Since both HHV-6 and EBV have been associated with an increased risk of autoimmune disease development, a group at the American University of Beirut studied whether viral DNA might be capable of triggering IL-17, a cytokine associated with autoimmune disease. They injected BALB/c mice intraperitoneally with either EBV or HHV-6A DNA. The mice were tested at three time points post-injection, and IL-17 was increased compared to the controls who were injected with water. IL-23 was also markedly elevated.
IL-17 is believed to be involved in the pathogenesis of autoimmune disease and inflammation, and is elevated in patients with multiple sclerosis, rheumatoid arthritis, lupus, and inflammatory bowel disease. IL-17 levels increased 2 to 11 fold after EBV genome copies were injected, and they increased 1.2 to 7 fold after an injection of HHV-6A. IL-10 was reduced after EBV injections but not after HHV-6A injections.
The authors point out that multiple pattern recognition receptors have been documented to respond to viral DNA, including toll receptors and that TLR3 and TLR9 have been implicated in the production of Th1 pro-inflammatory cytokines in response to HSV-1 DNA. Branka Horvat’s group in France showed that HHV-6A reactivation in CD46 transgenic mice was dependent on TLR9 (Reynaud 2014).
The authors hope to do further research to elucidate the precise roles played by viral DNA in triggering IL-17, and hope their findings will help assess disease risk and formulate new drug design and development.
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