{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wise HM"],"funding":["Intramural NIH HHS","Medical Research Council","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["e1002998"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3486900"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(11)"],"pubmed_abstract":["Segment 7 of influenza A virus produces up to four mRNAs. Unspliced transcripts encode M1, spliced mRNA2 encodes the M2 ion channel, while protein products from spliced mRNAs 3 and 4 have not previously been identified. The M2 protein plays important roles in virus entry and assembly, and is a target for antiviral drugs and vaccination. Surprisingly, M2 is not essential for virus replication in a laboratory setting, although its loss attenuates the virus. To better understand how IAV might replicate without M2, we studied the reversion mechanism of an M2-null virus. Serial passage of a virus lacking the mRNA2 splice donor site identified a single nucleotide pseudoreverting mutation, which restored growth in cell culture and virulence in mice by upregulating mRNA4 synthesis rather than by r"],"journal":["PLoS pathogens"],"pubmed_title":["Identification of a novel splice variant form of the influenza A virus M2 ion channel with an antigenically distinct ectodomain."],"pmcid":["PMC3486900"],"funding_grant_id":["088789","BBS/E/D/20241864","075450","G0700815","G0700848","G0801931"],"pubmed_authors":["Stuart AD","Hutchinson EC","Kang ZH","Wise HM","Digard P","Fodor E","Taubenberger JK","Jagger BW","Kash JC","Schwartzman LM","Firth AE","Gog JR","Robb N"],"additional_accession":[]},"is_claimable":false,"name":"Identification of a novel splice variant form of the influenza A virus M2 ion channel with an antigenically distinct ectodomain.","description":"Segment 7 of influenza A virus produces up to four mRNAs. Unspliced transcripts encode M1, spliced mRNA2 encodes the M2 ion channel, while protein products from spliced mRNAs 3 and 4 have not previously been identified. The M2 protein plays important roles in virus entry and assembly, and is a target for antiviral drugs and vaccination. Surprisingly, M2 is not essential for virus replication in a laboratory setting, although its loss attenuates the virus. To better understand how IAV might replicate without M2, we studied the reversion mechanism of an M2-null virus. Serial passage of a virus lacking the mRNA2 splice donor site identified a single nucleotide pseudoreverting mutation, which restored growth in cell culture and virulence in mice by upregulating mRNA4 synthesis rather than by r","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2025-07-09T03:05:08.388Z","creation":"2025-07-09T03:05:08.388Z"},"accession":"S-EPMC3486900","cross_references":{"pubmed":["23133386"],"doi":["10.1371/journal.ppat.1002998"]}}