{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T11:18:34Z","timestamp":1784719114629,"version":"3.55.0"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:00:00Z","timestamp":1782604800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:00:00Z","timestamp":1782604800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Viruses activate host defences by alerting interferon and other alarms. Viruses seeking latency must curtail this. Infected subjects would then have minimal immune system activation and remain healthy. However, a minority cannot prevent emergence of associated diseases. This conundrum remains despite our understanding (i) that interferon specifically suppresses the translation of viral mRNAs, but not host mRNAs, and (ii) that for the latent state only\n                    <jats:italic>one<\/jats:italic>\n                    latency\u2010maintaining mRNA may be needed. Critical are mRNA loadings with purine (R) bases, relative to pyrimidine bases (Y). Base composition and structural studies have established the\n                    <jats:italic>genome\u2010wide<\/jats:italic>\n                    potential of duplex DNA (hence transcripts thereof) to extruded stem\u2010loops, the stems of which require parity between R and Y bases. Sometimes conflicting with coding demands, parity\u2010violations (R\u2009&gt;\u2009Y)\n                    <jats:italic>decrease<\/jats:italic>\n                    this potential in exons (and hence in mRNAs). Thus, one mRNA (EBNA\u20101) of the Epstein\u2013Barr virus (EBV) is successful in\n                    <jats:italic>not alerting<\/jats:italic>\n                    hosts to immune awareness. However, Y\u2010rich transcripts might occasionally arise in the highly polymorphic \u2018junk DNA\u2019, long known as pervasively transcribed. Thus, within a minor subset of the infected population, some may,\n                    <jats:italic>by chance<\/jats:italic>\n                    , have randomly mutated to create pyrimidine\u2010loaded regions that would form forbidden double\u2010stranded RNA duplexes with purine\u2010loaded EBNA\u20101 mRNAs. Thus, immune systems would\n                    <jats:italic>awaken<\/jats:italic>\n                    . Other viruses, differing in types\/extents of latency, have evolved different survival strategies. Thus, mRNAs of the\n                    <jats:italic>extremely<\/jats:italic>\n                    latent human T cell leukaemia virus (HTLV1) are Y\u2010loaded (Y\u2009&gt;\u2009R), but a single latency transcript is highly R\u2010loaded. In contrast, most mRNAs of\n                    <jats:italic>less extremely<\/jats:italic>\n                    latent retrovirus (HIV1) are expressed with R\u2009&gt;\u2009Y.\n                  <\/jats:p>","DOI":"10.1111\/sji.70135","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T04:16:45Z","timestamp":1782706605000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The\n                    <scp>EBNA<\/scp>\n                    \u20101 Conundrum: Does Epstein\u2013Barr Virus Invoke Autoimmune Pathology in a Population Subset by Poorly Purine\u2010Loading Its Major Latency\u2010Maintaining Transcript?"],"prefix":"10.1111","volume":"104","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4844-1417","authenticated-orcid":false,"given":"Donald R.","family":"Forsdyke","sequence":"first","affiliation":[{"name":"Department of Biomedical and Molecular Sciences Queen's University  Kingston Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,28]]},"reference":[{"key":"e_1_2_13_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10739-011-9274-8"},{"key":"e_1_2_13_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtbi.2024.111943"},{"key":"e_1_2_13_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-319-28755-3"},{"key":"e_1_2_13_5_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pcbi.1014287"},{"key":"e_1_2_13_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1119(00)00472-8"},{"key":"e_1_2_13_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/jtbi.2000.2233"},{"key":"e_1_2_13_8_1","doi-asserted-by":"publisher","DOI":"10.1006\/scdb.1998.0241"},{"key":"e_1_2_13_9_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1010774"},{"key":"e_1_2_13_10_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1010387"},{"key":"e_1_2_13_11_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.2519445123"},{"key":"e_1_2_13_12_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.abm7930"},{"key":"e_1_2_13_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41584-024-01167-9"},{"key":"e_1_2_13_14_1","doi-asserted-by":"publisher","DOI":"10.3389\/fgene.2026.1775625"},{"key":"e_1_2_13_15_1","doi-asserted-by":"publisher","DOI":"10.1111\/sji.13314"},{"key":"e_1_2_13_16_1","volume-title":"Breaking Through. 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