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© Pierre Gounon
Virus influenza purifié, agent de la grippe. Ce virus enveloppé possède un génome fragmenté : 8 segments d'ARN négatif protégés par une nucléocapside.
Scientific Fields
Diseases
Organisms
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Technique

Published in Nature - 24 Jun 2015

Simon-Loriere E, Faye O, Faye O, Koivogui L, Magassouba N, Keita S, Thiberge JM, Diancourt L, Bouchier C, Vandenbogaert M, Caro V, Fall G, Buchmann JP, Matranga CB, Sabeti PC, Manuguerra JC, Holmes EC, Sall AA

Link to Pubmed [PMID] – 26106863

Nature 2015 Aug;524(7563):102-4

An epidemic of Ebola virus disease of unprecedented scale has been ongoing for more than a year in West Africa. As of 29 April 2015, there have been 26,277 reported total cases (of which 14,895 have been laboratory confirmed) resulting in 10,899 deaths. The source of the outbreak was traced to the prefecture of Guéckédou in the forested region of southeastern Guinea. The virus later spread to the capital, Conakry, and to the neighbouring countries of Sierra Leone, Liberia, Nigeria, Senegal and Mali. In March 2014, when the first cases were detected in Conakry, the Institut Pasteur of Dakar, Senegal, deployed a mobile laboratory in Donka hospital to provide diagnostic services to the greater Conakry urban area and other regions of Guinea. Through this process we sampled 85 Ebola viruses (EBOV) from patients infected from July to November 2014, and report their full genome sequences here. Phylogenetic analysis reveals the sustained transmission of three distinct viral lineages co-circulating in Guinea, including the urban setting of Conakry and its surroundings. One lineage is unique to Guinea and closely related to the earliest sampled viruses of the epidemic. A second lineage contains viruses probably reintroduced from neighbouring Sierra Leone on multiple occasions, while a third lineage later spread from Guinea to Mali. Each lineage is defined by multiple mutations, including non-synonymous changes in the virion protein 35 (VP35), glycoprotein (GP) and RNA-dependent RNA polymerase (L) proteins. The viral GP is characterized by a glycosylation site modification and mutations in the mucin-like domain that could modify the outer shape of the virion. These data illustrate the ongoing ability of EBOV to develop lineage-specific and potentially phenotypically important variation.