don't remember there being a thread on this, apologies if a repeat ... if correct, might account for many of the mysterious findings in ME
... "So there's something unique about EBV's role as a microbial agent," he said. And that, it turned out, was that EBV is the only human virus that can activate and survive in B cells, inducing clonal expansion and inhibiting apoptosis. Moreover, those B lymphocytes are precursors of the plasma cells that make antibodies characteristic and pathogenic in autoimmune disease.
Humans and EBV have evolved together for thousands of years, according to Marc S. Horwitz, PhD, of the University of British Columbia in Vancouver.
"The way the virus has learned to survive is to infect us and stay hidden inside a subset of cells for the remainder of our lives," Horwitz said in an interview.
But the cells this virus adapted to live in, B cells, are a poor host in some ways, he said. This is because B cells turn over rapidly and often, unlike many other tissues in the body.
"So the strategy EBV has developed to keep its host B cell alive but latent and hidden from attack by the immune system is by constantly poking the immune system's low level interferon response, which is akin to keeping the immune system on the edge of its seat and ready to pounce," said Horwitz, who is co-leader of the university's infection, inflammation, and immunity program.
In that hyperalert state, when the immune system detects a new threat its response could be excessive, which could push the individual over the edge into autoimmunity, he explained.
The T-Cell Connection
Many epidemiologic studies have found a strong familial component in autoimmune diseases. In a healthy host, EBV infection is tightly controlled by a subset of cytotoxic CD8+ cells, which destroy the infected cells. As Pender continued his research, he then suggested that this genetic component could be an inherited deficiency of CD8+ cells. ...