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Cell Rep. 2018 May 8;23(6):1806-1816. doi: 10.1016/j.celrep.2018.04.027.

Recently Identified Mutations in the Ebola Virus-Makona Genome Do Not Alter Pathogenicity in Animal Models.

Author information

1
Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA. Electronic address: marzia@niaid.nih.gov.
2
Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA.
3
Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA.
4
Ministry of Health and Social Welfare, Monrovia, Liberia.
5
Centre des Operations d'Urgence, Centre pour le Développement des Vaccins (CVD-Mali), Centre National d'Appui à la lutte contre la Maladie, Ministère de la Sante et de l'Hygiène Publique, Bamako, Mali.
6
Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, MT, USA. Electronic address: feldmannh@niaid.nih.gov.

Abstract

Ebola virus (EBOV), isolate Makona, the causative agent of the West African EBOV epidemic, has been the subject of numerous investigations to determine the genetic diversity and its potential implication for virus biology, pathogenicity, and transmissibility. Despite various mutations that have emerged over time through multiple human-to-human transmission chains, their biological relevance remains questionable. Recently, mutations in the glycoprotein GP and polymerase L, which emerged and stabilized early during the outbreak, have been associated with improved viral fitness in cell culture. Here, we infected mice and rhesus macaques with EBOV-Makona isolates carrying or lacking those mutations. Surprisingly, all isolates behaved very similarly independent of the genotype, causing severe or lethal disease in mice and macaques, respectively. Likewise, we could not detect any evidence for differences in virus shedding. Thus, no specific biological phenotype could be associated with these EBOV-Makona mutations in two animal models.

KEYWORDS:

Ebola Makona; Ebola virus; GP mutation A82V; L mutation D759G; West African epidemic; glycoprotein GP; pathogenicity; polymerase L

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