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IFITM1 启动子甲基化与 SARS-CoV-2 感染严重程度的关联。

Association of IFITM1 Promoter Methylation with Severity of SARS-CoV-2 Infection.

出版信息

Clin Lab. 2023 Apr 1;69(4). doi: 10.7754/Clin.Lab.2022.220622.

DOI:10.7754/Clin.Lab.2022.220622
PMID:37057950
Abstract

BACKGROUND

During viral infections such as SARS-CoV-2, epigenetic changes within the promoter region of the immune system genes would possibly occur and have an effect on the immune system response as well as disease outcome. We aimed to evaluate and compare the methylation level of the IFITM1 gene promoter in different stages of COVID-19 disease with a healthy control group.

METHODS

In this cross-sectional study, 75 COVID-19 patients (25 mild, 25 severe, and 25 critical in addition to 25 age- and gender-matched healthy volunteers) have been included. DNA was extracted from the peripheral white blood cells using a commercial DNA extraction kit. PCR was performed using two types of primers designed for the methylated and unmethylated forms of the IFITM1 gene promoter.

RESULTS

The mean age of the patient and healthy volunteer groups was 52.733 ± 13.780 and 49.120 ± 12.490, respectively. Out of a hundred participants, 52 were male. The results demonstrated that severe (p = 0.03, OR 6.729) and critical (p = 0.001, OR 11.156) patients were much more likely to show methylation of the IFITM1 gene in contrast with mild patients. Moreover, IFITM1 methylation was significantly higher in COVID-19 patients in comparison with the healthy volunteer group (p = 0.004, OR 3.17). Furthermore, IFITM1 methylation in male patients with critical status, (p = 0.01) was significantly higher than in male patients with mild status. In addition, IFITM1 methylation of male (p = 0.03) and female (p = 0.01) critical patients was considerably higher compared to males and females of volunteer group.

CONCLUSIONS

Increased methylation of the IFITM1 gene in the severe and critical stage of COVID-19 diseases may indicate the role of SARS-CoV-2 infection in increasing methylation of this antiviral gene. This might be involved in suppressing the immune system, promoting SARS-CoV-2 replication and disease outcome.

摘要

背景

在 SARS-CoV-2 等病毒感染期间,免疫系统基因启动子区域的表观遗传变化可能会发生,并对免疫系统反应和疾病结局产生影响。我们旨在评估和比较 COVID-19 疾病不同阶段与健康对照组之间 IFITM1 基因启动子的甲基化水平。

方法

在这项横断面研究中,纳入了 75 名 COVID-19 患者(25 名轻症、25 名重症和 25 名危重症,以及 25 名年龄和性别匹配的健康志愿者)。使用商业 DNA 提取试剂盒从外周白细胞中提取 DNA。使用针对 IFITM1 基因启动子甲基化和非甲基化形式设计的两种引物进行 PCR。

结果

患者组和健康志愿者组的平均年龄分别为 52.733 ± 13.780 和 49.120 ± 12.490。在 100 名参与者中,有 52 名男性。结果表明,与轻症患者相比,重症(p = 0.03,OR 6.729)和危重症(p = 0.001,OR 11.156)患者更有可能表现出 IFITM1 基因的甲基化。此外,与健康志愿者组相比,COVID-19 患者的 IFITM1 甲基化水平显著升高(p = 0.004,OR 3.17)。此外,在处于危急状态的男性患者中,IFITM1 甲基化(p = 0.01)显著高于处于轻症状态的男性患者。此外,与志愿者组的男性和女性相比,处于危急状态的男性(p = 0.03)和女性(p = 0.01)的 IFITM1 甲基化水平显著升高。

结论

COVID-19 疾病严重和危急阶段 IFITM1 基因的甲基化增加可能表明 SARS-CoV-2 感染在增加这种抗病毒基因的甲基化方面起作用。这可能与抑制免疫系统、促进 SARS-CoV-2 复制和疾病结局有关。

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