borrelia plasmids can be thought of as so-called ” mini-chromosomes”.
The functions of the totality of proteins are only partially understood. In the case of the “mystery” proteins, the proteins are named “hypothetical”. And no attempt to
link any “hypothetical protein” to a function is designated.
It is clear that more than 1000 ORF cassettes ( chromosome and plasmids added together)
are associated with each individual isolate of Borrelia spirochete (singular).
So in the realm of gene “equivalents = ORF’s”, there is huge complexity.
Borrelia spirochetes are notorious for their exchanges of DNA from one spirochete to another. These lateral DNA transfers shuffle the DNA deck of cards for each and every Borrelia spirochete….And thus there is DNA flux.
DNA fluxes cause antigenic variability and also produce changes in Borrelia spirochetal
tissue tropisms and biological aggressiveness ( virulence).
So …it is complicated.
Now add the newest dimension of DNA complexity, namely the Endosymbiont Borrelia state , where Borrelia spirochetes live inside of Nematode worms.
Endosymbiont Borrelia dwelling inside of parasitic worms are exposed to Nematode-initiated DNA exchanges i.e. Worm DNA to Borrelia DNA exchanges. These further complicate the genetic profiles: DNA – worm fluxes and DNA Borrelia-in-worm fluxes.
In the special case of Multiple Sclerosis there are the following ongoing events:
1. Borrelia species pathogenesis of Myelin Injury
2. Worm toxic protein pathogenesis of Myelin injury
3. Combined worm-and-Borrelia novel DNA as initiators of myelin injuries.