Endotheliopathy and Platelet Dysfunction as Hallmarks of Fatal Lassa Fever
Lucy E. Horton1
, Robert W. Cross1
, Jessica N. Hartnett, Emily J. Engel, Saori Sakabe, Augustine Goba, Mambu Momoh, John Demby Sandi, Thomas W. Geisbert, Robert F. Garry, John S. Schieffelin, Donald S. Grant, and Brian M. Sullivan
Author affiliations: The Scripps Research Institute, La Jolla, California, USA (L.E. Horton, S. Sakabe, B.M. Sullivan); University of Texas Medical Brach, Galveston, Texas, USA (R.W. Cross, T.W. Geisbert); Tulane University School of Medicine, New Orleans, Louisiana, USA (J.N. Hartnett, E.J. Engel, R.F. Garry, J.S. Schieffelin); Kenema Government Hospital, Kenema, Sierra Leone (A. Goba, M. Momoh, J.D. Sandi, D.S. Grant); Ministry of Health and Sanitation, Freetown, Sierra Leone (A. Goba, M. Momoh, J.D. Sandi); Eastern Polytechnic Institute, Kenema (M. Momoh, D.S. Grant); Njala University, Moyamba, Sierra Leone (J.D. Sandi); University of Sierra Leone, Freetown (D.S. Grant)
Figure 7. Representative platelet aggregometry performed on a 1:1 mix of platelet-rich plasma from a healthy control (HC) participant and platelet-poor plasma dialyzed to remove EDTA from either healthy controls or acute Lassa fever (LF) patients, Sierra Leone, 2015–2018. Aggregation was stimulated by addition of 5 μmol ADP. Plasma from fatal LF cases caused a decrease in aggregation at 4 min compared with peak aggregation, but plasma from LF survivor and non–LF febrile controls (NLFCs) showed no disaggregation by 4 min. A) Percent aggregation over 4 min. B) Aggregation at 4 min divided by the maximum aggregation in assays by using plasma from 14 fatal LF cases, 7 nonfatal LF cases, and 5 NLFC cases. Only assays using plasma from fatal cases showed disaggregation by the experimental endpoint. Error bars shows SD; horizontal lines indicate means. HC, healthy control; LF, Lassa fever; NLFC, non-LF febrile control.
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