The interplay between Epstein–Barr virus and B lymphocytes: implications for infection, immunity, and disease

Abstract

Human B cells are the primary targets of Epstein Barr virus (EBV) infection. In most cases EBV infection is asymptomatic because of a highly effective host immune response but some individuals develop self-limiting infectious mononucleosis, while others develop EBV-associated lymphoid or epithelial malignancies. The viral and immune factors that determine the outcome of infection are not understood. The EBV life cycle includes a lytic phase, culminating in the production of new viral particles, and a latent phase, during which the virus remains largely silent for the lifetime of the host in memory B cells. Thus, in healthy individuals there is a tightly orchestrated interplay between EBV and the host that allows the virus to persist. To promote viral persistence EBV has evolved a variety of strategies to modulate the host immune response including inhibition of immune cell function, blunting of apoptotic pathways, and interfering with antigen processing and presentation pathways. In this article we focus on mechanisms by which dysregulation of the host B cell, and immune modulation, by the virus can contribute to development of EBV+ B cell lymphomas.

Simultaneously increased expression of microRNA‐155 and suppressor of cytokine signaling 1 (SOCS1) gene in the peripheral blood mononuclear cells of patients with primary Sjögren's syndrome

“…The miR‐155 is encoded within B cell integration ( Bic ) gene located on chromosome 21 . The interplay between EBV and B‐lymphocytes in the context of infection, immunity and diseases is widely known . The involvement of EBV infection in the insurgence and persistence of Sjögren's syndrome is also an accepted aspect in the pathogenesis of the disease .…”

The Latent Membrane Protein 1 (LMP1)

“…In addition to B95.8-LMP1, a large number of LMP1 sequence variants have been isolated predominantly from NPC samples or healthy carriers of different geographical regions of the world (Hu et al 1991;Miller et al 1994;Sandvej et al 1997;Hatton et al 2014;Lorenzetti et al 2012;Renzette et al 2014). Due to space limitations, a detailed description of such LMP1 variants cannot be given here.…”

Transplant Games Promote Donation, Showcase Healthy Recipients

“…Analysis of the signaling properties of the SLCL-derived LMP1 molecules revealed gain of function mutations that differ from the B95.8 form of LMP1 (14). Thus we, and others, have suggested that EBV genomic diversity could play a role in viral function and pathogenesis (3,33,34). Here we provide the first analysis of the miRNA profiles in latency III EBV þ B cell lines from PTLD patients with lymphomas that were naturally infected by EBV in vivo, compared to the miRNA profile found in conventional latency III LCL generated from B95.8 infection in vitro.…”

“…However, EBV infection can also lead to the development of a variety of lymphoid and epithelial malignancies. In immunosuppressed transplant recipients, EBV is associated with posttransplant lymphoproliferative disorder (PTLD) which can manifest as aggressive B cell lymphomas (3). While impaired T cell immunity is considered to be the major factor contributing to the outgrowth of these EBV þ B cells, the intrinsic viral factors that drive lymphoma expansion are not well understood.…”