Epstein–Barr virus and multiple sclerosis

Authors

DOI:

https://doi.org/10.14739/2310-1237.2020.3.221870

Keywords:

Epstein–Barr virus, HHV-4, multiple sclerosis, demyelination, B lymphocytes, microglia

Abstract

 

Multiple sclerosis (MS) is a chronic inflammation of the central nervous system, a characteristic feature of which is the gradual development of focal and irreversible demyelination of the membranes of nerve structures in the spinal cord and brain, which leads to a gradual accumulation of neurological deficit and disability.

Aim – substantiation of the role of Epstein–Barr virus infection in the etiology and pathogenesis of MS based on the analysis of modern literary sources.

Herpes gamma viruses remain one of the most important suspects in the etiology of MS, including Epstein–Barr virus (EBV), which causes a lifelong infectious process in the human body. Human gammaherpesvirus 4 (HHV-4) can realize its pathogenic potential by performing lytic replication or lead to a delay in replication or reactivation of infection in both epithelial cells and B lymphocytes.

Taking into account current data on the biological properties of EBV and analyzing the role of this herpes virus in the pathogenesis of neurodegenerative diseases, this review was generated. Due to its molecular structure, EBV has specific biological properties, among which one of the most important is its tropism for the host’s immune tissue, in particular, B-lymphocytes, which obviously determines the life-long persistence of the virus. Thus, forming a latent process in the human body due to replicative cycles in B cells, EBV, on the one hand, controls the primary response of B lymphocytes, which leads to a deficiency of both humoral and cellular immunity factors. On the other hand, it contributes to the persistence of HHV-4 and the development of an infectious process constant with periods of reactivation.

With this in mind, an important detail that may link EBV infection with MS is that the development of the clinical picture and its course bears some similarity to natural HHV-4 infection, probably following the biological cycle of the virus over a certain period of time. Therefore, based on the found indirect relationship between EBV infection and MS, as well as on the indicated immunological and genetic mechanisms that are involved in neuroinflammatory processes, it is impossible not to take into account the role of herpes viruses in the development of the disease. But why, among a large population of HHV-4 carriers, only a small percentage develop EBV-associated MS remains to be seen.

Analyzing the conducted studies in which different results were obtained on the effect of EBV infection on different periods of MS development (by initiating the triggering or maintaining the inflammatory process or participating in its progression), it has now become clear that if the etiological role of EBV in this disease is present, then the course of the disease is not may not be related to HHV-4 biological cycles.

Conclusions. Currently, a direct connection is established between EBV infection and the development of MS. However, it is also impossible to refute and even more so to reject the role of human gammaherpesvirus 4 in the pathogenesis of multiple sclerosis.

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Skliar AI, Torianyk II, Osolodchenko TP, Ponomarenko SV. Epstein–Barr virus and multiple sclerosis. Pathologia [Internet]. 2020Dec.29 [cited 2026May19];17(3). Available from: https://pat.zsmu.edu.ua/article/view/221870

Issue

Section

Review