Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models

Abstract Rift Valley fever virus (RVFV) leads to varied clinical manifestations in animals and in humans that range from moderate fever to fatal illness, suggesting that host immune responses are important determinants of the disease severity. We investigated the immune basis for the extreme suscept...

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Autores principales:	Rashida Lathan, Dominique Simon-Chazottes, Grégory Jouvion, Ophélie Godon, Marie Malissen, Marie Flamand, Pierre Bruhns, Jean-Jacques Panthier
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/41caf67618af4a78ae89676304210b46
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spelling	oai:doaj.org-article:41caf67618af4a78ae89676304210b462021-12-02T12:30:45ZInnate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models10.1038/s41598-017-07543-82045-2322https://doaj.org/article/41caf67618af4a78ae89676304210b462017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07543-8https://doaj.org/toc/2045-2322Abstract Rift Valley fever virus (RVFV) leads to varied clinical manifestations in animals and in humans that range from moderate fever to fatal illness, suggesting that host immune responses are important determinants of the disease severity. We investigated the immune basis for the extreme susceptibility of MBT/Pas mice that die with mild to acute hepatitis by day 3 post-infection compared to more resistant BALB/cByJ mice that survive up to a week longer. Lower levels of neutrophils observed in the bone marrow and blood of infected MBT/Pas mice are unlikely to be causative of increased RVFV susceptibility as constitutive neutropenia in specific mutant mice did not change survival outcome. However, whereas MBT/Pas mice mounted an earlier inflammatory response accompanied by higher amounts of interferon (IFN)-α in the serum compared to BALB/cByJ mice, they failed to prevent high viral antigen load. Several immunological alterations were uncovered in infected MBT/Pas mice compared to BALB/cByJ mice, including low levels of leukocytes that expressed type I IFN receptor subunit 1 (IFNAR1) in the blood, spleen and liver, delayed leukocyte activation and decreased percentage of IFN-γ-producing leukocytes in the blood. These observations are consistent with the complex mode of inheritance of RVFV susceptibility in genetic studies.Rashida LathanDominique Simon-ChazottesGrégory JouvionOphélie GodonMarie MalissenMarie FlamandPierre BruhnsJean-Jacques PanthierNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rashida Lathan Dominique Simon-Chazottes Grégory Jouvion Ophélie Godon Marie Malissen Marie Flamand Pierre Bruhns Jean-Jacques Panthier Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
description	Abstract Rift Valley fever virus (RVFV) leads to varied clinical manifestations in animals and in humans that range from moderate fever to fatal illness, suggesting that host immune responses are important determinants of the disease severity. We investigated the immune basis for the extreme susceptibility of MBT/Pas mice that die with mild to acute hepatitis by day 3 post-infection compared to more resistant BALB/cByJ mice that survive up to a week longer. Lower levels of neutrophils observed in the bone marrow and blood of infected MBT/Pas mice are unlikely to be causative of increased RVFV susceptibility as constitutive neutropenia in specific mutant mice did not change survival outcome. However, whereas MBT/Pas mice mounted an earlier inflammatory response accompanied by higher amounts of interferon (IFN)-α in the serum compared to BALB/cByJ mice, they failed to prevent high viral antigen load. Several immunological alterations were uncovered in infected MBT/Pas mice compared to BALB/cByJ mice, including low levels of leukocytes that expressed type I IFN receptor subunit 1 (IFNAR1) in the blood, spleen and liver, delayed leukocyte activation and decreased percentage of IFN-γ-producing leukocytes in the blood. These observations are consistent with the complex mode of inheritance of RVFV susceptibility in genetic studies.
format	article
author	Rashida Lathan Dominique Simon-Chazottes Grégory Jouvion Ophélie Godon Marie Malissen Marie Flamand Pierre Bruhns Jean-Jacques Panthier
author_facet	Rashida Lathan Dominique Simon-Chazottes Grégory Jouvion Ophélie Godon Marie Malissen Marie Flamand Pierre Bruhns Jean-Jacques Panthier
author_sort	Rashida Lathan
title	Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
title_short	Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
title_full	Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
title_fullStr	Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
title_full_unstemmed	Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
title_sort	innate immune basis for rift valley fever susceptibility in mouse models
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/41caf67618af4a78ae89676304210b46
work_keys_str_mv	AT rashidalathan innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT dominiquesimonchazottes innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT gregoryjouvion innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT opheliegodon innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT mariemalissen innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT marieflamand innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT pierrebruhns innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels AT jeanjacquespanthier innateimmunebasisforriftvalleyfeversusceptibilityinmousemodels
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Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models

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