Pichindé viral infection of strain 13 guinea pigs is a model for Lassa fever virus in humans. Infected animals show impaired platelet function and altered coagulation parameters. Human endothelial cells and the human endothe1ia1-1 ike cell line, EA926, were infected with Pichinde virus. Following infection, cultures were monitored by phase contract microscopy for cytopathic effect (CPE). Assays of supernatant were used to document viral growth and to measure those endothelial-produced

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... that might affect hemostasis. In addition, the cells were stimulated with phorbol ester (PMA), which stimulates the production of prostacyclin. Infection showed no noticeable effect on the endothelial cells or EA926 cells which were untreated with PMA. PHA-treated EA926 cells were subject to CPE. Factor VIII antigen was not significantly affected by viral infection, PMA treatment, or endotoxin exposure. The production of PGFl, measured as an estimate of prostacyclin synthesis, was dependent on the concentration of stimulating PMA. Infected cultures showed decreased responsiveness to PMA stimulation when infected by increasing concentrations of Pichindé. The most noticeable effect was noted when cultures were infected with a multiplicity of infection of 0.1 and 100 ng/ml PMA. Thromboxane B2 an estimate of thromboxane A2, showed no significant change. No detectable leukotriene C4 was produced and no significant change in leukotriene B4 was measured. The decreased prostacyclin production by the infected endothelial cells may indicate a role for the endothelium in the hemorrhagic syndrome that accompanies some viral diseases.