AustralieFrV1, PubMed, Checkpoint, bibRecord, 003370

Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.

Identifieur interne : 003370 ( PubMed/Checkpoint ); précédent : 003369; suivant : 003371

Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.

Auteurs : Yee Suan Poo [Australie] ; Penny A. Rudd [Australie] ; Joy Gardner [Australie] ; Jane A C. Wilson [Australie] ; Thibaut Larcher [France] ; Marie-Anne Colle [France] ; Thuy T. Le [Australie] ; Helder I. Nakaya [Brésil] ; David Warrilow [Australie] ; Richard Allcock [Australie] ; Helle Bielefeldt-Ohmann [Australie] ; Wayne A. Schroder [Australie] ; Alexander A. Khromykh [Australie] ; José A. Lopez [Australie] ; Andreas Suhrbier [Australie]

Source :

PLoS neglected tropical diseases [ 1935-2735 ] ; 2014.

RBID : pubmed:25474568

Descripteurs français

KwdFr :
- ARN viral (analyse), Animaux, Anticorps antiviraux (immunologie), Cellules tueuses naturelles (immunologie), Femelle, Fièvre chikungunya (génétique), Fièvre chikungunya (immunologie), Fièvre chikungunya (virologie), Lymphocytes B (immunologie), Lymphocytes T (immunologie), Maladie aigüe, Maladie chronique, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL, Souris de lignée NOD, Souris knockout, Virus du chikungunya (immunologie).
MESH :
- analyse : ARN viral.
- génétique : Fièvre chikungunya.
- immunologie : Anticorps antiviraux, Cellules tueuses naturelles, Fièvre chikungunya, Lymphocytes B, Lymphocytes T, Virus du chikungunya.
- virologie : Fièvre chikungunya.
- Animaux, Femelle, Maladie aigüe, Maladie chronique, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL, Souris de lignée NOD, Souris knockout.

English descriptors

KwdEn :
- Acute Disease, Animals, Antibodies, Viral (immunology), B-Lymphocytes (immunology), Chikungunya Fever (genetics), Chikungunya Fever (immunology), Chikungunya Fever (virology), Chikungunya virus (immunology), Chronic Disease, Disease Models, Animal, Female, Killer Cells, Natural (immunology), Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Knockout, RNA, Viral (analysis), T-Lymphocytes (immunology).
MESH :
- chemical , analysis : RNA, Viral.
- chemical , immunology : Antibodies, Viral.
- genetics : Chikungunya Fever.
- immunology : B-Lymphocytes, Chikungunya Fever, Chikungunya virus, Killer Cells, Natural, T-Lymphocytes.
- virology : Chikungunya Fever.
- Acute Disease, Animals, Chronic Disease, Disease Models, Animal, Female, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Knockout.

Abstract

The recent epidemic of the arthritogenic alphavirus, chikungunya virus (CHIKV) has prompted a quest to understand the correlates of protection against virus and disease in order to inform development of new interventions. Herein we highlight the propensity of CHIKV infections to persist long term, both as persistent, steady-state, viraemias in multiple B cell deficient mouse strains, and as persistent RNA (including negative-strand RNA) in wild-type mice. The knockout mouse studies provided evidence for a role for T cells (but not NK cells) in viraemia suppression, and confirmed the role of T cells in arthritis promotion, with vaccine-induced T cells also shown to be arthritogenic in the absence of antibody responses. However, MHC class II-restricted T cells were not required for production of anti-viral IgG2c responses post CHIKV infection. The anti-viral cytokines, TNF and IFNγ, were persistently elevated in persistently infected B and T cell deficient mice, with adoptive transfer of anti-CHIKV antibodies unable to clear permanently the viraemia from these, or B cell deficient, mice. The NOD background increased viraemia and promoted arthritis, with B, T and NK deficient NOD mice showing high-levels of persistent viraemia and ultimately succumbing to encephalitic disease. In wild-type mice persistent CHIKV RNA and negative strand RNA (detected for up to 100 days post infection) was associated with persistence of cellular infiltrates, CHIKV antigen and stimulation of IFNα/β and T cell responses. These studies highlight that, secondary to antibodies, several factors are involved in virus control, and suggest that chronic arthritic disease is a consequence of persistent, replicating and transcriptionally active CHIKV RNA.

DOI: 10.1371/journal.pntd.0003354
PubMed: 25474568

Affiliations:

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Le document en format XML

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<author><name sortKey="Le, Thuy T" sort="Le, Thuy T" uniqKey="Le T" first="Thuy T" last="Le">Thuy T. Le</name>
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<author><name sortKey="Nakaya, Helder I" sort="Nakaya, Helder I" uniqKey="Nakaya H" first="Helder I" last="Nakaya">Helder I. Nakaya</name>
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<author><name sortKey="Allcock, Richard" sort="Allcock, Richard" uniqKey="Allcock R" first="Richard" last="Allcock">Richard Allcock</name>
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<wicri:regionArea>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia; School of Natural Sciences, Griffith University, Nathan</wicri:regionArea>
<wicri:noRegion>Nathan</wicri:noRegion>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term>
<term>Animals</term>
<term>Antibodies, Viral (immunology)</term>
<term>B-Lymphocytes (immunology)</term>
<term>Chikungunya Fever (genetics)</term>
<term>Chikungunya Fever (immunology)</term>
<term>Chikungunya Fever (virology)</term>
<term>Chikungunya virus (immunology)</term>
<term>Chronic Disease</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Killer Cells, Natural (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Knockout</term>
<term>RNA, Viral (analysis)</term>
<term>T-Lymphocytes (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (analyse)</term>
<term>Animaux</term>
<term>Anticorps antiviraux (immunologie)</term>
<term>Cellules tueuses naturelles (immunologie)</term>
<term>Femelle</term>
<term>Fièvre chikungunya (génétique)</term>
<term>Fièvre chikungunya (immunologie)</term>
<term>Fièvre chikungunya (virologie)</term>
<term>Lymphocytes B (immunologie)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Maladie aigüe</term>
<term>Maladie chronique</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris de lignée NOD</term>
<term>Souris knockout</term>
<term>Virus du chikungunya (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>RNA, Viral</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN viral</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Chikungunya Fever</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Fièvre chikungunya</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Anticorps antiviraux</term>
<term>Cellules tueuses naturelles</term>
<term>Fièvre chikungunya</term>
<term>Lymphocytes B</term>
<term>Lymphocytes T</term>
<term>Virus du chikungunya</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>B-Lymphocytes</term>
<term>Chikungunya Fever</term>
<term>Chikungunya virus</term>
<term>Killer Cells, Natural</term>
<term>T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Fièvre chikungunya</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Chikungunya Fever</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term>
<term>Animals</term>
<term>Chronic Disease</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Knockout</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Maladie aigüe</term>
<term>Maladie chronique</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris de lignée NOD</term>
<term>Souris knockout</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The recent epidemic of the arthritogenic alphavirus, chikungunya virus (CHIKV) has prompted a quest to understand the correlates of protection against virus and disease in order to inform development of new interventions. Herein we highlight the propensity of CHIKV infections to persist long term, both as persistent, steady-state, viraemias in multiple B cell deficient mouse strains, and as persistent RNA (including negative-strand RNA) in wild-type mice. The knockout mouse studies provided evidence for a role for T cells (but not NK cells) in viraemia suppression, and confirmed the role of T cells in arthritis promotion, with vaccine-induced T cells also shown to be arthritogenic in the absence of antibody responses. However, MHC class II-restricted T cells were not required for production of anti-viral IgG2c responses post CHIKV infection. The anti-viral cytokines, TNF and IFNγ, were persistently elevated in persistently infected B and T cell deficient mice, with adoptive transfer of anti-CHIKV antibodies unable to clear permanently the viraemia from these, or B cell deficient, mice. The NOD background increased viraemia and promoted arthritis, with B, T and NK deficient NOD mice showing high-levels of persistent viraemia and ultimately succumbing to encephalitic disease. In wild-type mice persistent CHIKV RNA and negative strand RNA (detected for up to 100 days post infection) was associated with persistence of cellular infiltrates, CHIKV antigen and stimulation of IFNα/β and T cell responses. These studies highlight that, secondary to antibodies, several factors are involved in virus control, and suggest that chronic arthritic disease is a consequence of persistent, replicating and transcriptionally active CHIKV RNA.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25474568</PMID>
<DateCreated><Year>2014</Year>
<Month>12</Month>
<Day>05</Day>
</DateCreated>
<DateCompleted><Year>2016</Year>
<Month>01</Month>
<Day>25</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>02</Month>
<Day>20</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1935-2735</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>8</Volume>
<Issue>12</Issue>
<PubDate><Year>2014</Year>
<Month>Dec</Month>
</PubDate>
</JournalIssue>
<Title>PLoS neglected tropical diseases</Title>
<ISOAbbreviation>PLoS Negl Trop Dis</ISOAbbreviation>
</Journal>
<ArticleTitle>Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.</ArticleTitle>
<Pagination><MedlinePgn>e3354</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pntd.0003354</ELocationID>
<Abstract><AbstractText>The recent epidemic of the arthritogenic alphavirus, chikungunya virus (CHIKV) has prompted a quest to understand the correlates of protection against virus and disease in order to inform development of new interventions. Herein we highlight the propensity of CHIKV infections to persist long term, both as persistent, steady-state, viraemias in multiple B cell deficient mouse strains, and as persistent RNA (including negative-strand RNA) in wild-type mice. The knockout mouse studies provided evidence for a role for T cells (but not NK cells) in viraemia suppression, and confirmed the role of T cells in arthritis promotion, with vaccine-induced T cells also shown to be arthritogenic in the absence of antibody responses. However, MHC class II-restricted T cells were not required for production of anti-viral IgG2c responses post CHIKV infection. The anti-viral cytokines, TNF and IFNγ, were persistently elevated in persistently infected B and T cell deficient mice, with adoptive transfer of anti-CHIKV antibodies unable to clear permanently the viraemia from these, or B cell deficient, mice. The NOD background increased viraemia and promoted arthritis, with B, T and NK deficient NOD mice showing high-levels of persistent viraemia and ultimately succumbing to encephalitic disease. In wild-type mice persistent CHIKV RNA and negative strand RNA (detected for up to 100 days post infection) was associated with persistence of cellular infiltrates, CHIKV antigen and stimulation of IFNα/β and T cell responses. These studies highlight that, secondary to antibodies, several factors are involved in virus control, and suggest that chronic arthritic disease is a consequence of persistent, replicating and transcriptionally active CHIKV RNA.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Poo</LastName>
<ForeName>Yee Suan</ForeName>
<Initials>YS</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rudd</LastName>
<ForeName>Penny A</ForeName>
<Initials>PA</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gardner</LastName>
<ForeName>Joy</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wilson</LastName>
<ForeName>Jane A C</ForeName>
<Initials>JA</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Larcher</LastName>
<ForeName>Thibaut</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Institut National de Recherche Agronomique, Unité Mixte de Recherche 703, Oniris, Nantes, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Colle</LastName>
<ForeName>Marie-Anne</ForeName>
<Initials>MA</Initials>
<AffiliationInfo><Affiliation>Institut National de Recherche Agronomique, Unité Mixte de Recherche 703, Oniris, Nantes, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Le</LastName>
<ForeName>Thuy T</ForeName>
<Initials>TT</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nakaya</LastName>
<ForeName>Helder I</ForeName>
<Initials>HI</Initials>
<AffiliationInfo><Affiliation>School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Warrilow</LastName>
<ForeName>David</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Public Health Virology Laboratory, Department of Health, Queensland Government, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Allcock</LastName>
<ForeName>Richard</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Lotterywest State Biomedical Facility Genomics, Royal Perth Hospital, Perth, Western Australia, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bielefeldt-Ohmann</LastName>
<ForeName>Helle</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schroder</LastName>
<ForeName>Wayne A</ForeName>
<Initials>WA</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Khromykh</LastName>
<ForeName>Alexander A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo><Affiliation>School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lopez</LastName>
<ForeName>José A</ForeName>
<Initials>JA</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Natural Sciences, Griffith University, Nathan, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Suhrbier</LastName>
<ForeName>Andreas</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute, and the Australian Infectious Diseases Research Centre, Brisbane, Queensland, Australia; School of Medicine/School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, Australia; School of Natural Sciences, Griffith University, Nathan, Australia.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>12</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS Negl Trop Dis</MedlineTA>
<NlmUniqueID>101291488</NlmUniqueID>
<ISSNLinking>1935-2727</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000914">Antibodies, Viral</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
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<country name="Brésil"><region name="État de São Paulo"><name sortKey="Nakaya, Helder I" sort="Nakaya, Helder I" uniqKey="Nakaya H" first="Helder I" last="Nakaya">Helder I. Nakaya</name>
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   |texte=   Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.
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	Serveur d'exploration sur les relations entre la France et l'Australie
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur les relations entre la France et l'Australie

Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.

Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection.

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