Epstein-Barr virus immunossuppression of innate immunity mediated by phagocytes

Epstein-Barr virus (EBV) is an oncogenic human herpesvirus that persistently infects approximately 90% of the world's population. Such a remarkably sustained of viral infectivity relies on EBV's ability to evade the host immune defenses. A crucial part of this anti-EBV response is mediated by cytotoxic CD8+ T lymphocytes, which maintain a life-long control over proliferating latently-infected B cells in order to prevent these from giving rise to lymphomatous diseases. On the other hand, little has been done to assess the role of phagocytes-mediated innate immunity in the pathogenesis of EBV infection. In the course of primary EBV infection, episodes of neutropenia and monocytopenia can be observed during the acute phase of infection. According to the role of those cells in the non specific and specific immunity, such a decrease in circulating phagocytes may then temporarily affect the immune defense and potentially influence the outcome of EBV infection. Recent studies have demonstrated that EBV infects both neutrophils and monocytes and modulates several of their biological functions. This review covers the current state of our knowledge relative to the role of neutrophils and monocytes in EBV pathogenesis and describes the nature of countermeasures deployed by EBV against these cells.