The Journal of Infectious Diseases · 2011 · 67 citations · 41 references
Life SciencesInfectious DiseasesMicrobiologyHost-pathogen InteractionsMolecular VirologyVirologyAnimal VirusesHost-virus InteractionsViral InfectionsViral PathogenesisViral TropismVirus-host InteractionsBat InteractionBat ReservoirsBats As Reservoir HostsPrimate Infectious DiseasesViral Entry ComplexesViral Entry ReceptorsViral Genome ReleaseViral Release Mechanisms
Infection with Ebola virus (EBOV) causes hemorrhagic fever in humans with high case-fatality rates. The EBOV-glycoprotein (EBOV-GP) facilitates viral entry and promotes viral release from human cells. African fruit bats are believed not to develop disease upon EBOV infection and have been proposed as a natural reservoir of EBOV. We compared EBOV-GP interactions with human cells and cells from African fruit bats. We found that susceptibility to EBOV-GP-dependent infection was not limited to bat cells from potential reservoir species, and we observed that GP displayed similar biological properties in human and bat cells. The only exception was GP localization, which was to a greater extent intracellular in bat cells as compared to human cells. Collectively, our results suggest that GP interactions with fruit bat and human cells are similar and do not limit EBOV tropism for certain bat species.
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Fruit bats as reservoirs of Ebola virus
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