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Latent EBV infection in B cells and autoimmune disease

natasa778

Senior Member
Messages
1,774
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. ...


full article
http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/43797
 

A.B.

Senior Member
Messages
3,780
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

When I became ill, I no longer had the seasonal infections that people usually get every now and then, or when I did get them, the symptoms were barely more than a midly sore throat. I wonder if EBV's strategy would look just like that in practice?
 

anciendaze

Senior Member
Messages
1,841
That web page also has a link to a free pdf of a review article by Michael Pender which is worth reading. The one disagreement I have is with the idea that the CD8+ deficiency must be inherited. I think there is now considerable evidence the deficiency is so specific it must be caused by a particular pathogen. There is also more than one highly-specific deficiency, which points in the same direction -- a pathogen is protecting itself.
 

natasa778

Senior Member
Messages
1,774
The one disagreement I have is with the idea that the CD8+ deficiency must be inherited.

Deficiency as in low levels, or a more general dysregulation - as in present in sufficient, or even excessive numbers, but not doing their job?

What are the findings on CD8+ in ME and are they consistent? Have there been attempts to correlate their levels or similar to severity of any of the symptoms? Asking 'cos of this paper that recently came out, where the CD8+ levels were shown directly correlated to the degree of neurological impairment and executive dysfunction in autism (also confirmed via frontal cortex EEG abnormalities). The working hypothesis there is that increased CD8+ levels are not merely a correlation but actually enter the brain and cause neurological impairments ...
Poorer executive performance as the level of CD3+ CD8+ lymphocyte increased. ► Executive dysfunction is associated with abnormal cortical connectivity. ► Executive dysfunction and disordered cortical connectivity exacerbate as a function of the increased level of CD3+ CD8+

http://www.sciencedirect.com/science/article/pii/S1750946713000366

If this is really the case, something is pushing those levels up ...
http://www.sciencedirect.com/science/article/pii/S1750946713000366
 

anciendaze

Senior Member
Messages
1,841
Deficiency as in low levels, or a more general dysregulation - as in present in sufficient, or even excessive numbers, but not doing their job?

What are the findings on CD8+ in ME and are they consistent? Have there been attempts to correlate their levels or similar to severity of any of the symptoms? Asking 'cos of this paper that recently came out, where the CD8+ levels were shown directly correlated to the degree of neurological impairment and executive dysfunction in autism (also confirmed via frontal cortex EEG abnormalities). The working hypothesis there is that increased CD8+ levels are not merely a correlation but actually enter the brain and cause neurological impairments ...


http://www.sciencedirect.com/science/article/pii/S1750946713000366

If this is really the case, something is pushing those levels up ...
Generally, Pender is talking about deficiency as in low numbers. And, no, CD8+ T cell numbers are not consistently low in ME. The new research on very specific subsets of T cells might explain why, earlier research didn't make fine enough distinctions. We also have to deal with the problem of feedback in the immune system, which can result in numbers being pushed up in response to a problem which consumes immune cells.

I've been watching for reports of CD8+ T cells entering the brain in ME ever since I read about finding some in the dorsal root ganglia at autopsy, or nodules of Nageotte, which indicate earlier damage by invasive T-cells. (These also occur in familial dysautonomia and Sjögren's syndrome.) This would go along with increased numbers rather than deficiencies.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,079
Location
australia (brisbane)
The griffith uni research says our cd8 function is low but didnt mention our numbers. Generally ebv causing increase in cd8 numbers as does cmv and possibly hhv6. My cd8 has been high since ive had cfs.
 

Christopher

Senior Member
Messages
576
Location
Pennsylvania
Generally, Pender is talking about deficiency as in low numbers. And, no, CD8+ T cell numbers are not consistently low in ME. The new research on very specific subsets of T cells might explain why, earlier research didn't make fine enough distinctions. We also have to deal with the problem of feedback in the immune system, which can result in numbers being pushed up in response to a problem which consumes immune cells.

I've been watching for reports of CD8+ T cells entering the brain in ME ever since I read about finding some in the dorsal root ganglia at autopsy, or nodules of Nageotte, which indicate earlier damage by invasive T-cells. (These also occur in familial dysautonomia and Sjögren's syndrome.) This would go along with increased numbers rather than deficiencies.

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