Bahrikarehmi Laleh, Kuruca Nilufer, Say Coskun Umut Safiye, Nursal Ayse Feyda, Albayrak Harun, Yigit Serbulent
Department of Medical Biology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey.
Department of Pathology, Faculty of Veterinary, Ondokuz Mayis University, Samsun, Turkey.
Nucleosides Nucleotides Nucleic Acids. 2025;44(10):827-835. doi: 10.1080/15257770.2024.2423887. Epub 2024 Nov 4.
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 and 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 936 C > T (rs3025039) and - 604 T > C (rs2071559) variants. The results were statistically analyzed.
The 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 (). There was a statistically significant association between the controls and the patients in terms of 936 C > T C/C versus C/T + T/T (, OR:3.273, 95%Cl: 1.44-7.63). The - 604 T > C variant's allele and genotype distribution were not significantly different between the patients and controls.
This study suggests the 936 C > T variant is a genetic marker of sensitivity to CCHF among the Turkish population and may help protect against the disease.
克里米亚-刚果出血热(CCHF)是一种急性病毒性出血热疾病,在人类中的死亡率很高。出血倾向是由凝血功能障碍以及由此导致的血管损伤引起的毛细血管通透性增加所致。血管内皮生长因子(VEGF)和VEGF受体-2,即激酶插入结构域包含受体(KDR),在血管生成和血管新生中发挥作用。据报道,CCHF存在内皮功能障碍。本研究旨在评估VEGF和KDR基因变异是否与土耳其人群中CCHF的发生有关。
本研究共纳入101名受试者,其中包括51例CCHF患者和50名健康对照。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法对VEGF 936 C > T(rs3025039)和KDR - 604 T > C(rs2071559)变异进行基因分型。对结果进行统计学分析。
患者和对照组之间VEGF 936 C > T基因型和等位基因分布确实存在显著差异。携带C/C基因型和C等位基因的受试者患CCHF 的风险高于对照组()。在VEGF 936 C > T C/C与C/T + T/T方面,对照组和患者之间存在统计学显著关联(,比值比:3.273,95%置信区间:1.44 - 7.63)。KDR - 604 T > C变异的等位基因和基因型分布在患者和对照组之间无显著差异。
本研究表明,VEGF 936 C > T变异是土耳其人群中对CCHF敏感的遗传标志物,可能有助于预防该疾病。