Abstract
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.
Highlights
Ebola virus (EBOV) infection in humans is characterized by severe, often fatal disease
We report changes that occurred in human PBMCs during EBOV infection
The dramatic loss of intermediate and nonclassical monocytes was striking in all 4 patients during the acute phase, in line with prior observations of monocyte loss in patients with Ebola virus disease (EVD) [2]
Summary
Ebola virus (EBOV) infection in humans is characterized by severe, often fatal disease. One way in which researchers have circumvented the difficulties surrounding the use of primary human samples from patients with EVD is by exposing human immune cells to EBOV in vitro to understand how viral infection alters cell function. EBOV productively infects monocytes and monocyte-derived macrophages in vitro, stimulates production of inflammatory cytokines, and actively inhibits IFN-α production by these cells [15, 16]. Monocyte-derived DCs, while able to support viral replication, do not produce inflammatory cytokines and are impaired in their ability to stimulate T cells [18, 19]. Since it is well established that T cell activation occurs during human EVD [4, 23], the status of pDCs in patients with EVD is an unexplored area of importance
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