Date: Wed, 5 Oct 2005 14:35:06 -0400
From: "Eddie Bollenbach"

During an acute polio infection the gray matter (Polios) in the spinal cord becomes inflamed (itis). Polio virus is a very small virus that mutates readily because the size of the genetic string is so small it has no room for the correction proteins present in the genetic material of larger organsisms. So it quickly changes into various viral types which cannot kill cells or burst cells.

Motor neurons of the gray matter die in two ways during a polio infection. 1. They die due to the effects of inflammation 2. They die as the polio virus completes its reproductive cycle and bursts the cells. I think it may be relevant to who gets PPS as to which of these two factors dominate during the original polio infection. I have no evidence for this. But, with little inflammation cells die by polio virus damage and may contain inside the cell many mutated polio virus particles. So we would have shrunken cells with a lot of polio virus* inside that could last a lifetime. At some point these viruses** in stasis could come into contact with glia (support cells which have immune function in the brain and spinal cord) stimulating an immune reaction. It is also possible that at some point, maybe simply time, enough mutant virus particles are released so that they can be detected, along with the immune cells and biochemicals like cytokines, in the spinal cord as several researchers have found (Sharief 1991)***.

So:

1. The virus in mutated form is inside cells if you have had polio
2. Immune reactions toward the virus have been detected but only in patients with PPS

The logic of how PPS happens seems compelling in light of these facts. Overuse has never been shown in any data to cause PPS. Our data****, along with data from Dalakas at NIH, have shown there is no connection. Once muscles are weak from PPS it is clear they should not be overused.

Eddie
Contact Professor Edward P. Bollenbach
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• *Eddie: The particles that didn't mutate would have escaped from the cell during the normal life cycle of the virus. But polio virus has RNA genes and is small and doesn't have the genes to make repair proteins. So if the genes mutate, as they do frequently,* *many will be unable to escape. Hence the large number of defective mutated particles. I think a lot of the motor neurons contain this type of material. But they wouldn't be able to signal and evoke an immune response unless they escape from the cells that hold them. So, I envisage some defective particles leaking into the spinal fluid and uping the immune response, possibly in stages, until those with PPS begin to lose their resiliency and develop inflammation.

• ** Eddie: The term "virus", singular virion, or virus particle are interchangeable. They are called particles because biologically they don't do metabolism and so traditionally they weren't classified as life. They can't reproduce on their own either but need a host cell from a different species. In that sentence I meant a damaged cell, shrunken and crenulated, able to perform minimal function but full of virus particles or even dead cells forming debris in the cord but packed with poliovirus.

• ***Intrathecal immune response in patients with the post-polio syndrome [Abstract]; Sharief MK, Hentges R, Ciardi M.; N Engl J Med. 1991 Sep 12;325(11):749-55.

• **** Post-Polio Questionnaire authored by Bollenbach and Falconer Jan. 2000