Viral DNA in submandibular gland tissue with an inflammatory disorder

dc.contributor.authorKeski-Säntti Noora
dc.contributor.authorWaltimo Elin
dc.contributor.authorMäkitie Antti
dc.contributor.authorHagström Jaana
dc.contributor.authorSöderlund-Venermo Maria
dc.contributor.authorAtula Timo
dc.contributor.authorHaglund Caj
dc.contributor.authorSinkkonen Saku T.
dc.contributor.authorJauhiainen Maria
dc.contributor.organizationfi=hammaslääketieteen laitos|en=Institute of Dentistry|
dc.contributor.organization-code1.2.246.10.2458963.20.64787032594
dc.converis.publication-id393413037
dc.converis.urlhttps://research.utu.fi/converis/portal/Publication/393413037
dc.date.accessioned2025-08-27T12:55:35Z
dc.date.available2025-08-27T12:55:35Z
dc.description.abstract<p>Background</p><p>The etiology behind different types of chronic sialadenitis (CS), some of which exhibit IgG4 overexpression, is unknown. Further, IgG4-related disease (IgG4-RD) commonly affects the submandibular gland, but its relationship to IgG4-overexpressing CS, and the antigen triggering IgG4 overexpression, remain unknown.</p><p>Materials and Methods<br>By qPCR, we assessed the presence of 21 DNA-viruses causing IgG4 overexpression in submandibular gland tissue from patients with IgG4-positive and IgG4-negative CS. Healthy submandibular glands and glands with sialolithiasis without CS were used as controls. We examined the distribution of HHV-7, HHV-6B and B19V DNA, within virus PCR-positive tissues with RNAscope in-situ hybridization (RISH).</p><p>Results<br>We detected DNA from seven viruses in 48/61 samples. EBV DNA was more prevalent within the IgG4-positive samples (6/29; 21%) than the IgG4-negative ones (1/19; 5.3%). B19V DNA was more prevalent within the IgG4-negative samples (5/19; 26%) than the IgG4-positive ones (4/29; 14%). The differences in virus prevalence were not statistically significant. Of the IgG4-RD samples (n = 3) one contained HHV-6B DNA. RISH only showed signals of HHV-7.</p><p>Conclusions<br>None of the studied viruses are implicated as triggering IgG4-overexpression in CS. Although our results do not confirm viral etiology in the examined conditions, they provide valuable information on the prevalence of viruses in both diseased and healthy submandibular gland tissue.</p>
dc.identifier.eissn2000-2297
dc.identifier.jour-issn2000-2297
dc.identifier.olddbid199878
dc.identifier.oldhandle10024/182905
dc.identifier.urihttps://www.utupub.fi/handle/11111/44621
dc.identifier.urlhttps://doi.org/10.1080/20002297.2024.2345941
dc.identifier.urnURN:NBN:fi-fe2025082788885
dc.language.isoen
dc.okm.affiliatedauthorHagström, Jaana
dc.okm.discipline1183 Plant biology, microbiology, virologyen_GB
dc.okm.discipline3111 Biomedicineen_GB
dc.okm.discipline1183 Kasvibiologia, mikrobiologia, virologiafi_FI
dc.okm.discipline3111 Biolääketieteetfi_FI
dc.okm.internationalcopublicationnot an international co-publication
dc.okm.internationalityInternational publication
dc.okm.typeA1 ScientificArticle
dc.publisherTaylor & Francis
dc.publisher.countryUnited Kingdomen_GB
dc.publisher.countryBritanniafi_FI
dc.publisher.country-codeGB
dc.relation.articlenumber2345941
dc.relation.doi10.1080/20002297.2024.2345941
dc.relation.ispartofjournalJournal of Oral Microbiology
dc.relation.issue1
dc.relation.volume16
dc.source.identifierhttps://www.utupub.fi/handle/10024/182905
dc.titleViral DNA in submandibular gland tissue with an inflammatory disorder
dc.year.issued2024

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