Risks Posed by Reston, the Forgotten Ebolavirus

ABSTRACT Out of the five members of the Ebolavirus family, four cause life-threatening disease, whereas the fifth, Reston virus (RESTV), is nonpathogenic in humans. The reasons for this discrepancy remain unclear. In this review, we analyze the currently available information to provide a state-of-t...

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Autores principales:	Diego Cantoni, Arran Hamlet, Martin Michaelis, Mark N. Wass, Jeremy S. Rossman
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2016
Materias:	Ebolavirus pathogenicity Reston Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/b5a56c02dfd946c096db82e2c53fdd30
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spelling	oai:doaj.org-article:b5a56c02dfd946c096db82e2c53fdd302021-11-15T15:22:04ZRisks Posed by Reston, the Forgotten Ebolavirus10.1128/mSphere.00322-162379-5042https://doaj.org/article/b5a56c02dfd946c096db82e2c53fdd302016-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mSphere.00322-16https://doaj.org/toc/2379-5042ABSTRACT Out of the five members of the Ebolavirus family, four cause life-threatening disease, whereas the fifth, Reston virus (RESTV), is nonpathogenic in humans. The reasons for this discrepancy remain unclear. In this review, we analyze the currently available information to provide a state-of-the-art summary of the factors that determine the human pathogenicity of Ebolaviruses. RESTV causes sporadic infections in cynomolgus monkeys and is found in domestic pigs throughout the Philippines and China. Phylogenetic analyses revealed that RESTV is most closely related to the Sudan virus, which causes a high mortality rate in humans. Amino acid sequence differences between RESTV and the other Ebolaviruses are found in all nine Ebolavirus proteins, though no one residue appears sufficient to confer pathogenicity. Changes in the glycoprotein contribute to differences in Ebolavirus pathogenicity but are not sufficient to confer pathogenicity on their own. Similarly, differences in VP24 and VP35 affect viral immune evasion and are associated with changes in human pathogenicity. A recent in silico analysis systematically determined the functional consequences of sequence variations between RESTV and human-pathogenic Ebolaviruses. Multiple positions in VP24 were differently conserved between RESTV and the other Ebolaviruses and may alter human pathogenicity. In conclusion, the factors that determine the pathogenicity of Ebolaviruses in humans remain insufficiently understood. An improved understanding of these pathogenicity-determining factors is of crucial importance for disease prevention and for the early detection of emergent and potentially human-pathogenic RESTVs.Diego CantoniArran HamletMartin MichaelisMark N. WassJeremy S. RossmanAmerican Society for MicrobiologyarticleEbolaviruspathogenicityRestonMicrobiologyQR1-502ENmSphere, Vol 1, Iss 6 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	Ebolavirus pathogenicity Reston Microbiology QR1-502
spellingShingle	Ebolavirus pathogenicity Reston Microbiology QR1-502 Diego Cantoni Arran Hamlet Martin Michaelis Mark N. Wass Jeremy S. Rossman Risks Posed by Reston, the Forgotten Ebolavirus
description	ABSTRACT Out of the five members of the Ebolavirus family, four cause life-threatening disease, whereas the fifth, Reston virus (RESTV), is nonpathogenic in humans. The reasons for this discrepancy remain unclear. In this review, we analyze the currently available information to provide a state-of-the-art summary of the factors that determine the human pathogenicity of Ebolaviruses. RESTV causes sporadic infections in cynomolgus monkeys and is found in domestic pigs throughout the Philippines and China. Phylogenetic analyses revealed that RESTV is most closely related to the Sudan virus, which causes a high mortality rate in humans. Amino acid sequence differences between RESTV and the other Ebolaviruses are found in all nine Ebolavirus proteins, though no one residue appears sufficient to confer pathogenicity. Changes in the glycoprotein contribute to differences in Ebolavirus pathogenicity but are not sufficient to confer pathogenicity on their own. Similarly, differences in VP24 and VP35 affect viral immune evasion and are associated with changes in human pathogenicity. A recent in silico analysis systematically determined the functional consequences of sequence variations between RESTV and human-pathogenic Ebolaviruses. Multiple positions in VP24 were differently conserved between RESTV and the other Ebolaviruses and may alter human pathogenicity. In conclusion, the factors that determine the pathogenicity of Ebolaviruses in humans remain insufficiently understood. An improved understanding of these pathogenicity-determining factors is of crucial importance for disease prevention and for the early detection of emergent and potentially human-pathogenic RESTVs.
format	article
author	Diego Cantoni Arran Hamlet Martin Michaelis Mark N. Wass Jeremy S. Rossman
author_facet	Diego Cantoni Arran Hamlet Martin Michaelis Mark N. Wass Jeremy S. Rossman
author_sort	Diego Cantoni
title	Risks Posed by Reston, the Forgotten Ebolavirus
title_short	Risks Posed by Reston, the Forgotten Ebolavirus
title_full	Risks Posed by Reston, the Forgotten Ebolavirus
title_fullStr	Risks Posed by Reston, the Forgotten Ebolavirus
title_full_unstemmed	Risks Posed by Reston, the Forgotten Ebolavirus
title_sort	risks posed by reston, the forgotten ebolavirus
publisher	American Society for Microbiology
publishDate	2016
url	https://doaj.org/article/b5a56c02dfd946c096db82e2c53fdd30
work_keys_str_mv	AT diegocantoni risksposedbyrestontheforgottenebolavirus AT arranhamlet risksposedbyrestontheforgottenebolavirus AT martinmichaelis risksposedbyrestontheforgottenebolavirus AT marknwass risksposedbyrestontheforgottenebolavirus AT jeremysrossman risksposedbyrestontheforgottenebolavirus
_version_	1718428093002022912

Risks Posed by Reston, the Forgotten Ebolavirus

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