Analysis of Programmed Cell Death-1 (PD-1) Gene Variations (re11568821 and rs41386349) in HTLV-1 Infection Using One Primer Pair and Proviral Load.

IF 2.1 3区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Molecular Evolution Pub Date : 2023-08-01 DOI:10.1007/s00239-023-10104-5

Yalda Amiri Hezave, Zohreh Sharifi, Fahime Ranjbar Kermani

{"title":"Analysis of Programmed Cell Death-1 (PD-1) Gene Variations (re11568821 and rs41386349) in HTLV-1 Infection Using One Primer Pair and Proviral Load.","authors":"Yalda Amiri Hezave, Zohreh Sharifi, Fahime Ranjbar Kermani","doi":"10.1007/s00239-023-10104-5","DOIUrl":null,"url":null,"abstract":"<p><p>About 90% of people infected with Human T lymphotropic virus type-1 (HTLV-1) virus are asymptomatic, so it can be said that the prevalence of this virus is not completely clear. During chronic infection, the expression of programmed cell death-1 (PD-1) protein increases and causes exhausted phenotype in T cells. Considering the role of host genetics and immune responses in HTLV-1 infection, in this case-control study, included 81 asymptomatic carriers (ACs) and 162 healthy controls (HCs), rs11568821 and rs41386349 polymorphisms of PD-1 gene were evaluated by Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method which investigated by one primer pair for both polymorphisms also, proviral load (PVL) measured by quantitative real-time PCR (Q-RT-PCR). The results showed that the mutant allele of rs11568821 (A) and rs41386349 (T) polymorphisms is associated with an increase in HTLV-1 infection significantly (p = 0.019 and p = 0.000 respectively). But there was no significant relationship between PVL and polymorphisms.</p>","PeriodicalId":16366,"journal":{"name":"Journal of Molecular Evolution","volume":null,"pages":null},"PeriodicalIF":2.1000,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Molecular Evolution","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s00239-023-10104-5","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

About 90% of people infected with Human T lymphotropic virus type-1 (HTLV-1) virus are asymptomatic, so it can be said that the prevalence of this virus is not completely clear. During chronic infection, the expression of programmed cell death-1 (PD-1) protein increases and causes exhausted phenotype in T cells. Considering the role of host genetics and immune responses in HTLV-1 infection, in this case-control study, included 81 asymptomatic carriers (ACs) and 162 healthy controls (HCs), rs11568821 and rs41386349 polymorphisms of PD-1 gene were evaluated by Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method which investigated by one primer pair for both polymorphisms also, proviral load (PVL) measured by quantitative real-time PCR (Q-RT-PCR). The results showed that the mutant allele of rs11568821 (A) and rs41386349 (T) polymorphisms is associated with an increase in HTLV-1 infection significantly (p = 0.019 and p = 0.000 respectively). But there was no significant relationship between PVL and polymorphisms.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

利用一对引物和前病毒负载分析HTLV-1感染中PD-1基因变异(re11568821和rs41386349)

人类T淋巴细胞嗜型病毒(HTLV-1)感染者约90%无症状，因此可以说这种病毒的流行情况尚不完全清楚。在慢性感染期间，程序性细胞死亡-1 (PD-1)蛋白的表达增加并导致T细胞衰竭表型。考虑到宿主遗传和免疫应答在HTLV-1感染中的作用，本研究选取81例无症状携带者(ACs)和162例健康对照(hc)，采用聚合酶链反应-限制性片段长度多态性(PCR- rflp)方法对PD-1基因rs11568821和rs41386349的多态性进行了检测，并采用实时荧光定量PCR (Q-RT-PCR)技术测定了PD-1基因的前病毒载量(PVL)。结果显示，rs11568821 (A)和rs41386349 (T)突变等位基因多态性与HTLV-1感染增加显著相关(p = 0.019和p = 0.000)。但PVL与多态性之间无显著相关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Journal of Molecular Evolution 生物-进化生物学

CiteScore

5.50

自引率

2.60%

发文量

审稿时长

3 months

期刊介绍： Journal of Molecular Evolution covers experimental, computational, and theoretical work aimed at deciphering features of molecular evolution and the processes bearing on these features, from the initial formation of macromolecular systems through their evolution at the molecular level, the co-evolution of their functions in cellular and organismal systems, and their influence on organismal adaptation, speciation, and ecology. Topics addressed include the evolution of informational macromolecules and their relation to more complex levels of biological organization, including populations and taxa, as well as the molecular basis for the evolution of ecological interactions of species and the use of molecular data to infer fundamental processes in evolutionary ecology. This coverage accommodates such subfields as new genome sequences, comparative structural and functional genomics, population genetics, the molecular evolution of development, the evolution of gene regulation and gene interaction networks, and in vitro evolution of DNA and RNA, molecular evolutionary ecology, and the development of methods and theory that enable molecular evolutionary inference, including but not limited to, phylogenetic methods.