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Adipocytes are susceptible to Ebola Virus infection
Journal article   Open access   Peer reviewed

Adipocytes are susceptible to Ebola Virus infection

Francoise A. Gourronc, Michael Rebagliati, Breanna Kramer-Riesberg, Anthony M. Fleck, Justin J. Patten, Kathleen Geohegan-Barek, Kelly N. Messingham, Robert A. Davey, Wendy Maury and Aloysius J. Klingelhutz
Virology (New York, N.Y.), Vol.573, pp.12-22
05/27/2022
DOI: 10.1016/j.virol.2022.05.007
PMCID: PMC9413353
PMID: 35690007
url
https://doi.org/10.1016/j.virol.2022.05.007View
Published (Version of record) Open Access

Abstract

Adipose tissue is an endocrine organ with strong proinflammatory capacity; however, the role of this tissue in highly pathogenic virus infections has not been extensively examined. We show that mice infected with a mouse-adapted Ebola Virus (EBOV) exhibit increasing levels of viral transcript in visceral and subcutaneous adipose tissue over the course of infection. Human adipocytes were found to be susceptible to EBOV. Endocytosis and macropinocytosis inhibitors effectively blocked infection of adipocytes by a replication competent recombinant VSV virus that expresses EBOV glycoprotein (EBOV-GP/rVSV). While EBOV-GP/rVSV infection of adipocytes caused a robust induction of interferon responsive genes, EBOV infection resulted in modest upregulation of these genes. However, both EBOV-GP/rVSV- and EBOV induced comparable and significant induction of the proinflammatory genes CXCL8, IL6, CCL2, and F3 (Tissue Factor). Our results suggest that adipocytes in adipose tissue may contribute to the inflammatory response and coagulopathy that occur during EBOV pathogenesis. •Ebola virus can infect differentiated human adipocytes.•Inhibitors of macropinocytosis or clathrin-dependent endocytosis inhibit Ebola virus GP-mediated infection of human adipocytes.•Infection of human adipocytes by Ebola virus elicits a proinflammatory response that includes transcriptional upregulation of cytokine, chemokine, and coagulation factor gene, all of which could contribute to pathogenesis.

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