Deficient EBV-Specific B- and T-Cell Response in Patients with Chronic Fatigue Syndrome

[alex3619]

Notice that this kind of pathology violates Koch's postulates. Neither EBV nor h. pylori alone is responsible.

Most of these are long term human pathogens (HIV is an exception). They co-evolved, with humans and other viable species as hosts. We are the environment they co-evolved in. As such it can be expected that they will have capacity to take advantage of other co-infections they have co-evolved with.

Occam's Razor is about simpler hypotheses having preferences. Its not a law, its a heuristic. Further, I think it was once said (Albert Einstein?) that explanations should be as simple as necessary, but no simpler. In other words, they must explain all the relevant data, and as new data is found that violates them then even more complex hypotheses should be adopted. Biological findings are not set in stone, and even long-standing findings should be considered changeable.

I think a lot of the argument for Occam's Razor arises in harder sciences like physics. Simpler equations are often preferred. Biology is messy. We are talking of systems of things interacting. Reductionism and critical rationalism, and heuristics like Occam's Razor, start to meet their limits here, and really fail when it comes to psychology or psychiatry.

 

[MeSci]

PLoS One. 2014 Mar 10;9(3):e90855. doi: 10.1371/journal.pone.0090855. eCollection 2014.
Direct Infection of Dendritic Cells during Chronic Viral Infection Suppresses Antiviral T Cell Proliferation and Induces IL-10 Expression in CD4 T Cells.
Baca Jones C, Filippi C, Sachithanantham S, Rodriguez-Calvo T, Ehrhardt K, von Herrath M.
Author information

Abstract
Elevated levels of systemic IL-10 have been associated with several chronic viral infections, including HCV, EBV, HCMV and LCMV. In the chronic LCMV infection model, both elevated IL-10 and enhanced infection of dendritic cells (DCs) are important for viral persistence.

This report highlights the relationship between enhanced viral tropism for DCs and the induction of IL-10 in CD4 T cells, which we identify as the most frequent IL-10-expressing cell type in chronic LCMV infection.

Here we report that infected CD8αneg DCs express elevated IL-10, induce IL-10 expression in LCMV specific CD4 T cells, and suppress LCMV-specific T cell proliferation. DCs exposed in vivo to persistent LCMV retain the capacity to stimulate CD4 T cell proliferation but induce IL-10 production by both polyclonal and LCMV-specific CD4 T cells.

Our study delineates the unique effects of direct infection versus viral exposure on DCs. Collectively these data point to enhanced infection of DCs as a key trigger of the IL-10 induction cascade resulting in maintenance of elevated IL-10 expression in CD4 T cells and inhibition of LCMV-specific CD4 and CD8 T cell proliferation.

Introduction
The host-pathogen relationship in chronic viral infections requires the establishment of equilibrium between the host immune response and viral replication. While this balance of competing interests aids in protecting the host from the immunopathologic consequences of continuous inflammation, such a truce can also result in the prolonged persistence of the virus within its host. Studies over the last decade have identified several characteristics common to multiple persistent viral infections including elevated levels of systemic IL-10 and T cell exhaustion [1]–[8].......

Click on link above for full free abstract:

and we have higher levels of IL-10 than controls according to this paper.

 

[wastwater]

I'm likely missing a gene IRF4 interferon regulatory factor 4 that gives rise to problems with EBV
Hope they continued this work
I don't know if this would make me a candidate for rituximab and what that would do
If b cells are undifferentiated does that make them anaplastic

 

[katcoff]

Interesting, partially explains why ebv keeps popping up in the cfs/me arguement. I guess they cant say its not an issue in cfs/me but also cant specifically say it is an issue. Explains the t cell dysfunctions found in us as well as the nk dysfunctions.

It might explain why some(cfsers) say they have never had ebv, their immune system cant produce antibodies to it, even though common information on ebv is that most adults have had ebv. When i hear someone (adult)with cfs/me hasnt had ebv, my thoughts are that maybe they have but their immune system isnt showing its so??

I've had CFS/ME for many years. Back when, I tested negative for mono, which I assume looked for EBV (or whatever). So yes,it makes me wonder if the real problem is lack of adequate immune reaction to the virus, a lack I still have.