Antiviral host defense through selective translational inhibition

通过选择性翻译抑制进行抗病毒宿主防御

基本信息

批准号：
8473888
负责人：
MICHAEL DAVID
金额：
$ 28.42万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN DIEGO
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-06-01 至 2016-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8473888
关键词：
AIDS/HIV problem ATP phosphohydrolase Affect Alternative Splicing Anti-Retroviral Agents Antigens Antiviral Agents Antiviral Response Area Attenuated Binding Biogenesis Biological Process Caenorhabditis elegans Cells Charge Codon Nucleotides Communicable Diseases DNA Development Diagnostic Disease Dominant-Negative Mutation Drosophila genus ERG gene Employee Strikes Event Family Generations Genes Genetic Transcription Goals HIV HIV Infections Homologous Gene Host Defense Human IRF3 gene Immune response Infection Infection prevention Influenza Interferon-alpha Interferon-beta Interferons Kinetics Length Light Location Mediating Messenger RNA Molecular Molecular Mechanisms of Action Multi-Drug Resistance Mus N-terminal Nucleic Acid Binding Organism Pathway interactions Pharmaceutical Preparations Positioning Attribute Poxviridae Process Production Protein Binding Protein Biosynthesis Protein Inhibition Protein Isoforms Protein Synthesis Inhibition Proteins RNA Helicase Reporting Retroviridae Reverse Transcription Role Shapes Specificity Staging System Testing Therapeutic Therapeutic Intervention Transfer RNA Translational Repression Viral Viral Proteins Virus Yeasts base member microbial novel pathogen preference prognostic prospective protein expression protein function tool viral RNA

AIDS/HIV problem ATP phosphohydrolase Affect Alternative Splicing Anti-Retroviral Agents Antigens Antiviral Agents Antiviral Response Area Attenuated Binding Biogenesis Biological Process Caenorhabditis elegans Cells Charge Codon Nucleotides Communicable Diseases DNA Development Diagnostic Disease Dominant-Negative Mutation Drosophila genus ERG gene Employee Strikes Event Family Generations Genes Genetic Transcription Goals HIV HIV Infections Homologous Gene Host Defense Human IRF3 gene Immune response Infection Infection prevention Influenza Interferon-alpha Interferon-beta Interferons Kinetics Length Light Location Mediating Messenger RNA Molecular Molecular Mechanisms of Action Multi-Drug Resistance Mus N-terminal Nucleic Acid Binding Organism Pathway interactions Pharmaceutical Preparations Positioning Attribute Poxviridae Process Production Protein Binding Protein Biosynthesis Protein Inhibition Protein Isoforms Protein Synthesis Inhibition Proteins RNA Helicase Reporting Retroviridae Reverse Transcription Role Shapes Specificity Staging System Testing Therapeutic Therapeutic Intervention Transfer RNA Translational Repression Viral Viral Proteins Virus Yeasts base member microbial novel pathogen preference prognostic prospective protein expression protein function tool viral RNA

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项目摘要

DESCRIPTION (provided by applicant): HIV continues to be one of the most prevalent infectious diseases in this world. Our discovery of a novel cellular factor that inhibits the production of HIV by infected cells provides a new target for the development of a novel class of anti-viral drugs and may additionally carry diagnostic and prognostic value. Furthermore, based on the molecular basis of the antiviral activity we hypothesize that other viruses such as Influenza will also be subject to inhibition by huSlfn11.

描述（由申请人提供）：HIV仍然是这个世界上最普遍的传染病之一。我们发现了一种新型细胞因子，该细胞因子抑制受感染细胞的HIV产生，为开发新型的抗病毒药物的发展提供了一个新的靶标，并可能还具有诊断和预后价值。此外，基于抗病毒活性的分子基础，我们假设其他病毒（例如流感病毒）也将受到HUSLFN11的抑制作用。