{"title":"拉脱维亚队列中艾滋病毒感染和肺结核患者的 HLA II 类 DRB1、DQA1 和 DQB1 基因座。","authors":"Alena Soha, Inga Azina, Baiba Rozentale, Ksenija Kramicha, Gunta Sture, Oksana Savicka, Galina Titovica","doi":"10.5114/ceji.2024.138738","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Until the COVID-19 pandemic, tuberculosis (TB) was the leading cause of death from a single infectious agent, ranking above HIV/AIDS. It is also the key cause of death among people infected with HIV. Tuberculosis incidence in Latvia has decreased by 25% during the last 30 years, but the mortality level of TB remains significant. The HLA class II genes are responsible for antigen presentation and regulation of immune responses, which plays an important role in individual susceptibility to infection disease. Whether or not differential HLA polymorphism contributes to TB with HIV infection and TB without HIV infection in Latvian patients is unknown.</p><p><strong>Material and methods: </strong>For the detection of HLA class II DQA1, DQB1, and DRB1 alleles a total of 616 subjects were enrolled, including 80 primary active TB (PATB) patients, 168 HIV-1/TB patients, 168 HIV-1 patients and 200 HC individuals.</p><p><strong>Results: </strong>For immunodeficiency caused by TB, HIV-1 or HIV-1/TB coinfection, alleles DRB1*12:01, 14:01, 16:01, DQA1*01:02, 01:03, 02:01, 06:01, DQB1*03:03, 06:01 are identified as protective, but DRB1*07:01, 11:01, 15:01, DQA1*02:01, 03:01, DQB1*03:01, 05:01 are identified as risk alleles.</p><p><strong>Conclusions: </strong>The results of our experimental pilot studies demonstrated that HLA class II genes may contribute to the genetic risk of TB and HIV-1/TB co-infection, possibly by reducing the presentation of protective Mycobacterium tuberculosis antigens to T-helpers. It is necessary to conduct repetitive, multicentre, and large sample studies in order to draw more scientific conclusions and to confirm the relationship between TB, HIV and HIV-1/TB co-infection susceptibility and gene polymorphisms.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11130985/pdf/","citationCount":"0","resultStr":"{\"title\":\"HLA class II DRB1, DQA1, DQB1 loci in patients with HIV infection and tuberculosis in a Latvian cohort group.\",\"authors\":\"Alena Soha, Inga Azina, Baiba Rozentale, Ksenija Kramicha, Gunta Sture, Oksana Savicka, Galina Titovica\",\"doi\":\"10.5114/ceji.2024.138738\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Until the COVID-19 pandemic, tuberculosis (TB) was the leading cause of death from a single infectious agent, ranking above HIV/AIDS. It is also the key cause of death among people infected with HIV. Tuberculosis incidence in Latvia has decreased by 25% during the last 30 years, but the mortality level of TB remains significant. The HLA class II genes are responsible for antigen presentation and regulation of immune responses, which plays an important role in individual susceptibility to infection disease. Whether or not differential HLA polymorphism contributes to TB with HIV infection and TB without HIV infection in Latvian patients is unknown.</p><p><strong>Material and methods: </strong>For the detection of HLA class II DQA1, DQB1, and DRB1 alleles a total of 616 subjects were enrolled, including 80 primary active TB (PATB) patients, 168 HIV-1/TB patients, 168 HIV-1 patients and 200 HC individuals.</p><p><strong>Results: </strong>For immunodeficiency caused by TB, HIV-1 or HIV-1/TB coinfection, alleles DRB1*12:01, 14:01, 16:01, DQA1*01:02, 01:03, 02:01, 06:01, DQB1*03:03, 06:01 are identified as protective, but DRB1*07:01, 11:01, 15:01, DQA1*02:01, 03:01, DQB1*03:01, 05:01 are identified as risk alleles.</p><p><strong>Conclusions: </strong>The results of our experimental pilot studies demonstrated that HLA class II genes may contribute to the genetic risk of TB and HIV-1/TB co-infection, possibly by reducing the presentation of protective Mycobacterium tuberculosis antigens to T-helpers. It is necessary to conduct repetitive, multicentre, and large sample studies in order to draw more scientific conclusions and to confirm the relationship between TB, HIV and HIV-1/TB co-infection susceptibility and gene polymorphisms.</p>\",\"PeriodicalId\":9694,\"journal\":{\"name\":\"Central European Journal of Immunology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11130985/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Central European Journal of Immunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5114/ceji.2024.138738\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/4/19 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Central European Journal of Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5114/ceji.2024.138738","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/4/19 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
导言:在 COVID-19 大流行之前,结核病(TB)是单一传染源导致死亡的主要原因,高于艾滋病毒/艾滋病。它也是艾滋病毒感染者的主要死因。过去 30 年间,拉脱维亚的结核病发病率下降了 25%,但结核病死亡率仍然很高。HLA 二类基因负责抗原呈递和免疫反应的调节,在个人感染疾病的易感性中起着重要作用。在拉脱维亚患者中,不同的 HLA 多态性是否会导致感染 HIV 的肺结核和未感染 HIV 的肺结核,目前尚不清楚:为检测 HLA II 类 DQA1、DQB1 和 DRB1 等位基因,共招募了 616 名受试者,其中包括 80 名原发性活动性肺结核(PATB)患者、168 名 HIV-1/TB 患者、168 名 HIV-1 患者和 200 名艾滋病毒感染者:结果:对于由肺结核、HIV-1 或 HIV-1/TB 合并感染引起的免疫缺陷,等位基因 DRB1*12:01、14:01、16:01、DQA1*01:02、01:03、02:01、06:01、DQB1*03:03、06:01 被确定为保护性等位基因,但 DRB1*07:01、11:01、15:01、DQA1*02:01、03:01、DQB1*03:01、05:01 被确定为风险等位基因:我们的实验性试点研究结果表明,HLA II 类基因可能会降低结核分枝杆菌抗原对 T 辅助细胞的保护作用,从而导致结核病和 HIV-1/TB 合并感染的遗传风险。有必要进行重复性、多中心和大样本研究,以便得出更科学的结论,并确认结核病、艾滋病毒和艾滋病毒-1/结核病合并感染易感性与基因多态性之间的关系。
HLA class II DRB1, DQA1, DQB1 loci in patients with HIV infection and tuberculosis in a Latvian cohort group.
Introduction: Until the COVID-19 pandemic, tuberculosis (TB) was the leading cause of death from a single infectious agent, ranking above HIV/AIDS. It is also the key cause of death among people infected with HIV. Tuberculosis incidence in Latvia has decreased by 25% during the last 30 years, but the mortality level of TB remains significant. The HLA class II genes are responsible for antigen presentation and regulation of immune responses, which plays an important role in individual susceptibility to infection disease. Whether or not differential HLA polymorphism contributes to TB with HIV infection and TB without HIV infection in Latvian patients is unknown.
Material and methods: For the detection of HLA class II DQA1, DQB1, and DRB1 alleles a total of 616 subjects were enrolled, including 80 primary active TB (PATB) patients, 168 HIV-1/TB patients, 168 HIV-1 patients and 200 HC individuals.
Results: For immunodeficiency caused by TB, HIV-1 or HIV-1/TB coinfection, alleles DRB1*12:01, 14:01, 16:01, DQA1*01:02, 01:03, 02:01, 06:01, DQB1*03:03, 06:01 are identified as protective, but DRB1*07:01, 11:01, 15:01, DQA1*02:01, 03:01, DQB1*03:01, 05:01 are identified as risk alleles.
Conclusions: The results of our experimental pilot studies demonstrated that HLA class II genes may contribute to the genetic risk of TB and HIV-1/TB co-infection, possibly by reducing the presentation of protective Mycobacterium tuberculosis antigens to T-helpers. It is necessary to conduct repetitive, multicentre, and large sample studies in order to draw more scientific conclusions and to confirm the relationship between TB, HIV and HIV-1/TB co-infection susceptibility and gene polymorphisms.