
doi: 10.2222/jsv.65.71
pmid: 26923960
Ebola virus is an enveloped virus with filamentous structure and causes a severe hemorrhagic fever in human and nonhuman primates. Host cell entry is the first essential step in the viral life cycle, which has been extensively studied as one of the therapeutic targets. A virus factor of cell entry is a surface glycoprotein (GP), which is an only essential viral protein in the step, as well as the unique particle structure. The virus also interacts with a lot of host factors to successfully enter host cells. Ebola virus at first binds to cell surface proteins and internalizes into cells, followed by trafficking through endosomal vesicles to intracellular acidic compartments. There, host proteases process GPs, which can interact with an intracellular receptor. Then, under an appropriate circumstance, viral and endosomal membranes are fused, which is enhanced by major structural changes of GPs, to complete host cell entry. Recently the basic research of Ebola virus infection mechanism has markedly progressed, largely contributed by identification of host factors and detailed structural analyses of GPs. This article highlights the mechanism of Ebola virus host cell entry, including recent findings.
Membrane Glycoproteins, Cells, Multivesicular Bodies, Virus Attachment, Hydrogen-Ion Concentration, Virus Internalization, Ebolavirus, Virus Replication, Cell Physiological Phenomena, Viral Proteins, Host-Pathogen Interactions, Animals, Humans, Receptors, Virus, Peptide Hydrolases
Membrane Glycoproteins, Cells, Multivesicular Bodies, Virus Attachment, Hydrogen-Ion Concentration, Virus Internalization, Ebolavirus, Virus Replication, Cell Physiological Phenomena, Viral Proteins, Host-Pathogen Interactions, Animals, Humans, Receptors, Virus, Peptide Hydrolases
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