Monday, July 18, 2011

RES: Chronic fatigue syndrome, the immune system and viral infection - clarification

Note: There has been some confusion regarding what "recent" criteria
meant in this study. For clarification, authors used the 2003 Canadian
Consensus criteria for this paper.

At the NIH ME/CFS State of the Knowledge Workshop in April, there was
discussion with Dr. Keith Kelly, who is also the editor of Brain
Behavior and Immunology, about publishing a paper setting out a
standard criteria for stating exactly how ME and CFS patients in
studies are defined. Currently there are five definitions all of which
delineate very different populations and some of which may include
people who have no disease, but have an affective disorder only.
Determining which criteria was used and how it was used can be quite
confusing for authors and readers alike.

Brain Behav Immun. 2011 Jul 2. [Epub ahead of print]

Chronic fatigue syndrome, the immune system and viral infection.

Bansal AS, Bradley AS, Bishop KN, Kiani S, Ford B.
Dept. of Immunology, Epsom and St. Helier University Hospitals NHS
Trust, Carshalton, Surrey, SM5 1AA and Chronic Illness Research Team,
Stratford Campus, University of East London, London E15 4LZ, UK.

Abstract

The chronic fatigue syndrome (CFS), as defined by recent criteria, is
a heterogeneous disorder with a common set of symptoms that often
either follows a viral infection or a period of stress. Despite many
years of intense investigation there is little consensus on the
presence, nature and degree of immune dysfunction in this condition.

However, slightly increased parameters of inflammation and
pro-inflammatory cytokines such as interleukin (IL) 1, IL6 and tumour
necrosis factor (TNF) =CE=B1 are likely present. Additionally, impaired
natural killer cell function appears evident. Alterations in T cell
numbers have been described by some and not others.

While the prevalence of positive serology for the common herpes
viruses appears no different from healthy controls, there is some
evidence of viral persistence and inadequate containment of viral
replication. The ability of certain herpes viruses to impair the
development of T cell memory may explain this viral persistence and
the continuation of symptoms.

New therapies based on this understanding are more likely to produce
benefit than current methods.

Copyright =C2=A9 2011. Published by Elsevier Inc.

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