virus name = Epstein Barr virus. propose a potential antigen for a vaccination. discuss how it does or does not fill the criteria of a good antigen. (300 word)
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Introduction
Primates and their γ-herpesviruses enjoy a largely peaceful coexistence where a balance of power has been reached over evolutionary time. Coevolution probably began before primate speciation and has allowed these viruses to develop sophisticated systems for the evasion of host immune responses. As a consequence, herpesvirus vaccines have been especially difficult to design because of viral latency, persistence, and immune modulation. Epstein–Barr virus (EBV) persists for the life of the individual in the face of a range of antibody responses, some of which are virus-neutralizing in vitro and a multitude of cell-mediated responses, including viral-specific CD8+ T-cells, CD4+ T-cells and NK cells. At least 95% of the adult population is infected with EBV and, for the vast majority, there are no clinical consequences whatsoever and an asymptomatic carrier state is maintained. It is not clear whether advantages are conferred to humans by lifelong EBV infection, but it is possible that some immunological effects, such as bias of the T-cell receptor repertoire are provided on a population-wide basis. Whether unselective mass vaccination of healthy individuals to prevent or modify EBV infection may cause more problems than it would solve must be considered.
M. A. Epstein first put forward ideas on the , and activated B-cell expressing the full panel of EBV latent genes in the growth program or Latency Ⅲ, and B-cells in Latency Ⅱ which may subsequently generate the memory reservoir B-cells (Thorley-Lawson, 2001). Cells in Latency Ⅲ have only been found in the germinal center of lymphoid follicles and these are regions in which cytotoxic T-cells (CTL) are poorly represented probably because EBV-specific CD8 T-cells lack homing receptors for lymphoid infection sites (Chen et al., 2001). CD4+ T-cells are detectable at low frequency within B-cell follicles and may, therefore, interact directly with EBV-infected B-cells at this site. It is possible that CD4+ T-cells primed by gp350 or latency antigen vaccination would become reactivated on viral challenge (Adhikary et al., 2006). Such cells could influence the course of IM by inducing apoptosis of EBV-infected B-cells within infected lymph nodes and by down.