Although latent HHV-6 and HHV-7 were both more prevalent in the whole blood of fibromyalgia patients than in controls, only HHV-6 was found to be significantly correlated with nerve fiber damage severity. 51% of fibromyalgia patients had detectable HHV-6 DNA in whole blood compared to just 6% of controls. 17% of fibromyalgia patients had detectable DNA in the plasma compared to none of the controls.
While HHV-6 has been a virus of interest in the context of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME), HHV-6 has not been studied in fibromyalgia, a related disease in several respects. Studies have found that up to 70% of people with fibromyalgia meet criteria for ME/CFS. Viral infections have been considered as possible triggers of both disorders, but so far, their exact roles have proved elusive. In the first study to examine potential HHV-6 involvement in fibromyalgia, a significant association was found between active or latent HHV-6 and nerve fiber damage among patients with the disease.
The investigators used quantitative sensory testing (QST) to determine the extent to which A delta and C nerve fibers were damaged. The unmyelinated C fibers are responsible for warmth sensation and deep and burning pain, while the thinly myelinated A delta fibers are involved in sensing cold sensation and sharp pain. Reduced or elevated sensation and/or pain to heat and/or cold in hands and/or feet represented abnormal QST findings. Of 43 patients, 39 (91%) showed abnormalities in 1-3 thermal QST modalities, which is indicative of light to severe A delta and C nerve fiber damage.
The team also performed qualitative, nested PCR on whole blood samples from patients and controls to test for presence of HHV-6 and HHV-7 DNA. They found that half of controls and 84% of patients had one or both viruses in their blood (p=0.013), and a significantly higher rate of HHV-6/7 coinfection was found among patients compared to controls (33% vs 5%, respectively). In total, HHV-6 genomic sequences were found in 23/43 (51%) patients vs 3/50 (6%) controls (p<0.001). There was less of a difference between prevalence of HHV-7 DNA among patients and controls, but like HHV-6, rates of detection were significantly higher among patients than controls (75.5% vs 52%).
Plasma viremia, which is considered a proxy for active infection, was only present in fibromyalgia patients (6/36, 17%); no active infection was detected in controls. Of the active infections, HHV-6 was found alone in 2 samples, HHV-7 single infection was found in 2 samples, and coinfections, in which both HHV-6 and -7 DNA were present in plasma, were also detected in 2 patients. Quantitative PCR determined that median HHV-6 and HHV-7 loads were higher in whole blood from patients compared to controls (815.8 and 311 copies/106 cells vs 125.5 and 173.12 copies/106 cells).
Among patients with active or latent HHV-6, abnormal QST results were more pronounced than in those without the virus in their whole blood or plasma. It remains to be determined whether the presence of HHV-6 and higher viral loads are a cause or effect of fibromyalgia, but it is known that HHV-6 infects nervous tissue and induces cellular dysfunction in affected areas. It is possible that persistent HHV-6 infection could directly or indirectly damage C and A delta nerve fibers, leading to fibromyalgia development and/or exacerbation.
For more information on HHV-6 in diseases affecting the peripheral or central nervous system, visit our webpage on the topic.
Find the full paper here: Krumina 2019.