Antiviral microRNA expression signatures are altered in subacute sclerosing panencephalitis

Tufekci K. U., Allmer J., Carman K. B., BAYRAM E., TOPÇU Y., Hiz S., ...More

NEUROLOGICAL SCIENCES AND NEUROPHYSIOLOGY, vol.38, no.3, pp.166-172, 2021 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 38 Issue: 3
  • Publication Date: 2021
  • Doi Number: 10.4103/nsn.nsn_57_21
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.166-172
  • Keywords: Antiviral microRNA, measles virus, microRNA, subacute sclerosing panencephalitis, INFORMATION, CYTOSCAPE, TARBASE
  • Dokuz Eylül University Affiliated: Yes


Background: Subacute sclerosing panencephalitis (SSPE) is a chronic, progressive disease caused by a persistent infection of the measles virus. Despite extensive efforts, the exact neurodegeneration mechanism in SSPE remains unknown. MicroRNAs (miRNAs) have emerged as an essential part of cellular antiviral defense mechanisms and can be modulated by antiviral cytokines Such as interferon-beta (IFN-beta). Aims and Objectives: In this study, we aimed to elucidate the role of antiviral miRNAs in the pathogenesis of SSPE and analyze the interaction between host antiviral miRNAs and virus genes. Materials and Methods: Thirty-seven patients who were followed with SSPE and age-matched healthy children were included in the study. Peripheral blood mononuclear cell levels of miR-196b, miR-296, miR-431, and miR-448 were analyzed using quantitative polymerase chain reaction. Target predictions and pathway constructions of deregulated miRNAs were assessed. Results: Here, we showed that IFN-beta-modulated miR-196b, miR-296, and miR-431 were significantly upregulated in patients with SSPE compared with healthy controls. Besides, sequence complementarity analysis showed that miR-296 and miR-196b predicted binding regions in measles virus genomic RNA. Conclusion: Our findings suggest that antiviral miRNAs are upregulated in patients with SSPE, which could be a part of the host antiviral defense mechanism.