Une première épidémie de fièvre à virus Ebola en Afrique de l’Ouest

Reynard, Olivier; Volchkov, Viktor E.; Peyrefitte, Christophe N.

doi:10.1051/medsci/20143006018

Cited by 11 publications

(9 citation statements)

References 14 publications

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“…The first Ebolavirus species was discovered in 1976 in the Democratic Republic of Congo (previously called Zaire), near the Ebola River (2). Subsequently, 28 outbreaks appeared sporadically until March 2014, when the most devastating outbreak occurred in western Africa, including the countries of Guinea, Liberia, and Sierra Leone (3)(4)(5)(6). Most outbreaks are caused by the Zaire Ebola virus subspecies (7), which is the most pathogenic (case fatality rate, up to 90%).…”

Section: Importancementioning

confidence: 99%

Enhancement of Ebola Virus Infection via Ficolin-1 Interaction with the Mucin Domain of GP Glycoprotein

Favier¹,

Gout

Reynard

et al. 2016

J Virol

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Ebola virus infection requires the surface viral glycoprotein to initiate entry into the target cells. The trimeric glycoprotein is a highly glycosylated viral protein which has been shown to interact with host C-type lectin receptors and the soluble complement recognition protein mannose-binding lectin, thereby enhancing viral infection. Similarly to mannose-binding lectin, ficolins are soluble effectors of the innate immune system that recognize particular glycans at the pathogen surface. In this study, we demonstrate that ficolin-1 interacts with the Zaire Ebola virus (EBOV) glycoprotein, and we characterized this interaction by surface plasmon resonance spectroscopy. Ficolin-1 was shown to bind to the viral glycoprotein with a high affinity. This interaction was mediated by the fibrinogen-like recognition domain of ficolin-1 and the mucin-like domain of the viral glycoprotein. Using a ficolin-1 control mutant devoid of sialic acid-binding capacity, we identified sialylated moieties of the mucin domain to be potential ligands on the glycoprotein. In cell culture, using both pseudotyped viruses and EBOV, ficolin-1 was shown to enhance EBOV infection independently of the serum complement. We also observed that ficolin-1 enhanced EBOV infection on human monocyte-derived macrophages, described to be major viral target cells,. Competition experiments suggested that although ficolin-1 and mannose-binding lectin recognized different carbohydrate moieties on the EBOV glycoprotein, the observed enhancement of the infection likely depended on a common cellular receptor/partner. In conclusion, ficolin-1 could provide an alternative receptor-mediated mechanism for enhancing EBOV infection, thereby contributing to viral subversion of the host innate immune system. E bola virus (EBOV), a member of the Filoviridae family, can cause a severe, often fatal, hemorrhagic fever (HF) in humans and nonhuman primates (1). The first Ebolavirus species was discovered in 1976 in the Democratic Republic of Congo (previously called Zaire), near the Ebola River (2). Subsequently, 28 outbreaks appeared sporadically until March 2014, when the most devastating outbreak occurred in western Africa, including the countries of Guinea, Liberia, and Sierra Leone (3-6). Most outbreaks are caused by the Zaire Ebola virus subspecies (7), which is the most pathogenic (case fatality rate, up to 90%). EBOV is classified in the category A agents of the Centers for Disease Control and Prevention (CDC) because it represents a substantial threat to public health, and consequently, its handling requires a biosafety level 4 (BSL-4) laboratory. The development of effective therapies against EBOV became an urgent priority during the spread of the most recent epidemics throughout Africa, which, in addition to causing the loss of thousands of human lives, caused economic and social instability (8).The trimeric transmembrane glycoprotein (GP) of EBOV plays a crucial role in EBOV infection by mediating its cellular attachment and entry into host cells (9, 1...

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Section: Importancementioning

confidence: 99%

Enhancement of Ebola Virus Infection via Ficolin-1 Interaction with the Mucin Domain of GP Glycoprotein

Favier¹,

Gout

Reynard

et al. 2016

J Virol

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“…1B). As of 19 August 2014, 2240 cases and 1229 deaths have been documented (4, 5). Its emergence in the major cities of Conakry (Guinea), Freetown (Sierra Leone), Monrovia (Liberia), and Lagos (Nigeria) raises the specter of increasing local and international dissemination.…”

mentioning

confidence: 99%

Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak

Gire

Goba²,

Andersen

et al. 2014

Science

1,123

1,192

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In its largest outbreak, Ebola virus disease is spreading through Guinea, Liberia, Sierra Leone, and Nigeria. We sequenced 99 Ebola virus genomes from 78 patients in Sierra Leone to ∼2000× coverage. We observed a rapid accumulation of interhost and intrahost genetic variation, allowing us to characterize patterns of viral transmission over the initial weeks of the epidemic. This West African variant likely diverged from central African lineages around 2004, crossed from Guinea to Sierra Leone in May 2014, and has exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources. Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.

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“…Dans le cas des virus, ces zoonoses peuvent être à l'origine d'émergences entraînant des pathologies sévères chez l'homme, avec des impacts sanitaires et économiques considérables, comme l'épi-démie de maladie à virus Ebola d'une ampleur inédite qui a récemment frappé l'Afrique de l'Ouest [1]. Mais comment défi-nit-on un virus émergent et peut-on anticiper la survenue de ces épidémies ?…”

Section: Zoonoses Virales Et éMergence : La Recherche Ne Fait Que Comunclassified

Zoonoses virales et émergence : la recherche ne fait que commencer

Salvetti¹,

Baize²

2015

Med Sci (Paris)

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Une première épidémie de fièvre à virus Ebola en Afrique de l’Ouest

Cited by 11 publications

References 14 publications

Enhancement of Ebola Virus Infection via Ficolin-1 Interaction with the Mucin Domain of GP Glycoprotein

Enhancement of Ebola Virus Infection via Ficolin-1 Interaction with the Mucin Domain of GP Glycoprotein

Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak

Zoonoses virales et émergence : la recherche ne fait que commencer

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