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Shed GP of Ebola Virus Triggers Immune Activation and Increased Vascular Permeability


Ebola virus, a member of the Filoviridae family, causes lethal hemorrhagic fever in man and primates, displaying up to 90% mortality rates. Viral infection is typified by an excessive systemic inflammatory response resembling septic shock. It also damages endothelial cells and creates difficulty in coagulation, ultimately leading to haemorrhaging, organ failure and death. A unique feature of EBOV is that following infection high amounts of truncated surface GP, named shed GP, are released from infected cells and are detected in the blood of patients and experimentally infected animals. However the role of shed GP in virus replication and pathogenicity is not yet clearly defined. Here we show that shed GP released from virus-infected cells binds and activates non-infected DCs and macrophages causing the massive release of pro- and anti-inflammatory cytokines and also affects vascular permeability. These activities could be at the heart of the excessive and dysregulated inflammatory host reactions to infection and thus contribute to high virus pathogenicity.


Vyšlo v časopise: Shed GP of Ebola Virus Triggers Immune Activation and Increased Vascular Permeability. PLoS Pathog 10(11): e32767. doi:10.1371/journal.ppat.1004509
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004509

Souhrn

Ebola virus, a member of the Filoviridae family, causes lethal hemorrhagic fever in man and primates, displaying up to 90% mortality rates. Viral infection is typified by an excessive systemic inflammatory response resembling septic shock. It also damages endothelial cells and creates difficulty in coagulation, ultimately leading to haemorrhaging, organ failure and death. A unique feature of EBOV is that following infection high amounts of truncated surface GP, named shed GP, are released from infected cells and are detected in the blood of patients and experimentally infected animals. However the role of shed GP in virus replication and pathogenicity is not yet clearly defined. Here we show that shed GP released from virus-infected cells binds and activates non-infected DCs and macrophages causing the massive release of pro- and anti-inflammatory cytokines and also affects vascular permeability. These activities could be at the heart of the excessive and dysregulated inflammatory host reactions to infection and thus contribute to high virus pathogenicity.


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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

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PLOS Pathogens


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