Abstract

The filoviruses Ebola (EBOV) and Marburg (MARV) cause fatal disease in humans and nonhuman primates but cause subclinical infections in bats. The Egyptian rousette bat (ERB, Rousettus aegyptiacus) is a natural MARV reservoir. To understand the nature of this resistance, we have analyzed how EBOV and MARV affect the transcriptomes of multiple ERB tissues. We found that while the primary locus of infection was the liver, gene expression was affected in multiple tissues, suggesting a systemic response. We have identified transcriptional changes indicative of inhibition of the complement system, induction of vasodilation, changes in coagulation, modulation of iron regulation, activation of a T cell response, and converting macrophages from the M1 to M2 state. We propose that these events are facets of a systemic anti-inflammatory state that enables effective control of the infection in bats and suggest that this state can inform how to control a filovirus infection in humans.

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