MicroRNA Expression Profiles in Patients With Acute Crimean Congo Hemorrhagic Fever Reveal Possible Adjustments to Cellular Pathways


Demir Z. C., Bastug A., Bodur H., ERGÜNAY K., ÖZKUL A.

JOURNAL OF MEDICAL VIROLOGY, cilt.89, sa.3, ss.417-422, 2017 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 89 Sayı: 3
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1002/jmv.24667
  • Dergi Adı: JOURNAL OF MEDICAL VIROLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.417-422
  • Anahtar Kelimeler: Crimean Congo Hemorrhagic Fever, miRNA, pathogenesis, HEPATITIS-C VIRUS, DENGUE VIRUS, VIRAL LOAD, INFECTION, REPLICATION, PATHOGENESIS, RECOGNITION, SUPPRESSOR, RESPONSES, PROTEIN
  • Ankara Üniversitesi Adresli: Evet

Özet

Several viral diseases are associated with altered microRNA (miRNA) expression, which can provide vital information about how cellular pathways respond to infection. However, the miRNA profile of Crimean Congo Hemorrhagic Fever (CCHFV) infections are not known. To address this gap, we performed real-time PCR-based miRNA analysis in individuals with acute Crimean Congo Hemorrhagic Fever (CCHFV) infections, with the goal of identifying pathways that might be associated with this disease. Peripheral blood mononuclear cells were analysed in eight individuals with detectable viral RNA and compared to five healthy subjects. A total of 106 differentially expressed miRNAs were identified, of which 19 miRNAs were either fivefold prominently up-or down-regulation. Several miRNAs associated with cytokine expression, some of which were previously associated with Dengue and Hantavirus infections were revealed. Moreover, possible mechanisms related to secretion of adhesion molecules and viral escape from innate immunity were identified. Pathway enrichment analyses further revealed the putative involvement of TNF-alfa, TGF-beta, MAPK, WNT, and neurotrophin signaling pathways in disease pathogenesis. (C) 2016 Wiley Periodicals, Inc.