Romanova E N, Govorin A V
Ter Arkh. 2013;85(3):58-62.
To study the specific features of cytokine gene polymorphisms (such as TNF G308A, IL10 C592A, IL10 C819T, IL10 G1082A) and vascular tone regulatory gene polymorphism (eNOS C786T) in patients with influenza A/H1N1 complicated by pneumonia.
Patients treated for pneumonia in the presence of influenza A/H1N1, divided into 3 groups: 1) 37 patients with severe pneumonia; 2) 74 with mild pneumonia; and 3) 68 healthy individuals, were examined. Molecular genetic testing was made using a polymerase chain reaction technique. Serum TNFalpha, IL-10 and s-ICAM-1 concentrations were measured by enzyme immunoassay.
As compared to the control group, the patients with influenza-related pneumonia were more frequently homozygous for the G allele of the TNF 308 G/A polymorphism. The IL-10 G allele (1082 G/A) was considerably prevalent as homozygous carriage and the IL-10 G allele (592 G/A) was as a homozygous type to a greater extent. An abnormal zygote of the eNOS T/T (786 C/T) polymorphism was found to be prevalent among the patients with influenza-related pneumonia; on the contrary, there were mainly heterozygous C/T carriers in the control group. In the C/T genotype group, the level of soluble intercellular adhesion molecule 1 (sICAM-1) was lower than in other polymorphic variants (786 C/T). CONCLUSION; The study of the patients' genetic status in influenza A/H1N1 will be able to evaluate the severity of the disease and to predict possible complications.
研究甲型H1N1流感合并肺炎患者细胞因子基因多态性（如肿瘤坏死因子G308A、白细胞介素10 C592A、白细胞介素10 C819T、白细胞介素10 G1082A）及血管张力调节基因多态性（内皮型一氧化氮合酶C786T）的特点。
对因甲型H1N1流感合并肺炎接受治疗的患者进行分组检查，分为3组：1）37例重症肺炎患者；2）74例轻症肺炎患者；3）68名健康个体。采用聚合酶链反应技术进行分子遗传学检测。通过酶免疫测定法测定血清肿瘤坏死因子α、白细胞介素10和可溶性细胞间黏附分子1的浓度。
与对照组相比，甲型H1N1流感相关肺炎患者中肿瘤坏死因子308 G/A多态性的G等位基因纯合子更为常见。白细胞介素10 G等位基因（1082 G/A）作为纯合子携带相当普遍，白细胞介素10 G等位基因（592 G/A）在很大程度上为纯合子类型。在内皮型一氧化氮合酶T/T（C786T）多态性中，异常纯合子在甲型H1N1流感相关肺炎患者中较为普遍；相反，对照组中主要是杂合子C/T携带者。在C/T基因型组中，可溶性细胞间黏附分子1（sICAM-1）水平低于其他多态性变体（C786T）。结论：对甲型H1N1流感患者的基因状态进行研究，将能够评估疾病的严重程度并预测可能的并发症。
