Figure 2.

Representation of the interaction between EBV, HHV-6, HERV and vitamin D in triggering MS. Vitamin D deficiency has been proposed to influence the risk of MS in individuals infected with EBV due to the overlap between the receptor-binding sites of EBNA-2 (a protein produced by EBV) and vitamin D. Additionally, high levels of vitamin D may inhibit EBV infection through apoptosis, while HHV-6 can activate latent EBV in B cells. In patients with MS, an interaction between vitamin D and HERV has also been observed. There is an inverse correlation between HERV-W DNA levels and vitamin D levels and high vitamin D levels may inhibit HERV transactivation. Furthermore, low vitamin D levels increase the risk of MS in individuals with high titers of anti-HHV-6A antibodies. EBV has the ability to induce the expression of certain HERV genes and the activation of HERV-W during infectious mononucleosis has been proposed as a potential effector in the pathogenesis of MS. It is important to note that while these relationships have been identified, the precise mechanisms and their significance in MS development and progression require further investigation. The interplay between EBV, HHV, HERV and vitamin D in the context of MS is complex and multifaceted.