Adults with celiac disease exhibit overexpression of endogenous retroviruses, TRIM28, and SETDB1 despite gluten-free diet

•Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. health...

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Veröffentlicht in:Virus research Jg. 359; S. 199613
Hauptverfasser: Tovo, Pier-Angelo, Armandi, Angelo, Bruno, Mauro, Caviglia, Gian Paolo, Montanari, Paola, Pitoni, Demis, Calvi, Cristina, Frara, Simone, Dileo, Eleonora, Gambarino, Stefano, Galliano, Ilaria, Ribaldone, Davide Giuseppe, Bergallo, Massimiliano
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Netherlands Elsevier B.V 01.09.2025
Elsevier
Schlagworte:
Adult
Celiac disease
Celiac Disease - diet therapy
Celiac Disease - genetics
Celiac Disease - virology
Diet, Gluten-Free
Endogenous Retroviruses - genetics
epigenetics
Female
GFD
Histone-Lysine N-Methyltransferase - genetics
Human endogenous retroviruses
Humans
Male
Middle Aged
Prospective Studies
SETDB1
TRIM28
Tripartite Motif-Containing Protein 28 - blood
Tripartite Motif-Containing Protein 28 - genetics
Young Adult
Celiac disease
Human endogenous retroviruses
TRIM28
SETDB1
GFD
epigenetics
ISSN:0168-1702, 1872-7492, 1872-7492
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Zusammenfassung:•Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. healthy controls.•Persistent HERV activation may raise long-term autoimmune and cancer risks. Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
co-last author
ISSN:0168-1702
1872-7492
1872-7492
DOI:10.1016/j.virusres.2025.199613