Abstract
Epstein-Barr Virus (EBV) is an extremely successful human herpes virus, which infects essentially all human beings at some time during their life span. EBV infection and the associated immune response results in production of antibodies (seroconversion), which occurs mainly during the first years of life, but may also happen during adolescence or later in life. Infection of adolescents can result in infectious mononucleosis, an acute serious condition characterized by massive lymphocytosis. Transmission of EBV mainly occurs through saliva but can rarely be spread through semen or blood, e.g. through organ transplantations and blood transfusions. EBV transmission through oral secretions results in infection of epithelial cells of the oropharynx. From the epithelial cells EBV can infect B cells, which are the major reservoir for the virus, but other cell types may also become infected. As a result, EBV can shuttle between different cell types, mainly B cells and epithelial cells. Moreover, since the virus can switch between a latent and a lytic life cycle, EBV has the ability to cause chronic relapsing/reactivating infections. Chronic or recurrent EBV infection of epithelial cells has been linked to systemic lupus erythematosus and Sjögren’s syndrome, whereas chronic/recurrent infection of B cells has been associated with rheumatoid arthritis, multiple sclerosis and other diseases. Accordingly, since EBV can shuttle between epithelial cells and B cells, the systemic autoimmune diseases often occur as overlapping syndromes with symptoms and characteristic autoantibodies (e.g. antinuclear antibodies and rheumatoid factors) reflecting epithelial and/or B cell infection.
Highlights
Epstein-Barr VirusEpstein-Barr Virus (EBV) is a lymphotropic herpes virus and the causative agent of infectious mononucleosis (IM) [1,2,3,4]
Current treatments can be related to EBV infection, e.g. CD20 monoclonal antibodies (MAbs), which presumably diminish the burden of EBVinfected B cells, and Tumor necrosis factor (TNF) MAbs, which possibly diminish the burden of EBV infection by an anti-inflammatory effect [172,173,174]
In rheumatoid arthritis (RA), relapses most likely follow re-activation of EBV in B cells upon Ag stimulation. This results in production of EBVtransformed B cell blasts, which by their very nature will attempt homing to bones and will have a tendency to populate joints, where the concomitant lytic EBV production may result in EBV infection of synovial epithelial cells
Summary
Epstein-Barr Virus (EBV) is a lymphotropic herpes virus and the causative agent of infectious mononucleosis (IM) [1,2,3,4]. EBV can occasionally reactivate, e.g. in response to antigen stimulation of memory B cells, resulting in lytic production of virions upon expression of an ordered sequence of viral genes [55,56,57] This in turn mounts an increased immune response against EBV, neutralizing infected cells and forcing the virus into latency again. To be able to exit from the host cell in a controlled process, and to be able to infect other cells, several viral gPs have to be inserted into the envelope membrane as mentioned above These proteins are targets for innate immune recognition and antibody (Ab) production, as described in the preceding paragraph, but extensive glycosylation with host-derived glycans affords considerable protection against pattern recognition (scavenger) receptor (including complement) and Ab recognition (“glycan shielding”). The presence of DNA Abs and other ANAs would seem to be compatible with infection by a DNA virus in combination with inefficient removal of apoptotic and necrotic material
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