| Literature DB >> 27651412 |
Gary Wong1, Xiangguo Qiu2, Marc-Antoine de La Vega3, Lisa Fernando4, Haiyan Wei4, Alexander Bello2, Hugues Fausther-Bovendo4, Jonathan Audet2, Andrea Kroeker4, Robert Kozak4, Kaylie Tran4, Shihua He4, Kevin Tierney4, Geoff Soule4, Estella Moffat5, Stephan Günther6, George F Gao7, Jim Strong4, Carissa Embury-Hyatt5, Gary Kobinger8.
Abstract
Enhanced virulence and/or transmission of West African Ebola virus (EBOV) variants, which are divergent from their Central African counterparts, are suspected to have contributed to the sizable toll of the recent Ebola virus disease (EVD) outbreak. This study evaluated the pathogenicity and shedding in rhesus macaques infected with 1 of 2 West African isolates (EBOV-C05 or EBOV-C07) or a Central African isolate (EBOV-K). All animals infected with EBOV-C05 or EBOV-C07 died of EVD, whereas 2 of 3 EBOV-K-infected animals died. The viremia level was elevated 10-fold in EBOV-C05-infected animals, compared with EBOV-C07- or EBOV-K-infected animals. More-severe lung pathology was observed in 2 of 6 EBOV-C05/C07-infected macaques. This is the first detailed analysis of the recently circulating EBOV-C05/C07 in direct comparison to EBOV-K with 6 animals per group, and it showed that EBOV-C05 but not EBOV-C07 can replicate at higher levels and cause more tissue damage in some animals. Increased virus shedding from individuals who are especially susceptible to EBOV replication is possibly one of the many challenges facing the community of healthcare and policy-making responders since the beginning of the outbreak. © Crown copyright 2016.Entities:
Keywords: Ebola virus; Kikwit; Makona; nonhuman primates; pathogenicity
Mesh:
Year: 2016 PMID: 27651412 PMCID: PMC5050479 DOI: 10.1093/infdis/jiw267
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226