Tuesday, July 19, 2011

Research paper: CFS, the immune system and viral infection, 2 July 2011

From the M.E. Association's website, a post by Tony Britton entitled 'Research paper: CFS, the immune system and viral infection, 2 July 2011':
From Brain, Behaviour and Immunity, the official journal of the Psychoneuroimmunology Research Society (PNIRS). 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) α 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 © 2011. Published by Elsevier Inc.

PMID: 21756995 [PubMed - as supplied by publisher]

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Tuesday, June 14, 2011

New study: Gene expression alterations at baseline and following moderate exercise in patients with CFS & FMS

RESEARCHERS behind a new study say they've discovered post-exercise differences in genetic expression that meet criteria for an objective biomarker for a subgroup of chronic fatigue syndrome (ME/CFS). They also say data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls. Further details in three reports reprinted here below.

(1) From Post Viral Fatigue Forum, 6 June 2011 www.postviralfatigue.me.uk Full copy:
New Study Claims Change in Gene Expression in CFS

Looks interesting: http://chronicfatigue.about.com/b/2011/06/06/genetic-expression-after-exercise-in-fibromyalgia-chronic-fatigue-syndrome.htm

Researchers analyzed blood samples before exercise to get a baseline, then took samples again half an hour, 8 hours, 24 hours and 48 hours after moderate exercise.

They found that:

- 71% of the ME/CFS group (34 of 48) had increased expression of 4 genes dealing with sensory and adrenergic receptors and cytokines for 48 hours after exercise; Those with the largest change in genetic expression also had the largest increase in post-exercise symptoms.

- The other 29% of the ME/CFS group (14 of 48) did not show the above changes but did have a decrease in expression of the adrenergic α-2A receptor; This group had significantly more orthostatic intolerance (dizziness upon standing) than the first group.

- Healthy controls and people with FMS had no post-exercises changes in the genes that were studied.

They [the researchers] say the data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls.

Seems encouraging to me.

B.
edited by Barbarian on 6/6/2011 [End]
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(2) From About.com Guide Fibromyalgia & Chronic Fatigue
6 June 2011 - http://chronicfatigue.about.com
By Adrienne Dellwo
Full copy:
Research Brief

Researchers behind a new study [full copy below, courtesy of PubMed] say they've discovered post-exercise differences in genetic expression that meet criteria for an objective biomarker for a subgroup of chronic fatigue syndrome (ME/CFS). They also say data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls.

Researchers analyzed blood samples before exercise to get a baseline, then took samples again half an hour, 8 hours, 24 hours and 48 hours after moderate exercise (maintaining maximum heart rate for 20 minutes.) They were looking for changes in genes that deal with sensory fatigue and muscle pain, which are common post-exercise symptoms of ME/CFS. The found that:

71% of the ME/CFS group (34 of 48) had increased expression of 4 genes dealing with sensory and adrenergic receptors and cytokines for 48 hours after exercise;
Those with the largest change in genetic expression also had the largest increase in post-exercise symptoms;

The other 29% of the ME/CFS group (14 of 48) did not show the above changes but did have a decrease in expression of the adrenergic α-2A receptor;
This group had significantly more orthostatic intolerance (dizziness upon standing) than the first group;

Healthy controls and people with FMS had no post-exercises changes in the genes that were studied;
However, those with FMS had baseline elevations in 3 genes -- 2 sensory ion channels and 1 cytokine -- that were not found in the other groups.
These differences in genetic expression could help explain post-exertional malaise (PEM), which is considered the hallmark symptom of ME/CFS. PEM causes a marked upswing in symptoms after exertion, and for some people it takes very little exertion -- such as taking a shower or walking to the mailbox -- to trigger this symptom. In the most severe cases, even sitting up for a few minutes can lead to PEM.

FMS involves a similar but generally less-severe reaction to over exertion or stressful events, and these genetic abnormalities could help shed light on this as well.

Researchers concluded that these findings could help establish an objective biomarker for diagnosing at least 1 subgroup of ME/CFS, guide treatment for both identified ME/CFS subgroups, and differentiate FMS from ME/CFS. [End]
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(3) From PubMed - May 2011 - National Center for Biotechnology Information, U.S. National Library of Medicine
http://www.ncbi.nlm.nih.gov/pubmed/21615807?forumid=331851
Full copy:
J Intern Med. 2011 May 26. doi: 10.1111/j.1365-2796.2011.02405.x. [Epub ahead of print]

Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.

Light AR, Bateman L, Jo D, Hughen RW, Vanhaitsma TA, White AT, Light KC.

Source
Department of Anesthesiology, University of Utah, Salt Lake City, UT The Brain Institute, University of Utah, Salt Lake City, UT Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT Department of Exercise and Sprt Science, University of Utah, Salt Lake City, UT.

Abstract
Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AT, Light KC (University of Utah Dept. Anesthesiology, Dept. Neurobiology and Anatomy, Dept. Exercise and Sport Science) Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.

Objectives: To determine mRNA expression differences in genes involved in signaling and modulating sensory fatigue, and muscle pain in patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia Syndrome (FM) at baseline, and following moderate exercise.

Design: Forty eight Patients with CFS-only, or CFS with comorbid FM, 18 Patients with FM that did not meet criteria for CFS, and 49 healthy Controls underwent moderate exercise (25 minutes at 70% maximum age predicted heart-rate). Visual-analogue measures of fatigue and pain were taken before, during, and after exercise. Blood samples were taken before, and 0.5, 8, 24, and 48 hours after exercise. Leukocytes were immediately isolated from blood, number coded for blind processing and analyses, and flash frozen. Using real-time, quantitative PCR, the amount of mRNA for 13 genes (relative to control genes) involved in sensory, adrenergic, and immune functions was compared between groups at baseline, and following exercise. Changes in amounts of mRNA were correlated with behavioral measures, and functional clinical assessments.

Results: No gene expression changes occurred following exercise in Controls. In 71% of CFS patients, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48 hours. These post-exercise increases correlated with behavioral measures of fatigue and pain. In contrast, for the other 29% of CFS patients, adrenergic α-2A receptor's transcription was decreased at all time points after exercise; other genes were not altered. History of orthostatic intolerance was significantly more common in the α-2A decrease subgroup. FM only patients showed no post-exercise alterations in gene expression, but their pre-exercise baseline mRNA for two sensory ion channels and one cytokine were significantly higher than Controls.

Conclusions: At least two subgroups of CFS patients can be identified by gene expression changes following exercise. The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine. The smaller subgroup contained most of the CFS patients with orthostatic intolerance, showed no post-exercise increases in any gene, and was defined by decreases in mRNA for α-2A. FM only patients can be identified by baseline increases in 3 genes. Post-exercise increases for 4 genes meet published criteria as an objective biomarker for CFS, and could be useful in guiding treatment selection for different subgroups.

Copyright © 2011 The Association for the Publication of the Journal of Internal Medicine.

PMID: 21615807 [PubMed - as supplied by publisher] [End]
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