Insilico Analysis of Codon 131 Polymorphism in FcγRIIA Gene and it is Association with Clinical Symptoms Persistence of Dengue Patients

E. Nugraheni, D. Ramadhani, M. Sariyanti, Ety Febrianti
{"title":"Insilico Analysis of Codon 131 Polymorphism in FcγRIIA Gene and it is Association with Clinical Symptoms Persistence of Dengue Patients","authors":"E. Nugraheni, D. Ramadhani, M. Sariyanti, Ety Febrianti","doi":"10.14710/dmj.v10i6.31010","DOIUrl":null,"url":null,"abstract":"Background. Dengue Hemorrhagic Fever (DHF) is infection caused by Dengue Virus. Failure of vascularization is a main symptom of Dengue Hemorrhagic Fever inducing mediator secretion by an immune cell. FcgRIIA  and CCL2 have a significant role in dengue pathogenesis and possibility in having a chance to cause dengue with a worse manifestation. Objective. Analysis of bio-informatic structure, function and expression of FcgRIIA  gene. Methods. Insilico analysis used NCBI database to find position and sequences. Analysis mutant use SNO and OMIM. Protein prediction withUniprot.  Result. FcgRIIA   human with access number of NM_001136219 by a length of 2429 bp has its full name as Fc Fragment of IgG receptor IIa, located in 1q23.3 chromosom. analyzed mutation was rs1801274 with type of missense protein residue function experiencing a change from Histidin (H) turning into Arginin (R) with allele of wild-type A and becoming G amino acid position of 166. there was structural difference of FcgRIIA   gene in wild type and mutant. Conclusion. Gene FcγRIIA  is a play a role of pathogenesis of dengue infection. Mutation in FcγRIIA  have polymorfisme at Dengue Hemorrage Fever","PeriodicalId":394284,"journal":{"name":"DIPONEGORO MEDICAL JOURNAL (JURNAL KEDOKTERAN DIPONEGORO)","volume":"12 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2021-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DIPONEGORO MEDICAL JOURNAL (JURNAL KEDOKTERAN DIPONEGORO)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14710/dmj.v10i6.31010","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Background. Dengue Hemorrhagic Fever (DHF) is infection caused by Dengue Virus. Failure of vascularization is a main symptom of Dengue Hemorrhagic Fever inducing mediator secretion by an immune cell. FcgRIIA  and CCL2 have a significant role in dengue pathogenesis and possibility in having a chance to cause dengue with a worse manifestation. Objective. Analysis of bio-informatic structure, function and expression of FcgRIIA  gene. Methods. Insilico analysis used NCBI database to find position and sequences. Analysis mutant use SNO and OMIM. Protein prediction withUniprot.  Result. FcgRIIA   human with access number of NM_001136219 by a length of 2429 bp has its full name as Fc Fragment of IgG receptor IIa, located in 1q23.3 chromosom. analyzed mutation was rs1801274 with type of missense protein residue function experiencing a change from Histidin (H) turning into Arginin (R) with allele of wild-type A and becoming G amino acid position of 166. there was structural difference of FcgRIIA   gene in wild type and mutant. Conclusion. Gene FcγRIIA  is a play a role of pathogenesis of dengue infection. Mutation in FcγRIIA  have polymorfisme at Dengue Hemorrage Fever
FcγRIIA基因密码子131多态性及其与登革热患者临床症状持续相关的计算机分析
背景。登革出血热是由登革病毒引起的感染。血管化失败是登革出血热诱导免疫细胞分泌介质的主要症状。FcgRIIA和CCL2在登革热发病机制中有重要作用,有机会引起表现较差的登革热。目标。FcgRIIA基因的生物信息学结构、功能及表达分析。方法。Insilico分析使用NCBI数据库查找位置和序列。用SNO和OMIM分析突变体。用uniprot预测蛋白质。结果。FcgRIIA人,接入号NM_001136219,全长2429 bp,全称IgG受体IIa Fc片段,位于1q23.3染色体上。所分析的突变为rs1801274,其错义蛋白残基功能由hitidin (H)转变为Arginin (R),其等位基因为野生型a,其G氨基酸位置为166。FcgRIIA基因在野生型和突变型中存在结构差异。结论。fc γ - riia基因在登革热感染的发病机制中起作用。登革出血热时fc - γ - riia突变多态
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 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信