HULC and 7SL RNA expression levels in patients with Crimean-Congo hemorrhagic fever

Bayyurt B., Arslan S., Engin A., Bakır M.

JOURNAL OF MEDICAL VIROLOGY, vol.90, pp.1822-1826, 2018 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 90
  • Publication Date: 2018
  • Doi Number: 10.1002/jmv.25264
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1822-1826
  • Keywords: Crimean-congo hemorrhagic fever (CCHF), gene expression, long non-coding RNAs (lncRNAs), SIGNAL RECOGNITION PARTICLE, NONCODING RNA, ORAL-CANCER, PROTEIN, VIRUS, APOBEC3G, HIV-1, GENE
  • Sivas Cumhuriyet University Affiliated: Yes


Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the Crimean-Congo hemorrhagic fever virus. Long non-coding RNAs (lncRNAs) are generally classified as transcripts longer than 200 nucleotides (nt). The various lncRNAs expressed in infected cells are responsible for regulating the expression of viral and host genes. This is the first study to investigate hepatocellular carcinoma upregulated long non-coding RNA (HULC) and 7SL RNA expression levels in patients with CCHF. Blood samples were taken from 100 individuals (60 patients and 40 controls), and total RNA isolation was performed. Quantitative polymerase chain reaction (qPCR) was performed using the SYBR Green method to determine HULC and 7SL RNA expression levels in the study population. Compared the patient and control groups, HULC was upregulated statistically significantly (P=0.04) and 7SL RNA was downregulated (P=0.93) in patients. Also, there was a statistically significant difference between fatal cases and surviving patients for HULC and 7SL RNA (P<0.01 and P=0.03, respectively). In addition, HULC expression was increased statistically significantly in fatal cases compared with surviving patients in terms of clinical parameters such as aspartate aminotransferase (P<0.01), alanine aminotransferase (P<0.01), international normalized ratio (P=0.05), prothrombin time (P=0.01), active partial thromboplastin time (P<0.01), and lactate dehydrogenase (P<0.01). These findings highlighted that HULC and 7SL RNA could be important mediators for studying the pathogenesis of CCHF and significant therapeutic targets of the disease.