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Regulation of Gammaherpesviral Late Gene Expression

γ疱疹病毒晚期基因表达的调控

基本信息

批准号：
9178643
负责人：
Britt A Glaunsinger
金额：
$ 37.03万
依托单位：
UNIVERSITY OF CALIFORNIA BERKELEY
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-11-13 至 2020-10-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9178643
关键词：
Acquired Immunodeficiency Syndrome Affinity Antiviral Agents Architecture Binding Biology Cancer Etiology Cells Cercopithecine Herpesvirus 1 Code Complex Congenital Disorders Cryoelectron Microscopy DNA DNA Polymerase II DNA Viruses DNA biosynthesis DNA-Directed RNA Polymerase Data Disease Double Stranded DNA Virus Electron Microscopy Eukaryota Eukaryotic Cell Gene Expression Genes Genetic Transcription Grant Herpesviridae Herpesviridae Infections Human Human Herpesvirus 8 Hybrids Imagery Immunocompromised Host Impairment Individual Infection Late Gene Transcriptions Late Promoters Life Life Cycle Stages Light Link Malignant Neoplasms Modeling Molecular Mimicry Mutation Negative Staining Patients Polymerase Population Process Proteins Recruitment Activity Regulation Reporting Role TATA-Box Binding Protein Transcription Coactivator Transcriptional Regulation Viral Viral Genes Viral Genome Viral Proteins Virion Virus Virus Assembly Virus Replication Visual base defined contribution experimental study gammaherpesvirus high throughput screening mammalian genome member mimicry mutant novel novel virus particle pathogen promoter protein protein interaction public health relevance transcription factor

项目摘要

DESCRIPTION (provided by applicant): Herpesviruses are endemic within the human population, and cause a wide range of life-threatening diseases. Members of the beta-herpesvirus (β-HV) and gamma-herpesvirus (γ-HV) subfamilies are extremely problematic in immunocompromised individuals, leading to severe congenital disorders and a variety of cancers. During the herpesviral replication cycle, viral genes are expressed temporally in an ordered cascade, with timing linked to appropriate life cycle stage needs. Following viral genome replication, a group of viral genes termed late genes (L) are robustly activated and produce proteins necessary for progeny virion assembly and egress. Mechanisms governing L gene expression in the β-HV and the γ-HV largely remain a mystery. However, shedding light on this aspect of herpesviral biology has become a high priority, in part due to recent discoveries demonstrating that mutants impaired in this final viral transcription cascade cannot produce progeny virions. An understanding of the regulatory features critical for L gene transcription may therefore reveal robust new targets for antiviral strategies. Our data demonstrate that late gene transcriptional regulation is unique, as it incorporates both molecular mimicry and selective recruitment of key host transcriptional machinery in a manner not previously observed in viral or host gene expression. Thus, the focus of this grant is to define the composition and regulation of this novel gene expression complex, as well as reveal how it may globally impact gene expression in infected cells.