It’s not every day that a noted researcher calls a study “the capstone” of his career or asserts that it’s more important than the rest of his 500 studies put together.
That’s pretty amazing but the exciting part for those of us with ME/CFS/FM is that the breakthrough describes how a common trigger of ME/CFS and possibly FM – an Epstein-Barr Virus infection – sets into motion a process that results in nasty autoimmune diseases like M.S. and lupus (and possibly ME/CFS/FM).
The research team’s decision to make their code available to others suggests we could know sooner rather than later if EBV has unleashed a similar disease process in ME/CFS/FM. If it has, then note that the search for a way to fix the damage is already underway. Find out more in a Simmaron Foundation sponsored blog
Health Rising’s Quickie Summer Donation Drive is On!The Autoimmune Virus? Groundbreaking EBV Finding Could Help Explain ME/CFS
Why does EBV not show up as elevated for my CFS blood? just past infection…
Update on my question. So EBV is no longer active but it triggers a gene(?). But something keeps the illness going. Like a bad feedback loop in the brain?……
it will show up in early antigen test
My son’s illness started at age 5, 1986, with a definite EBV infection ( documented by EBV panels in course of illness). He had multiple neurological symptoms beginning 2 weeks after initial illness. Also began having depression after being a very happy and active little boy.
I remember a number of friends who had mono in the 1960s. However, my son’s EBV symptom/ profile seemed different. I appreciate that EBV has been part of multiple experimental programs in using viruses to carry genetic information into cells. I would hope that someone would look carefully at the genetic manipulation of the EBV virus since the late 1970s.
Interesting. But one thing that isn’t really covered here, is why infection-triggered ME/CFS is 99% of the time ‘sudden onset’, and it almost always seems to occur right after a severe infection, where-as ME/CFS triggered by A.I. diseases is 99% of the time ‘gradual onset’, typically long after the AI disease has appeared.
Yes. Good point which was mentioned. I don’t think sudden onset accounts for such a large percentage of patients but it clearly does for many. I wonder if its too quick for the kind of process described. We’ll only know if the studies are done/
From https://en.wikipedia.org/wiki/Epstein-Barr_virus I got:
“In primary infection, EBV replicates in oro-pharyngeal epithelial cells and establishes Latency III, II, and I infections in B-lymphocytes. EBV latent infection of B-lymphocytes is necessary for virus persistence, subsequent replication in epithelial cells, and release of infectious virus into saliva. EBV Latency III and II infections of B-lymphocytes, Latency II infection of oral epithelial cells, and Latency II infection of NK- or T-cell can result in malignancies, marked by uniform EBV genome presence and gene expression.”
So primary infection is mainly through infection of epithelial cells. I guess those are more numerous (actually in primary infection it’s epithelial plus B-cells so it is more numerous then mainly B-cells only), making for a far stronger (higher viral counts/activity) initial infection and immune reaction. Also, in the active phase the virus (or cell containing the virus) is detectable/fightable by the immune system again making for a stronger immune reaction.
Shortly after the first infection likely many infected active EBV/epithelial cells are cleaned up by the immune system. That probably leaves, in the latent phase, lower numbers of EBV infected cells in the body then during peak infection. Also, viral “potency” is lower in latency as only part of the viral genes are expressed opposed to all during initial infection. The immune system will be far less active against EBV as well as the vast majority of infected cells will be undetectable by the immune system.
So I suppose:
* during initial infection EBV infected cells, viral activity strength (amount of virus genes expressed) per infected cell, virons and percentage of infected cells detectable/fightable by the immune system is far higher making up for a potential onslaught-like combined effect (sudden onset ME type)
* during latency all of the above factors are likely lower making for a less fierce but constant effect; as EBV seems to be a very opportunistic virus it takes advantage (by partial reactivation and/or multiplication) of every small infection/pathogen to gain further ground so every cold, flu, stomach infection, cold sore… has the potential to increase its combined strength IMO slowly increasing the strength of the bad constant influence latent EBV has (gradual onset type ME)