F — Filoviruses
Filoviruses include the ebola virus (EBOV) and Marburg virus (MARV). Ebola virus disease presents with fever, gastrointestinal symptoms, coagulopathy, multiorgan failure, and high mortality in severe outbreaks. Survivors may experience persistent viral reservoirs in immune-privileged sites (e.g., eye, testes). Research priorities include monoclonal antibody therapies, viral persistence mechanisms, and vaccine platforms such as recombinant vesicular stomatitis virus (rVSV)-based vaccines.
Filoviruses are enveloped, filamentous, negative-sense single-stranded RNA viruses. Their non-segmented genome encodes seven structural proteins, including the glycoprotein (GP), nucleoprotein (NP), RNA-dependent RNA polymerase (L), and VP35 and VP24, which play critical roles in immune evasion.
Entry occurs via macropinocytosis, followed by endosomal processing of GP and interaction with the intracellular receptor NPC1. Replication takes place in the cytoplasm within inclusion bodies. Filoviruses are highly cytopathic in vitro, but much of their in vivo pathology stems from dysregulated host responses.
A hallmark of filovirus infection is profound innate immune antagonism. VP35 inhibits RIG-I–mediated interferon signaling, while VP24 blocks STAT1 nuclear translocation, impairing interferon responses. Early infection of monocytes, macrophages, and dendritic cells promotes viral dissemination and massive cytokine release. This “cytokine storm,” along with endothelial dysfunction and coagulation abnormalities, drives vascular leakage and shock.
Filoviruses include the ebola virus (EBOV) and Marburg virus (MARV). Ebola virus disease presents with fever, gastrointestinal symptoms, coagulopathy, multiorgan failure, and high mortality in severe outbreaks. Survivors may experience persistent viral reservoirs in immune-privileged sites (e.g., eye, testes). Research priorities include monoclonal antibody therapies, viral persistence mechanisms, and vaccine platforms such as recombinant vesicular stomatitis virus (rVSV)-based vaccines.
Filoviruses are enveloped, filamentous, negative-sense single-stranded RNA viruses. Their non-segmented genome encodes seven structural proteins, including the glycoprotein (GP), nucleoprotein (NP), RNA-dependent RNA polymerase (L), and VP35 and VP24, which play critical roles in immune evasion.
Entry occurs via macropinocytosis, followed by endosomal processing of GP and interaction with the intracellular receptor NPC1. Replication takes place in the cytoplasm within inclusion bodies. Filoviruses are highly cytopathic in vitro, but much of their in vivo pathology stems from dysregulated host responses.
A hallmark of filovirus infection is profound innate immune antagonism. VP35 inhibits RIG-I–mediated interferon signaling, while VP24 blocks STAT1 nuclear translocation, impairing interferon responses. Early infection of monocytes, macrophages, and dendritic cells promotes viral dissemination and massive cytokine release. This “cytokine storm,” along with endothelial dysfunction and coagulation abnormalities, drives vascular leakage and shock.