Human herpesvirus-6 (HHV-6) has been associated with multiple autoimmune diseases, including Sjogren’s syndrome, multiple sclerosis, and systemic lupus erythematosus. A recent study led by Rizzo and Caselli from the University of Ferrara has found a possible link to another autoinflammatory process, Hashimoto’s Thyroiditis (HT). They found that HHV-6 infection correlated with higher levels of a particular type of NK cell associated with a potent release of cytokines.
The Italian group analyzed fine needle thyroid aspirates (FNAs) and blood from 8 HT patients and 8 controls. HHV-6 was found in 8/8 (100%) HT FNAs compared to only 2/8 (25%) control FNAs. Furthermore, the viral load in HT specimens was higher than in controls (mean 1.2 x 104 copies/ug DNA vs. mean 3.9 x 102 copies/ug DNA, respectively). Similarly, viral load was higher (mean 1.8 x 104 copies/ug DNA) and detected more often (8/8 HT specimens) in PBMCs than in controls, where the mean viral load was 3.7 x 102 copies/ug DNA in 3/8 (37%) samples.
The researchers also measured the antibody response and the percentages of natural killer (NK) cells. An antibody response directed against the HHV-6 U94/Rep protein was not only found to be more prevalent in HT patients than in controls (8/8 vs. 6/8), but the titer was also significantly higher in HT patients than in control subjects (1:1624 vs 1:543, p<0.01). In addition, a higher percentage and activation status of CD3-CD56bright NK cells were found in samples from HT patients compared to controls.
The authors believe that these results demonstrate a possible relationship between HHV-6 and the development of Hashimoto’s Thyroiditis. They point out that since CD3-CD56bright NK cells have the ability to produce abundant cytokines following activation, these NK cells might play an important role in disease activity and viral infection.
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