The effect of VEGF and KDR gene variants on Crimean-Congo hemorrhagic fever

• Published in: Nucleosides, nucleotides & nucleic acids Vol. 44; no. 10; pp. 827 - 835
• Main Authors: Bahrikarehmi, Laleh, Kuruca, Nilufer, Say Coskun, Umut Safiye, Nursal, Ayse Feyda, Albayrak, Harun, Yigit, Serbulent
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 03.10.2025
• Subjects: Adult; Alleles; Case-Control Studies; Crimean-Congo hemorrhagic fever; Female; Genetic Predisposition to Disease; Genotype; Hemorrhagic Fever, Crimean - genetics; Humans; kinase insert domain containing receptor; Male; Middle Aged; PCR; Polymorphism, Single Nucleotide; RFLP; Turkey; vascular endothelial growth factor; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor Receptor-2 - genetics; Turkey; kinase insert domain containing receptor; vascular endothelial growth factor; PCR; RFLP; Crimean-Congo hemorrhagic fever
• ISSN: 1525-7770; 1532-2335; 1532-2335
• DOI: 10.1080/15257770.2024.2423887

Crimean-Congo hemorrhagic fever (CCHF), an acute viral hemorrhagic fever disease, has a high mortality rate among humans. Hemorrhagic propensity is caused by coagulation malfunction and increased capillary permeability brought on by the resultant vascular injury. Vascular endothelial growth factor (VEGF) and VEGF receptor-2, or KDR (kinase insert domain containing receptor), are effective in vasculogenesis and angiogenesis. CCHF was stated to have endothelial dysfunction. This study aimed to evaluate whether the VEGF and KDR gene variants contribute to the development of CCHF in the Turkish population. A total of 101 subjects, including 51 CCHF patients and 50 healthy controls, were included in the study. The polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method was used to genotype VEGF 936 C > T (rs3025039) and KDR − 604 T > C (rs2071559) variants. The results were statistically analyzed. The VEGF 936 C > T genotype and allele distributions did differ significantly between the patients and the controls. The subjects carrying the C/C genotype and C allele had a higher risk of developing CCHF than the control group (p˂0.05). There was a statistically significant association between the controls and the patients in terms of VEGF 936 C > T C/C versus C/T + T/T (p˂0.05, OR:3.273, 95%Cl: 1.44-7.63). The KDR − 604 T > C variant's allele and genotype distribution were not significantly different between the patients and controls. This study suggests the VEGF 936 C > T variant is a genetic marker of sensitivity to CCHF among the Turkish population and may help protect against the disease.