Marburg- and Ebolaviruses

Olejnik, Judith, Hume, Adam J, Leung, Daisy W, Amarasinghe, Gaya K, Basler, Christopher F, Mühlberger, Elke, Judith Olejnik, Adam J. Hume, Daisy W. Leung, Gaya K. Amarasinghe, Christopher F. Basler, Elke Mühlberger, Hume, Adam J., Leung, Daisy W., Amarasinghe, Gaya K., Basler, Christopher F.

This chapter describes the various strategies filoviruses use to escape host immune responses with a focus on innate immune and cell death pathways. Since filovirus replication can be efficiently blocked by interferon (IFN), filoviruses have evolved mechanisms to counteract both type I IFN induction and IFN response signaling pathways. Intriguingly, marburg- and ebolaviruses use different strategies to inhibit IFN signaling. This chapter also summarizes what is known about the role of IFN-stimulated genes (ISGs) in filovirus infection. These fall into three categories: those that restrict filovirus replication, those whose activation is inhibited by filoviruses, and those that have no measurable effect on viral replication. In addition to innate immunity, mammalian cells have evolved strategies to counter viral infections, including the induction of cell death and stress response pathways, and we summarize our current knowledge of how filoviruses interact with these pathways. Finally, this chapter delves into the interaction of EBOV with myeloid dendritic cells and macrophages and the associated inflammatory response, which differs dramatically between these cell types when they are infected with EBOV. In summary, we highlight the multifaceted nature of the host-viral interactions during filoviral infections.