Neuropsychiatry problem is not the chief clinical presentation of 2014 Western Africa Ebola virus infection

Joob, Beuy; Wiwanitkit, Viroj

doi:10.1590/0004-282x20140179

Cited by 1 publication

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References 4 publications

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“…Direct targeting of bacterial enterotoxins using monoclonal antibodies and other approaches has shown potential (Liu et al, 2020;Shankar et al, 2020). Treatment of the hypovolemia induced by EBOV infection is crucial supportive care for Ebola patients (Chertow et al, 2014;Joob and Wiwanitkit, 2015;Kendall et al, 2015). Thus, the work we present here supports the idea that direct inhibition of EBOV delta peptide, or inhibition of critical biological pathways involved in the induction of diarrhea by the delta peptide, may provide a clinical benefit in this often-fatal disease.…”

Section: Discussionsupporting

confidence: 64%

Ebola virus delta peptide is an enterotoxin

et al. 2022

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During the 2013-2016 West African (WA) Ebola virus (EBOV) outbreak, severe gastrointestinal symptoms were common in patients and associated with poor outcome. Delta peptide is a conserved product of post-translational processing of the abundant EBOV soluble glycoprotein (sGP). The murine ligated ileal loop model was used to demonstrate that delta peptide is a potent enterotoxin. Dramatic intestinal fluid accumulation follows injection of biologically relevant amounts of delta peptide into ileal loops, along with gross alteration of villous architecture and loss of goblet cells. Transcriptomic analyses show that delta peptide triggers damage response and cell survival pathways and downregulates expression of transporters and exchangers. Induction of diarrhea by delta peptide occurs via cellular damage and regulation of genes that encode proteins involved in fluid secretion. While distinct differences exist between the ileal loop murine model and EBOV infection in humans, these results suggest that delta peptide may contribute to EBOVinduced gastrointestinal pathology.

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