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Purifying the Impure: Sequencing Metagenomes and Metatranscriptomes from Complex Animal-associated Samples
Published on: December 22, 2014
Microbial infections in eight genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis
Lihan Zhang1, John Gough, David Christmas
1Department of Cellular & Molecular Medicine, St George's University of London, London, UK.
Background:
The authors have previously reported genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on expression of 88 human genes.
Aim:
To attempt to reproduce these findings, determine the specificity of this signature to CFS/ME, and test for associations between CFS/ME subtype and infection.
Methods:
Expression levels of 88 human genes were determined in blood of 62 new patients with idiopathic CFS/ME (according to Fukuda criteria), six patients with Q-fever-associated CFS/ME from the Birmingham Q-fever outbreak (according to Fukuda criteria), 14 patients with endogenous depression (according to DSM-IV criteria) and 29 normal blood donors.
Results:
In patients with CFS/ME, differential expression was confirmed for all 88 genes. Q-CFS/ME had similar patterns of gene expression to idiopathic CFS/ME. Gene expression in patients with endogenous depression was similar to that in the normal controls, except for upregulation of five genes (APP, CREBBP, GNAS, PDCD2 and PDCD6). Clustering of combined gene data in CFS/ME patients for this and the authors' previous study (117 CFS/ME patients) revealed genomic subtypes with distinct differences in SF36 scores, clinical phenotypes, severity and geographical distribution. Antibody testing for Epstein-Barr virus, enterovirus, Coxiella burnetii and parvovirus B19 revealed evidence of subtype-specific relationships for Epstein-Barr virus and enterovirus, the two most common infectious triggers of CFS/ME.
Conclusions:
This study confirms the involvement of these genes in CFS/ME.
Insights
This study confirms genomic subtypes in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) using gene expression. These subtypes correlate with clinical features and specific infections, aiding in understanding CFS/ME.
Area of Science:
- Genomics
- Immunology
- Molecular Biology
Background:
- Previous research identified genomic subtypes in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) based on 88-gene expression.
- This study aimed to validate these findings and explore their specificity.
Purpose of the Study:
- To reproduce genomic subtype findings in CFS/ME.
- To determine if the gene expression signature is specific to CFS/ME.
- To investigate associations between CFS/ME subtypes and infectious triggers.
Main Methods:
- Gene expression profiling of 88 genes in blood samples from CFS/ME patients, Q-fever-associated CFS/ME patients, depression patients, and healthy controls.
- Statistical analysis including gene expression clustering and antibody testing for common infectious agents.
Main Results:
- Differential expression of all 88 genes was confirmed in CFS/ME patients.
- Genomic subtypes were identified in CFS/ME patients, correlating with clinical phenotypes, severity, and geographical distribution.
- Subtype-specific associations were found with Epstein-Barr virus and enterovirus infections.
Conclusions:
- The study validates the involvement of the 88-gene signature in CFS/ME.
- Genomic subtypes in CFS/ME are distinct and linked to clinical characteristics and specific viral triggers.
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