Inflammatory responses in Ebola virus‐infected patients

• Published in: Clinical and experimental immunology Vol. 128; no. 1; pp. 163 - 168
• Main Authors: BAIZE, S., LEROY, E. M., GEORGES, A. J., GEORGES‐COURBOT, M.‐C., CAPRON, M., BEDJABAGA, I., LANSOUD‐SOUKATE, J., MAVOUNGOU, E.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.04.2002; Blackwell; Oxford University Press; Blackwell Science Inc
• Subjects: Adult; Anti-Inflammatory Agents - blood; Antibodies, Viral - blood; Antigens, Viral - blood; Biological and medical sciences; Biomarkers - blood; Cytokines - blood; Disease Outbreaks; Ebolavirus - immunology; Female; Gabon - epidemiology; haemorrhagic fever; Hemorrhagic Fever, Ebola - diagnosis; Hemorrhagic Fever, Ebola - epidemiology; Hemorrhagic Fever, Ebola - immunology; Hemorrhagic Fever, Ebola - mortality; human; Human viral diseases; Humans; IL‐10; Immunoglobulin G - blood; Infectious diseases; Inflammation - blood; Inflammation Mediators - blood; innate immunity; Kinetics; Male; Marburg disease, ebola disease; Medical sciences; monocyte; Original; Prognosis; Survivors; Tropical viral diseases; Viral diseases; Gabon; Human; Prognosis; Monocyte; Pathophysiology; Interleukin 1 receptor antagonist; Mortality; Cytokine; Biological marker; Natural immunity; Inflammation; Ebola hemorrhagic fever; Virus; Infection; Ebola virus; Mononegavirales; Filoviridae; Viral disease; Interleukin 10; Filovirus; Tumor necrosis factor α; Macrophage; Biological receptor
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1046/j.1365-2249.2002.01800.x

SUMMARY Ebola virus subtype Zaire (Ebo‐Z) induces acute haemorrhagic fever and a 60–80% mortality rate in humans. Inflammatory responses were monitored in victims and survivors of Ebo‐Z haemorrhagic fever during two recent outbreaks in Gabon. Survivors were characterized by a transient release in plasma of interleukin‐1β (IL‐1β), IL‐6, tumour necrosis factor‐α (TNFα), macrophage inflammatory protein‐1α (MIP‐1α) and MIP‐1β early in the disease, followed by circulation of IL‐1 receptor antagonist (IL‐1RA) and soluble receptors for TNFα (sTNF‐R) and IL‐6 (sIL‐6R) towards the end of the symptomatic phase and after recovery. Fatal infection was associated with moderate levels of TNFα and IL‐6, and high levels of IL‐10, IL‐1RA and sTNF‐R, in the days before death, while IL‐1β was not detected and MIP‐1α and MIP‐1β concentrations were similar to those of endemic controls. Simultaneous massive activation of monocytes/macrophages, the main target of Ebo‐Z, was suggested in fatal infection by elevated neopterin levels. Thus, presence of IL‐1β and of elevated concentrations of IL‐6 in plasma during the symptomatic phase can be used as markers of non‐fatal infection, while release of IL‐10 and of high levels of neopterin and IL‐1RA in plasma as soon as a few days after the disease onset is indicative of a fatal outcome. In conclusion, recovery from Ebo‐Z infection is associated with early and well‐regulated inflammatory responses, which may be crucial in controlling viral replication and inducing specific immunity. In contrast, defective inflammatory responses and massive monocyte/macrophage activation were associated with fatal outcome.