Lassa fever causes multisystem disease and has a fatality rate <70%. Severe cases exhibit abnormal coagulation, endothelial barrier disruption, and dysfunctional platelet aggregation but the underlying mechanisms remain poorly understood.
In a new study published in the Center for Disease Control and Prevention’s Emerging Infectious Diseases Journal, researchers in Sierra Leone assessed Lassa fever patients’ day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function.
Evidence of impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections.
The data forms a basis for investigation into specific pathways that could provide targets of intervention to minimize the effects of host immunopathology and enable the immune system adequate time to clear the virus.
The researchers state that unavailability of samples and ELISA kits in Sierra Leone limited more extensive analyses of the data, specifically in cases in which analytes trended but did not reach statistical significance. More robust patient data and sample collection could help define hematological dysfunction during disease progression and correlate these markers with signs, such as facial and pulmonary edema.
Endotheliopathy and Platelet Dysfunction as Hallmarks of Fatal Lassa Fever. Emerging Infectious Diseases.
