Tufan Tukek, Sacide Pehlivan, Alpay Medetalibeyoglu, Istemi Serin, Yasemin Oyacı, Huzeyfe Arıcı, Naci Senkal, Mustafa Pehlivan, Ummuhan Isoglu-Alkac, Murat Kose
{"title":"细胞因子信号传导-1 (SOCS1)基因抑制因子多态性和启动子甲基化与COVID-19病程相关。","authors":"Tufan Tukek, Sacide Pehlivan, Alpay Medetalibeyoglu, Istemi Serin, Yasemin Oyacı, Huzeyfe Arıcı, Naci Senkal, Mustafa Pehlivan, Ummuhan Isoglu-Alkac, Murat Kose","doi":"10.1080/20477724.2022.2151861","DOIUrl":null,"url":null,"abstract":"<p><p>The suppressor of the cytokine signaling-1 (SOCS1) gene is a short sequence located on chromosome 16 that functions to induce an appropriate immune response and is an essential physiological regulator of interferon (IFN) signaling. In addition to comparing the global DNA and SOCS1 gene promoter methylation status between our patients with coronavirus disease 2019 (COVID-19) and healthy controls, this study demonstrates the effect of the SOCS1 rs33989964 polymorphism on patients with COVID-19. The study group included 139 patients diagnosed with COVID-19 in our hospital's clinics between June and December 2020, and the control group included 78 healthy individuals. After comparing the initial gene polymorphisms of the patients with the healthy control group, three separate clinical subgroups were formed. The gene polymorphism distribution and the methylation status of SOCS1 were examined in these clinical subgroups. Hypomethylation of the SOCS1 gene was observed in the COVID-19 patient group compared to the healthy control group (p = 0.001). Between the patients divided into two separate clinical subgroups, those with severe and mild infections, the Del/Del genotype of the SOCS1 gene was more common in patients with severe infection than in patients with mild infection (p = 0.018). Patients with the CA/CA and CA/Del genotypes were 0.201 times more likely to have a severe infection (95% CI: 0.057-0.716, p = 0.007). Having a non-Del/Del genotype was a protective factor against severe infection. The effect of the SOCS1 rs33989964 polymorphism and methylation status of the SOCS1 gene throughout the COVID-19 pandemic could be significant contributions to the literature.</p>","PeriodicalId":19850,"journal":{"name":"Pathogens and Global Health","volume":null,"pages":null},"PeriodicalIF":4.9000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10177741/pdf/","citationCount":"0","resultStr":"{\"title\":\"The suppressor of cytokine signaling-1 (<i>SOCS1</i>) gene polymorphism and promoter methylation correlate with the course of COVID-19.\",\"authors\":\"Tufan Tukek, Sacide Pehlivan, Alpay Medetalibeyoglu, Istemi Serin, Yasemin Oyacı, Huzeyfe Arıcı, Naci Senkal, Mustafa Pehlivan, Ummuhan Isoglu-Alkac, Murat Kose\",\"doi\":\"10.1080/20477724.2022.2151861\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The suppressor of the cytokine signaling-1 (SOCS1) gene is a short sequence located on chromosome 16 that functions to induce an appropriate immune response and is an essential physiological regulator of interferon (IFN) signaling. In addition to comparing the global DNA and SOCS1 gene promoter methylation status between our patients with coronavirus disease 2019 (COVID-19) and healthy controls, this study demonstrates the effect of the SOCS1 rs33989964 polymorphism on patients with COVID-19. The study group included 139 patients diagnosed with COVID-19 in our hospital's clinics between June and December 2020, and the control group included 78 healthy individuals. After comparing the initial gene polymorphisms of the patients with the healthy control group, three separate clinical subgroups were formed. The gene polymorphism distribution and the methylation status of SOCS1 were examined in these clinical subgroups. Hypomethylation of the SOCS1 gene was observed in the COVID-19 patient group compared to the healthy control group (p = 0.001). Between the patients divided into two separate clinical subgroups, those with severe and mild infections, the Del/Del genotype of the SOCS1 gene was more common in patients with severe infection than in patients with mild infection (p = 0.018). Patients with the CA/CA and CA/Del genotypes were 0.201 times more likely to have a severe infection (95% CI: 0.057-0.716, p = 0.007). Having a non-Del/Del genotype was a protective factor against severe infection. The effect of the SOCS1 rs33989964 polymorphism and methylation status of the SOCS1 gene throughout the COVID-19 pandemic could be significant contributions to the literature.</p>\",\"PeriodicalId\":19850,\"journal\":{\"name\":\"Pathogens and Global Health\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.9000,\"publicationDate\":\"2023-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10177741/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pathogens and Global Health\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/20477724.2022.2151861\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2022/11/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pathogens and Global Health","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/20477724.2022.2151861","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/11/29 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PARASITOLOGY","Score":null,"Total":0}
The suppressor of cytokine signaling-1 (SOCS1) gene polymorphism and promoter methylation correlate with the course of COVID-19.
The suppressor of the cytokine signaling-1 (SOCS1) gene is a short sequence located on chromosome 16 that functions to induce an appropriate immune response and is an essential physiological regulator of interferon (IFN) signaling. In addition to comparing the global DNA and SOCS1 gene promoter methylation status between our patients with coronavirus disease 2019 (COVID-19) and healthy controls, this study demonstrates the effect of the SOCS1 rs33989964 polymorphism on patients with COVID-19. The study group included 139 patients diagnosed with COVID-19 in our hospital's clinics between June and December 2020, and the control group included 78 healthy individuals. After comparing the initial gene polymorphisms of the patients with the healthy control group, three separate clinical subgroups were formed. The gene polymorphism distribution and the methylation status of SOCS1 were examined in these clinical subgroups. Hypomethylation of the SOCS1 gene was observed in the COVID-19 patient group compared to the healthy control group (p = 0.001). Between the patients divided into two separate clinical subgroups, those with severe and mild infections, the Del/Del genotype of the SOCS1 gene was more common in patients with severe infection than in patients with mild infection (p = 0.018). Patients with the CA/CA and CA/Del genotypes were 0.201 times more likely to have a severe infection (95% CI: 0.057-0.716, p = 0.007). Having a non-Del/Del genotype was a protective factor against severe infection. The effect of the SOCS1 rs33989964 polymorphism and methylation status of the SOCS1 gene throughout the COVID-19 pandemic could be significant contributions to the literature.
期刊介绍:
Pathogens and Global Health is a journal of infectious disease and public health that focuses on the translation of molecular, immunological, genomics and epidemiological knowledge into control measures for global health threat. The journal publishes original innovative research papers, reviews articles and interviews policy makers and opinion leaders on health subjects of international relevance. It provides a forum for scientific, ethical and political discussion of new innovative solutions for controlling and eradicating infectious diseases, with particular emphasis on those diseases affecting the poorest regions of the world.