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Highly pathogenic Ebola and Marburg filoviruses infect myeloid phagocytes, but viral attachment and entry occur through a complex series of events involving the interaction of several viral and host components. This chapter focuses on what is currently known about the cellular pathways exploited by filoviruses to gain access into myeloid phagocytes. These antigen-presenting cells are located at the mucosal portals of viral entry, and upon pathogen encounter, migrate to secondary lymphoid tissues to induce antiviral immunity. However, once infected, myeloid phagocytes may also contribute to systemic viral dissemination. Here we discuss the current therapeutic agents available for blocking filoviral entry into these cells as a strategy to limit viral dissemination and disease progression, which might trigger protective immune responses. The development of a combined therapy targeting the precise host factors that confer susceptibility to filoviral entry may also lead to a new generation of broad-spectrum antivirals with potential clinical applicability.

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