Part 1:
Dr Bieger talked about the question whether CFS could be causes by a viral infection. He distinguishes between post-viral CFS (40%-80% of cases)
and idiopathic CFS (20%-60% of cases). Post-viral CFS presents mainly as an immune-related infectious symptoms such as fatigue, none to low-grade
fever, recurring herpes infections, elevated inflammatory cytokine levels, NK-cell impairment and oxidative stress. Idiopathic CFS mainly presents
as inflammatory and neurological dysfucntion like fatigue, pain (FM), depression, insomnia, cognitive impairment and gut problems.
Possible post-infectious fatigue has been established for EBV, HHV6, CMV, ParvoB19, HBV, HCV, enteroviruses, Q-fever and Lyme disease infections.
Reactivated infections are likely complications of the original illness. This holds true for EBV, HHV6, HHV7, CMV. It is possible that CFS is also
caused by the retrovirus XMRV or HMRV. Usually we find immune dysfnction such as immune activation and deficiency like NK-cell defects or elevated
CD8/T-Cell activity and also various proinflammatory cytokines suggesting an immune activation or infectious disease. Also the genetic markers is
distinct from healthy controls in various ways.
He presented 2 cases where EBV and CMV titers were significantly elevated and to a certain degree the patients would benefit from anti-viral treatment.
Dr Bieger discussed the discovery of XMRV as a potential diagnostic marker for CFS. In collaboration with one of the best retro-virologist he tried
to detect XMRV through nPCR after the study in October 2009 had been published, but did not succed at first. This was possibly caused by isolating
the DNA right after the blood draw which - according to Dr. Mikovits - leads to the inability to detect the virus. For their next attempt they will be
working closely with Dr. Mikovtis (results are estimated to be available around January/February 2011).
The work of Lo/Alter released in August who found XMRV in 86,6% of patients vs 6.8% of healthy controls indicates that this discovery could bring
diagnostics a step forward.
When dealing with diagnosis of CFS and diagnostics we often find reactivated infections. The possible role of the XMRV/HMRV retrovirus is still unclear.
We often find immune dysfunction and we always fins inflammatory processes which manifest in diverging cytokine measurements
(e.g. IL-1, IL-6, TNFa, IL-17,TH1, IL-2, IFNg, IL-12, TGF, IL-10, IL-13,TH2, IL-4, IL-5, IL-8, IFN-g, NF-kB). The patterns of activation of these
cytokines in MCS, CFS anf FM are distinct.
Dr Bieger criticised that despite those measurable differences CFS is still regarded as a predominantly psychological or psychosomatic condition
in Germany and therefore all advancements in research happen in the US and not in Germany. In MCS we also find a strong cytokine activation. Those
form a network and when examining the links between the various cytokines we find a pattern that is clearly distinct form healthy controls and is
associated with infection. Thus what we know so far is that the immune system is activated, there is a dysfunction and there is possibly a chronic
reactivating underlying infection. NF-kappa-b is the most senstitive marker for immune system activation, becasue NF-kappa-b is a central switch in
all cells. Thus we can detect immune system activation even if other markers don' show anything. The following cytokines present the most diverging
values in all multi-system disorders.
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