L I Nikolaeva, M D Stuchinskaya, K P Telepenina, N G Shevchenko, V V Kuprianov, K G Krasnoslobodtsev, E A Mukasheva, S V Trushakova, I N Khlopova, I S Kruzhkova, L B Kisteneva, L V Kolobukhina, E I Burtseva
{"title":"影响干扰素-λ3产生的基因单核苷酸多态性与流感临床病程的关系分析","authors":"L I Nikolaeva, M D Stuchinskaya, K P Telepenina, N G Shevchenko, V V Kuprianov, K G Krasnoslobodtsev, E A Mukasheva, S V Trushakova, I N Khlopova, I S Kruzhkova, L B Kisteneva, L V Kolobukhina, E I Burtseva","doi":"10.36233/0507-4088-271","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Predisposition to different courses of the infectious process is largely associated with the polymorphisms in human genome, especially in genes encoding proteins of the immune system. In the early stages of influenza infection such components of innate immunity as interferons I (α/β) and III (λ) type play a significant role in limiting virus replication. The aim of the work was to investigate associations of single nucleotide polymorphism in <i>IFNL3</i> (rs8099917 T/G) and <i>IFNL4</i> (rs12979860 C/T) genes with different course of influenza, and identify genetic markers of influenza complicated by community-acquired pneumonia. The genes noted above affect the production of interferon-λ3, which is involved in restriction of the viral replication.</p><p><strong>Materials and methods: </strong>Samples from 456 patients with mild (<i>n </i>= 150), moderate (<i>n </i>= 173), and severe (<i>n </i>= 133) influenza were studied. The viral RNA was detected by reverse transcription and polymerase chain reaction (RT-PCR). Polymorphisms in <i>IFNL3</i> (rs8099917 T/G) and <i>IFNL4</i> (rs12979860 C/T) genes was detected by PCR. Statistical analysis was performed using SNPStats software.</p><p><strong>Results: </strong>Patients with the C/T or T/T genotype of <i>IFNL4</i> gene (rs12979860 C/T) were more likely to have pneumonia than those with the C/C genotype (OR 2.47 (1.31-4.63); <i>p </i>= 0.0044; <i>q</i> = 0.0059). The presence of one T allele increased the risk of developing pneumonia (OR 2.02 (1.05-4.02); <i>p </i>= 0.006; <i>q</i> = 0.008). In the presence of the T/T genotype, the risk increased more than twofold: OR 2.14 (1.31-3.48). Analysis of the SNP of <i>IFNL3</i> gene (rs8099917 T/G) revealed a weak association of the G allele with pneumonia (OR 1.86 (1.04-3.31); <i>p</i> = 0.03; <i>q </i>= 0.045).</p><p><strong>Conclusion: </strong>Genetic markers of increased risk of community-acquired pneumonia in influenza include the presence of the T allele in <i>IFNL4</i> gene (rs12979860 C/T) and, to a lesser extent, the G allele in <i>IFNL3</i> gene (rs8099917 T/G). Patients carrying these alleles have an increased risk of developing pneumonia, especially in old age.</p>","PeriodicalId":23669,"journal":{"name":"Voprosy virusologii","volume":"70 1","pages":"25-34"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Analysis of the association of influenza clinical course with single nucleotide polymorphisms in genes affecting the interferon-λ3 production.\",\"authors\":\"L I Nikolaeva, M D Stuchinskaya, K P Telepenina, N G Shevchenko, V V Kuprianov, K G Krasnoslobodtsev, E A Mukasheva, S V Trushakova, I N Khlopova, I S Kruzhkova, L B Kisteneva, L V Kolobukhina, E I Burtseva\",\"doi\":\"10.36233/0507-4088-271\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Predisposition to different courses of the infectious process is largely associated with the polymorphisms in human genome, especially in genes encoding proteins of the immune system. In the early stages of influenza infection such components of innate immunity as interferons I (α/β) and III (λ) type play a significant role in limiting virus replication. The aim of the work was to investigate associations of single nucleotide polymorphism in <i>IFNL3</i> (rs8099917 T/G) and <i>IFNL4</i> (rs12979860 C/T) genes with different course of influenza, and identify genetic markers of influenza complicated by community-acquired pneumonia. The genes noted above affect the production of interferon-λ3, which is involved in restriction of the viral replication.</p><p><strong>Materials and methods: </strong>Samples from 456 patients with mild (<i>n </i>= 150), moderate (<i>n </i>= 173), and severe (<i>n </i>= 133) influenza were studied. The viral RNA was detected by reverse transcription and polymerase chain reaction (RT-PCR). Polymorphisms in <i>IFNL3</i> (rs8099917 T/G) and <i>IFNL4</i> (rs12979860 C/T) genes was detected by PCR. Statistical analysis was performed using SNPStats software.</p><p><strong>Results: </strong>Patients with the C/T or T/T genotype of <i>IFNL4</i> gene (rs12979860 C/T) were more likely to have pneumonia than those with the C/C genotype (OR 2.47 (1.31-4.63); <i>p </i>= 0.0044; <i>q</i> = 0.0059). The presence of one T allele increased the risk of developing pneumonia (OR 2.02 (1.05-4.02); <i>p </i>= 0.006; <i>q</i> = 0.008). In the presence of the T/T genotype, the risk increased more than twofold: OR 2.14 (1.31-3.48). Analysis of the SNP of <i>IFNL3</i> gene (rs8099917 T/G) revealed a weak association of the G allele with pneumonia (OR 1.86 (1.04-3.31); <i>p</i> = 0.03; <i>q </i>= 0.045).</p><p><strong>Conclusion: </strong>Genetic markers of increased risk of community-acquired pneumonia in influenza include the presence of the T allele in <i>IFNL4</i> gene (rs12979860 C/T) and, to a lesser extent, the G allele in <i>IFNL3</i> gene (rs8099917 T/G). Patients carrying these alleles have an increased risk of developing pneumonia, especially in old age.</p>\",\"PeriodicalId\":23669,\"journal\":{\"name\":\"Voprosy virusologii\",\"volume\":\"70 1\",\"pages\":\"25-34\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-03-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Voprosy virusologii\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.36233/0507-4088-271\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Voprosy virusologii","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.36233/0507-4088-271","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
Analysis of the association of influenza clinical course with single nucleotide polymorphisms in genes affecting the interferon-λ3 production.
Introduction: Predisposition to different courses of the infectious process is largely associated with the polymorphisms in human genome, especially in genes encoding proteins of the immune system. In the early stages of influenza infection such components of innate immunity as interferons I (α/β) and III (λ) type play a significant role in limiting virus replication. The aim of the work was to investigate associations of single nucleotide polymorphism in IFNL3 (rs8099917 T/G) and IFNL4 (rs12979860 C/T) genes with different course of influenza, and identify genetic markers of influenza complicated by community-acquired pneumonia. The genes noted above affect the production of interferon-λ3, which is involved in restriction of the viral replication.
Materials and methods: Samples from 456 patients with mild (n = 150), moderate (n = 173), and severe (n = 133) influenza were studied. The viral RNA was detected by reverse transcription and polymerase chain reaction (RT-PCR). Polymorphisms in IFNL3 (rs8099917 T/G) and IFNL4 (rs12979860 C/T) genes was detected by PCR. Statistical analysis was performed using SNPStats software.
Results: Patients with the C/T or T/T genotype of IFNL4 gene (rs12979860 C/T) were more likely to have pneumonia than those with the C/C genotype (OR 2.47 (1.31-4.63); p = 0.0044; q = 0.0059). The presence of one T allele increased the risk of developing pneumonia (OR 2.02 (1.05-4.02); p = 0.006; q = 0.008). In the presence of the T/T genotype, the risk increased more than twofold: OR 2.14 (1.31-3.48). Analysis of the SNP of IFNL3 gene (rs8099917 T/G) revealed a weak association of the G allele with pneumonia (OR 1.86 (1.04-3.31); p = 0.03; q = 0.045).
Conclusion: Genetic markers of increased risk of community-acquired pneumonia in influenza include the presence of the T allele in IFNL4 gene (rs12979860 C/T) and, to a lesser extent, the G allele in IFNL3 gene (rs8099917 T/G). Patients carrying these alleles have an increased risk of developing pneumonia, especially in old age.
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The journal deals with advances in virology in Russia and abroad. It publishes papers dealing with investigations of viral diseases of man, animals and plants, the results of experimental research on different problems of general and special virology. The journal publishes materials are which promote introduction into practice of the achievements of the virological science in the eradication and incidence reduction of infectious diseases, as well as their diagnosis, treatment and prevention. The reader will find a description of new methods of investigation, new apparatus and devices.
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