KSHV Epigenetic Regulation

KSHV 表观遗传调控

基本信息

批准号：
10312714
负责人：
Jae U Jung
金额：
$ 43.12万
依托单位：
CLEVELAND CLINIC LERNER COM-CWRU
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-15 至 2024-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10312714
关键词：
3-Dimensional ATAC-seq Adopted Affect Auxins Bioinformatics Blood Cell Culture Techniques Cells ChIP-seq Chromatin Chromatin Conformation Capture and Sequencing Chromatin Loop Chromatin Structure Complication Development Endothelial Cells Epigenetic Process Epithelial Epithelial Cells Etiology Euchromatin Gene Expression Gene Expression Profile Genes Genetic Genetic Transcription Genomics Goals Grant HIV Infections Heterochromatin Histones Human Herpesvirus 8 Infection Integration Host Factors Kaposi Sarcoma Lead Lesion Lytic Malignant lymphoid neoplasm Mediating Modeling Mutation Oral Palate Kaposi&apos s Sarcoma Pattern Play Promoter Regions Regulation Role Route Saliva Seminal fluid Site Structure Technology Testing Tissue Model Viral Viral Genes Virus Replication base cell type chromosome conformation capture epigenetic regulation epigenome epigenomics global run on sequencing histone modification in vivo insight latent infection lytic gene expression lytic replication mutant next generation sequencing oral cavity epithelium oral infection oral lesion oral status oral tissue particle programs single-cell RNA sequencing three dimensional cell culture three-dimensional modeling transcription factor transcriptomics transmission process viral genomics

项目摘要

Project Summary/Abstract While KSHV can be detected in blood and occasionally in semen, it is frequently secreted in saliva which is believed to be the main route of spread. Nearly 25 years after the identification of KSHV, however, the initial steps in KSHV oral infection and the expressions of host and KSHV genes are still poorly understood. Our main question is: while KSHV establishes latency in most cells and KS lesions by default, why does it lead to spontaneous lytic replication in oral epithelial cells and oral lesions? Our hypothesis is: this difference is due to the differences of viral epigenetics and genomics. As the previous grant has been primarily focused on the epigenetic regulation of KSHV, the current study will characterize the high-order genomic organization of KSHV and investigate the transcriptomic and epigenomic regulations of KSHV at the single cell level using 3D organotypic oral tissue infection model that closely resembles in vivo oral transmission.

项目概要/摘要虽然 KSHV 可以在血液中检测到，偶尔在精液中检测到，但它经常分泌于唾液被认为是主要传播途径。在确认身份后近 25 年然而，KSHV 口腔感染的初始步骤以及宿主和 KSHV 基因的表达仍然知之甚少。我们的主要问题是：虽然 KSHV 在大多数单元中建立了延迟，并且默认为KS病变，为何会导致口腔上皮细胞和口腔黏膜自发裂解复制病变？我们的假设是：这种差异是由于病毒表观遗传学和基因组学。由于之前的资助主要集中在 KSHV 的表观遗传调控上，目前的研究将表征 KSHV 的高阶基因组组织并调查使用 3D 器官型口腔在单细胞水平上对 KSHV 进行转录组和表观基因组调控与体内口腔传播非常相似的组织感染模型。