Abstract
Epstein-Barr virus (EBV), also known as human herpesvirus 4, is a double-stranded DNA virus that is ubiquitous in 90–95% of the population as a gamma herpesvirus. It exists in two main states, latent infection and lytic replication, each encoding viral proteins with different functions. Human B-lymphocytes and epithelial cells are EBV-susceptible host cells. EBV latently infects B cells and nasopharyngeal epithelial cells throughout life in most immunologically active individuals. EBV-infected cells, free viruses, their gene products, and abnormally elevated EBV titers are observed in the cerebrospinal fluid. Studies have shown that EBV can infect neurons directly or indirectly via infected B-lymphocytes, induce neuroinflammation and demyelination, promote the proliferation, degeneration, and necrosis of glial cells, promote proliferative disorders of B- and T-lymphocytes, and contribute to the occurrence and development of nervous system diseases, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, acute cerebellar ataxia, meningitis, acute disseminated encephalomyelitis, and brain tumors. However, the specific underlying molecular mechanisms are unclear. In this paper, we review the mechanisms underlying the role of EBV in the development of central nervous system diseases, which could bebeneficial in providing new research ideas and potential clinical therapeutic targets for neurological diseases.
Highlights
Epstein-Barr virus (EBV) is an approximately 172-kb DNA, double-stranded gamma herpesvirus that contains a DNA-wrapped cyclic protein as the core, a nucleocapsid consisting of 162 capsules, a protein envelope located between the nucleocapsid and the envelope, and an outer envelope with an external virus-encoded membrane glycoprotein
In-depth studies have shown that EBV-encoded proteins (e.g., EBNA1, LMP1, LMP2A) derived from EBV-infected B cells are involved in the development of Multiple sclerosis (MS) by inducing neuroinflammation and regulating the immune function of B and T cells (Tarlinton et al, 2019)
One study found cross-reactivity between EBNA-1 and myelin oligodendrocyte glycoprotein (MOG), in which EBV infection triggered the production of anti-MOG antibodies thereby elevating MOG concentrations and inducing the development of Acute disseminated encephalomyelitis (ADEM) (Selter et al, 2010; Lalive et al, 2011; Nakamura et al, 2017)
Summary
Epstein-Barr virus (EBV) is an approximately 172-kb DNA, double-stranded gamma herpesvirus that contains a DNA-wrapped cyclic protein as the core, a nucleocapsid consisting of 162 capsules, a protein envelope located between the nucleocapsid and the envelope, and an outer envelope with an external virus-encoded membrane glycoprotein. In-depth studies have shown that EBV-encoded proteins (e.g., EBNA1, LMP1, LMP2A) derived from EBV-infected B cells are involved in the development of MS by inducing neuroinflammation and regulating the immune function of B and T cells (Tarlinton et al, 2019).
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