OsHV-1 countermeasures to the Pacific oyster's anti-viral response.
Identifieur interne : 002A79 ( Ncbi/Checkpoint ); précédent : 002A78; suivant : 002A80OsHV-1 countermeasures to the Pacific oyster's anti-viral response.
Auteurs : Timothy J. Green [Australie] ; Jean-Luc Rolland [France] ; Agnes Vergnes [France] ; David Raftos [Australie] ; Caroline Montagnani [France]Source :
- Fish & shellfish immunology [ 1095-9947 ] ; 2015.
Descripteurs français
- KwdFr :
- ARN double brin (génétique), ARN double brin (métabolisme), ARN messager (génétique), ARN messager (métabolisme), Animaux, Apoptose, Branchies (virologie), Crassostrea (immunologie), Crassostrea (virologie), Expression des gènes, Interactions hôte-pathogène, Poly I-C (pharmacologie), Protéines virales (génétique), Protéines virales (métabolisme), Virus à ADN (génétique), Virus à ADN (physiologie).
- MESH :
- génétique : ARN double brin, ARN messager, Protéines virales, Virus à ADN.
- immunologie : Crassostrea.
- métabolisme : ARN double brin, ARN messager, Protéines virales.
- pharmacologie : Poly I-C.
- physiologie : Virus à ADN.
- virologie : Branchies, Crassostrea.
- Animaux, Apoptose, Expression des gènes, Interactions hôte-pathogène.
English descriptors
- KwdEn :
- Animals, Apoptosis, Crassostrea (immunology), Crassostrea (virology), DNA Viruses (genetics), DNA Viruses (physiology), Gene Expression, Gills (virology), Host-Pathogen Interactions, Poly I-C (pharmacology), RNA, Double-Stranded (genetics), RNA, Double-Stranded (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Viral Proteins (genetics), Viral Proteins (metabolism).
- MESH :
- chemical , genetics : RNA, Double-Stranded, RNA, Messenger, Viral Proteins.
- chemical , metabolism : RNA, Double-Stranded, RNA, Messenger, Viral Proteins.
- chemical , pharmacology : Poly I-C.
- genetics : DNA Viruses.
- immunology : Crassostrea.
- physiology : DNA Viruses.
- virology : Crassostrea, Gills.
- Animals, Apoptosis, Gene Expression, Host-Pathogen Interactions.
Abstract
The host-pathogen interactions between the Pacific oyster (Crassostrea gigas) and Ostreid herpesvirus type 1 (OsHV-1) are poorly characterised. Herpesviruses are a group of large, DNA viruses that are known to encode gene products that subvert their host's antiviral response. It is likely that OsHV-1 has also evolved similar strategies as its genome encodes genes with high homology to C. gigas inhibitors of apoptosis (IAPs) and an interferon-stimulated gene (termed CH25H). The first objective of this study was to simultaneously investigate the expression of C. gigas and OsHV-1 genes that share high sequence homology during an acute infection. Comparison of apoptosis-related genes revealed that components of the extrinsic apoptosis pathway (TNF) were induced in response to OsHV-1 infection, but we failed to observe evidence of apoptosis using a combination of biochemical and molecular assays. IAPs encoded by OsHV-1 were highly expressed during the acute stage of infection and may explain why we didn't observe evidence of apoptosis. However, C. gigas must have an alternative mechanism to apoptosis for clearing OsHV-1 from infected gill cells as we observed a reduction in viral DNA between 27 and 54 h post-infection. The reduction of viral DNA in C. gigas gill cells occurred after the up-regulation of interferon-stimulated genes (viperin, PKR, ADAR). In a second objective, we manipulated the host's anti-viral response by injecting C. gigas with a small dose of poly I:C at the time of OsHV-1 infection. This small dose of poly I:C was unable to induce transcription of known antiviral effectors (ISGs), but these oysters were still capable of inhibiting OsHV-1 replication. This result suggests dsRNA induces an anti-viral response that is additional to the IFN-like pathway.
DOI: 10.1016/j.fsi.2015.09.025
PubMed: 26384844
Affiliations:
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Green</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Sciences, Macquarie University, NSW, 2109, Australia; Sydney Institute of Marine Science, Chowder Bay Road, Mosman, NSW, 2088, Australia. Electronic address: tim.green@mq.edu.au.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Biological Sciences, Macquarie University, NSW, 2109, Australia; Sydney Institute of Marine Science, Chowder Bay Road, Mosman, NSW, 2088</wicri:regionArea><wicri:noRegion>2088</wicri:noRegion></affiliation></author><author><name sortKey="Rolland, Jean Luc" sort="Rolland, Jean Luc" uniqKey="Rolland J" first="Jean-Luc" last="Rolland">Jean-Luc Rolland</name><affiliation wicri:level="3"><nlm:affiliation>IFREMER, IHPE, UMR 5244, Univ. Perpignan Via Domitia, CNRS, Univ. Montpellier, F-34095, Montpellier, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>IFREMER, IHPE, UMR 5244, Univ. 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Montpellier, F-34095, Montpellier</wicri:regionArea><placeName><region type="region" nuts="2">Occitanie (région administrative)</region><region type="old region" nuts="2">Languedoc-Roussillon</region><settlement type="city">Montpellier</settlement></placeName></affiliation></author></analytic><series><title level="j">Fish & shellfish immunology</title><idno type="eISSN">1095-9947</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Crassostrea (immunology)</term><term>Crassostrea (virology)</term><term>DNA Viruses (genetics)</term><term>DNA Viruses (physiology)</term><term>Gene Expression</term><term>Gills (virology)</term><term>Host-Pathogen Interactions</term><term>Poly I-C (pharmacology)</term><term>RNA, Double-Stranded (genetics)</term><term>RNA, Double-Stranded (metabolism)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Viral Proteins (genetics)</term><term>Viral Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN double brin (génétique)</term><term>ARN double brin (métabolisme)</term><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Animaux</term><term>Apoptose</term><term>Branchies (virologie)</term><term>Crassostrea (immunologie)</term><term>Crassostrea (virologie)</term><term>Expression des gènes</term><term>Interactions hôte-pathogène</term><term>Poly I-C (pharmacologie)</term><term>Protéines virales (génétique)</term><term>Protéines virales (métabolisme)</term><term>Virus à ADN (génétique)</term><term>Virus à ADN (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Double-Stranded</term><term>RNA, Messenger</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Double-Stranded</term><term>RNA, Messenger</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Poly I-C</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Viruses</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN double brin</term><term>ARN messager</term><term>Protéines virales</term><term>Virus à ADN</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Crassostrea</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Crassostrea</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN double brin</term><term>ARN messager</term><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Poly I-C</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus à ADN</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>DNA Viruses</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Branchies</term><term>Crassostrea</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Crassostrea</term><term>Gills</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Gene Expression</term><term>Host-Pathogen Interactions</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Expression des gènes</term><term>Interactions hôte-pathogène</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The host-pathogen interactions between the Pacific oyster (Crassostrea gigas) and Ostreid herpesvirus type 1 (OsHV-1) are poorly characterised. Herpesviruses are a group of large, DNA viruses that are known to encode gene products that subvert their host's antiviral response. It is likely that OsHV-1 has also evolved similar strategies as its genome encodes genes with high homology to C. gigas inhibitors of apoptosis (IAPs) and an interferon-stimulated gene (termed CH25H). The first objective of this study was to simultaneously investigate the expression of C. gigas and OsHV-1 genes that share high sequence homology during an acute infection. Comparison of apoptosis-related genes revealed that components of the extrinsic apoptosis pathway (TNF) were induced in response to OsHV-1 infection, but we failed to observe evidence of apoptosis using a combination of biochemical and molecular assays. IAPs encoded by OsHV-1 were highly expressed during the acute stage of infection and may explain why we didn't observe evidence of apoptosis. However, C. gigas must have an alternative mechanism to apoptosis for clearing OsHV-1 from infected gill cells as we observed a reduction in viral DNA between 27 and 54 h post-infection. The reduction of viral DNA in C. gigas gill cells occurred after the up-regulation of interferon-stimulated genes (viperin, PKR, ADAR). In a second objective, we manipulated the host's anti-viral response by injecting C. gigas with a small dose of poly I:C at the time of OsHV-1 infection. This small dose of poly I:C was unable to induce transcription of known antiviral effectors (ISGs), but these oysters were still capable of inhibiting OsHV-1 replication. This result suggests dsRNA induces an anti-viral response that is additional to the IFN-like pathway.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Languedoc-Roussillon</li><li>Occitanie (région administrative)</li></region><settlement><li>Montpellier</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="Green, Timothy J" sort="Green, Timothy J" uniqKey="Green T" first="Timothy J" last="Green">Timothy J. Green</name></noRegion><name sortKey="Raftos, David" sort="Raftos, David" uniqKey="Raftos D" first="David" last="Raftos">David Raftos</name></country><country name="France"><region name="Occitanie (région administrative)"><name sortKey="Rolland, Jean Luc" sort="Rolland, Jean Luc" uniqKey="Rolland J" first="Jean-Luc" last="Rolland">Jean-Luc Rolland</name></region><name sortKey="Montagnani, Caroline" sort="Montagnani, Caroline" uniqKey="Montagnani C" first="Caroline" last="Montagnani">Caroline Montagnani</name><name sortKey="Vergnes, Agnes" sort="Vergnes, Agnes" uniqKey="Vergnes A" first="Agnes" last="Vergnes">Agnes Vergnes</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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