{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T15:48:36Z","timestamp":1790524116811,"version":"4.1.0"},"reference-count":66,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2014,4,15]],"date-time":"2014-04-15T00:00:00Z","timestamp":1397520000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2014,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Syncytin-1, a fusogenic protein encoded by a human endogenous retrovirus of the W family (HERV-W) element (\n            <jats:italic>ERVWE1<\/jats:italic>\n            ), is expressed in the syncytiotrophoblast layer of the placenta. This locus is transcriptionally repressed in adult tissues through promoter CpG methylation and suppressive histone modifications. Whereas syncytin-1 appears to be crucial for the development and functioning of the human placenta, its ectopic expression has been associated with pathological conditions, such as multiple sclerosis and schizophrenia. We previously reported on the transactivation of HERV-W elements, including\n            <jats:italic>ERVWE1<\/jats:italic>\n            , during influenza A\/WSN\/33 virus infection in a range of human cell lines. Here we report the results of quantitative PCR analyses of transcripts encoding syncytin-1 in both cell lines and primary fibroblast cells. We observed that spliced\n            <jats:italic>ERVWE1<\/jats:italic>\n            transcripts and those encoding the transcription factor glial cells missing 1 (GCM1), acting as an enhancer element upstream of\n            <jats:italic>ERVWE1<\/jats:italic>\n            , are prominently upregulated in response to influenza A\/WSN\/33 virus infection in nonplacental cells. Knockdown of GCM1 by small interfering RNA followed by infection suppressed the transactivation of\n            <jats:italic>ERVWE1<\/jats:italic>\n            . While the infection had no influence on CpG methylation in the\n            <jats:italic>ERVWE1<\/jats:italic>\n            promoter, chromatin immunoprecipitation assays detected decreased H3K9 trimethylation (H3K9me3) and histone methyltransferase SETDB1 levels along with influenza virus proteins associated with\n            <jats:italic>ERVWE1<\/jats:italic>\n            and other HERV-W loci in infected CCF-STTG1 cells. The present findings suggest that an exogenous influenza virus infection can transactivate\n            <jats:italic>ERVWE1<\/jats:italic>\n            by increasing transcription of\n            <jats:italic>GCM1<\/jats:italic>\n            and reducing H3K9me3 in this region and in other regions harboring HERV-W elements.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Syncytin-1, a protein encoded by the\n            <jats:italic>env<\/jats:italic>\n            gene in the HERV-W locus\n            <jats:italic>ERVWE1<\/jats:italic>\n            , appears to be crucial for the development and functioning of the human placenta and is transcriptionally repressed in nonplacental tissues. Nevertheless, its ectopic expression has been associated with pathological conditions, such as multiple sclerosis and schizophrenia. In the present paper, we report findings suggesting that an exogenous influenza A virus infection can transactivate\n            <jats:italic>ERVWE1<\/jats:italic>\n            by increasing the transcription of\n            <jats:italic>GCM1<\/jats:italic>\n            and reducing the repressive histone mark H3K9me3 in this region and in other regions harboring HERV-W elements. These observations have implications of potential relevance for viral pathogenesis and for conditions associated with the aberrant transcription of HERV-W loci.\n          <\/jats:p>","DOI":"10.1128\/jvi.03628-13","type":"journal-article","created":{"date-parts":[[2014,1,30]],"date-time":"2014-01-30T04:17:19Z","timestamp":1391055439000},"page":"4328-4337","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":68,"title":["Transcriptional Derepression of the\n            <i>ERVWE1<\/i>\n            Locus following Influenza A Virus Infection"],"prefix":"10.1128","volume":"88","author":[{"given":"Fang","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoffer","family":"Nell\u00e5ker","sequence":"additional","affiliation":[{"name":"MRC Functional Genetics Unit, Department of 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