| Autor: |
McElroy AK; Viral Special Pathogens Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.; Division of Pediatric Infectious Diseases and Center for Vaccine Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA., Akondy RS; Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA., Mcllwain DR; Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA., Chen H; Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA., Bjornson-Hooper Z; Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA., Mukherjee N; Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA., Mehta AK; Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA., Nolan G; Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA., Nichol ST; Viral Special Pathogens Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, USA., Spiropoulou CF; Viral Special Pathogens Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. |
| Abstrakt: |
A complete understanding of human immune responses to Ebola virus infection is limited by the availability of specimens and the requirement for biosafety level 4 (BSL-4) containment. In an effort to bridge this gap, we evaluated cryopreserved PBMCs from 4 patients who survived Ebola virus disease (EVD) using an established mass cytometry antibody panel to characterize various cell populations during both the acute and convalescent phases. Acute loss of nonclassical monocytes and myeloid DCs, especially CD1c+ DCs, was noted. Classical monocyte proliferation and CD38 upregulation on plasmacytoid DCs coincided with declining viral load. Unsupervised analysis of cell abundance demonstrated acute declines in monocytic, NK, and T cell populations, but some populations, many of myeloid origin, increased in abundance during the acute phase, suggesting emergency hematopoiesis. Despite cell losses during the acute phase, upregulation of Ki-67 correlated with recovery of cell populations over time. These data provide insights into the human immune response during EVD. |
