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The study also identified a tendency for more prevalent human herpesvirus 6B in people with FM than in those without.
A new gut microbiome analysis has found significant differences in diversity between people with and without fibromyalgia (FM).1
“Despite significant information in the literature on FM pathophysiology and potential diagnostic mechanisms, it remains insufficient, as there is no definitive diagnostic procedure based on biological biomarkers,” lead investigator Lauma Ievena, PhD candidate,
The Institute of Microbiology and Virology of the Riga Stradiņš University Science Hub, Latvia, and colleagues wrote.1 “Thus, our study aims to identify the prevalence of HHV-6 A and B infection and changes in pro-inflammatory cytokines and microbiome, as well as measure the potential link between these parameters. Our goal is to gain information about measurable indicators with a biomarker potential that could help diagnose and assess FM by analyzing viral infections, cytokine profiles, gut microbiome, and their interactions.2”
Ievena and colleagues analyzed data from 17 participants diagnosed with FM and 24 apparently healthy participants. They used real-time polymerase chain reaction (qPCR), to detect the presence of human herpesvirus (HHV)-6A and B genomic sequences in DNA isolated from peripheral blood mononuclear cells (PBMCs) and buccal swabs. They measured HHV-6-specific IgG and IgM class antibodies and proinflammatory cytokine levels, using enzyme-linked immunosorbent assay (ELISA) and bead-based multiplex assays. They also analyzed the gut microbiome using next-generation sequencing.
The investigators found that HHV-6B was present in the PBMCS of 4 participants and the buccal swabs of 3 (23.5%) with FM compared with presence in the PBMCs of 4 control group participants (16.6%), although this difference was not statistically significant (P = 0.6975).1
Comparing cytokine levels between HHV-6B DNA-positive and negative patients with FM revealed significantly elevated levels of TNF-α (P = .03) in those that were positive. Notably, participants with FM and a body mass index (BMI) of 30 or higher had elevated of IL-1β, IL-2, TNF-α, and IL-17A/CTLA levels compared to those with the same BMI range in the control group, although these differences were also not statistically significant.1
Ievena and colleagues also found that the gut microbiome in participants with FM was less diverse than in the control group, as shown on a-diversity metrics with both Shannon’s (P = 0.03), and inverse Simpson’s (P = 0.03) indices being significantly higher in control group participants (4.11 ± 0.4 and 30.74 ± 13.9, respectively) than in participants with FM (3.78 ± 0.5 and 20.98 ± 13.7, respectively. Specifically, they found that FM gut microbiomes had depleted Dorea longicatena, Caprococcus catus, and Clostridiales bacterium NSJ 40 species; and enriched Lawsonibacter asaccharolyticus, Phocaeicola, Dysosmobacter sp., Victivallis, Enterocloster, Dysosmobacter sp. NSJ 60, and GGB79630 SGB13983 assembled genome of Firmicutes phylum species than those in the control group (all P < .0065).1
“This pilot study indicates a tendency where HHV-6B genome sequences are more frequently found in FM patients accompanied by higher plasma levels of TNF-α, compared to healthy individuals,” Ievena and colleagues concluded.1 “Additionally, significant differences were observed in the Shannon α-diversity and β-diversity of the gut microbiome between FM patients and matched healthy controls, indicating a shift in species abundance in the FM group.”