Adipocytes are susceptible to Ebola Virus infection.

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.