| Literature DB >> 27511894 |
Abhilash I Chiramel1, Logan Banadyga1, Jonathan D Dougherty1, Darryl Falzarano2, Cynthia Martellaro1, Dominique Brees3, R Travis Taylor4, Hideki Ebihara1, Sonja M Best1.
Abstract
Antiviral therapeutics with existing clinical safety profiles would be highly desirable in an outbreak situation, such as the 2013-2016 emergence of Ebola virus (EBOV) in West Africa. Although, the World Health Organization declared the end of the outbreak early 2016, sporadic cases of EBOV infection have since been reported. Alisporivir is the most clinically advanced broad-spectrum antiviral that functions by targeting a host protein, cyclophilin A (CypA). A modest antiviral effect of alisporivir against contemporary (Makona) but not historical (Mayinga) EBOV strains was observed in tissue culture. However, this effect was not comparable to observations for an alisporivir-susceptible virus, the flavivirus tick-borne encephalitis virus. Thus, EBOV does not depend on (CypA) for replication, in contrast to many other viruses pathogenic to humans. Published by Oxford University Press for the Infectious Diseases Society of America 2016. This work is written by (a) US Government employee(s) and is in the public domain in the US.Entities:
Keywords: Ebola virus; alisporivir; antivirals; cyclophilin A; flavivirus
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Year: 2016 PMID: 27511894 PMCID: PMC5050471 DOI: 10.1093/infdis/jiw241
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226