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Article: Human annexin A6 interacts with influenza a virus protein M2 and negatively modulates infection

TitleHuman annexin A6 interacts with influenza a virus protein M2 and negatively modulates infection
Authors
Issue Date2012
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2012, v. 86 n. 3, p. 1789-1801 How to Cite?
Abstract
The influenza A virus M2 ion channel protein has the longest cytoplasmic tail (CT) among the three viral envelope proteins and is well conserved between different viral strains. It is accessible to the host cellular machinery after fusion with the endosomal membrane and during the trafficking, assembly, and budding processes. We hypothesized that identification of host cellular interactants of M2 CT could help us to better understand the molecular mechanisms regulating the M2-dependent stages of the virus life cycle. Using yeast two-hybrid screening with M2 CT as bait, a novel interaction with the human annexin A6 (AnxA6) protein was identified, and their physical interaction was confirmed by coimmunoprecipitation assay and a colocalization study of virus-infected human cells. We found that small interfering RNA (siRNA)-mediated knockdown of AnxA6 expression significantly increased virus production, while its overexpression could reduce the titer of virus progeny, suggesting a negative regulatory role for AnxA6 during influenza A virus infection. Further characterization revealed that AnxA6 depletion or overexpression had no effect on the early stages of the virus life cycle or on viral RNA replication but impaired the release of progeny virus, as suggested by delayed or defective budding events observed at the plasma membrane of virus-infected cells by transmission electron microscopy. Collectively, this work identifies AnxA6 as a novel cellular regulator that targets and impairs the virus budding and release stages of the influenza A virus life cycle. © 2012, American Society for Microbiology.
Persistent Identifierhttp://hdl.handle.net/10722/161157
ISSN
2013 Impact Factor: 4.648
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, Hen_HK
dc.contributor.authorKien, Fen_HK
dc.contributor.authorManière, Men_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorLagarde, Nen_HK
dc.contributor.authorTse, KSen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorNal, Ben_HK
dc.date.accessioned2012-08-16T06:39:38Z-
dc.date.available2012-08-16T06:39:38Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Virology, 2012, v. 86 n. 3, p. 1789-1801en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/161157-
dc.description.abstractThe influenza A virus M2 ion channel protein has the longest cytoplasmic tail (CT) among the three viral envelope proteins and is well conserved between different viral strains. It is accessible to the host cellular machinery after fusion with the endosomal membrane and during the trafficking, assembly, and budding processes. We hypothesized that identification of host cellular interactants of M2 CT could help us to better understand the molecular mechanisms regulating the M2-dependent stages of the virus life cycle. Using yeast two-hybrid screening with M2 CT as bait, a novel interaction with the human annexin A6 (AnxA6) protein was identified, and their physical interaction was confirmed by coimmunoprecipitation assay and a colocalization study of virus-infected human cells. We found that small interfering RNA (siRNA)-mediated knockdown of AnxA6 expression significantly increased virus production, while its overexpression could reduce the titer of virus progeny, suggesting a negative regulatory role for AnxA6 during influenza A virus infection. Further characterization revealed that AnxA6 depletion or overexpression had no effect on the early stages of the virus life cycle or on viral RNA replication but impaired the release of progeny virus, as suggested by delayed or defective budding events observed at the plasma membrane of virus-infected cells by transmission electron microscopy. Collectively, this work identifies AnxA6 as a novel cellular regulator that targets and impairs the virus budding and release stages of the influenza A virus life cycle. © 2012, American Society for Microbiology.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_HK
dc.relation.ispartofJournal of Virologyen_HK
dc.titleHuman annexin A6 interacts with influenza a virus protein M2 and negatively modulates infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1098-5514 (Electronic) 0022-538X (Linkin&volume=86&issue=3&spage=1789&epage=801&date=2012&atitle=Human+annexin+A6+interacts+with+influenza+a+virus+protein+M2+and+negatively+modulates+infectionen_US
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailNal, B: bnal@hkucc.hku.hken_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityNal, B=rp00541en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.06003-11en_HK
dc.identifier.pmid22114333-
dc.identifier.pmcidPMC3264383-
dc.identifier.scopuseid_2-s2.0-84863158307en_HK
dc.identifier.hkuros203742en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863158307&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume86en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1789en_HK
dc.identifier.epage1801en_HK
dc.identifier.isiWOS:000299308000045-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMa, H=55272776400en_HK
dc.identifier.scopusauthoridKien, F=7004231633en_HK
dc.identifier.scopusauthoridManière, M=55272041700en_HK
dc.identifier.scopusauthoridZhang, Y=35239223600en_HK
dc.identifier.scopusauthoridLagarde, N=16203012000en_HK
dc.identifier.scopusauthoridTse, KS=55272891000en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridNal, B=6506672380en_HK
dc.identifier.citeulike10252092-

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