THE ROLE OF CYTOMEGALOVIRUS PHOSPHOPROTEIN 65 IN VIRUS REPLICATON IN VIVO

巨细胞病毒磷酸蛋白65在体内病毒复制中的作用

基本信息

项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The cytomegalovirus (CMV) protein pp65 modulates the host immune response. At the same time it is also the primary antiviral target of cellular immune responses. pp65 is the most abundant component of the Rhesus CMV (RhCMV) and human CMV (HCMV) tegument, a protein-rich layer between the capsid and the envelope that is released into the cytoplasm. Interestingly, pp65 is not required for in vitro growth of either virus. This allowed us to generate a pp65-deficient RhCMV to examine whether 1) The protein's immunomodulatory functions are critical for virus survival in vivo; or 2) The demonstrated immunogenicity of pp65 limits virus replication in the presence of functional immunity. Infection of rhesus macaques (RMs) with mutant RhCMV will allow examination of the importance of pp65 for CMV infection in vivo. Therefore we will infect CMV-na¿ve RM with a pp65-deleted recombinant virus and evaluate whether this virus is able to establish primary and chronic infection and, if so, how virological and immunological parameters compare to previous observations made during infection with wild type RhCMV. Depending on the outcome of this experiment, we will then evaluate whether pp65-deleted virus is able to re-infect these animals. If pp65-encoded functions are required for productive in vivo infection, we expect replication of the deletion virus to be either undetectable or less robust than that measured for wild type RhCMV. Conversely, if the pp65 immunogenicity is crucial to the ability of the host immune response to control virus infection we predict that replication of the pp65-deleted virus will be greater than that for wild type RhCMV. The outcome of these experiments has implications both for the design of CMV vaccines and antiviral treatments as well as the development of CMV as a vaccine vector.
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项目成果

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VICTOR Robert DEFILIPPIS其他文献

VICTOR Robert DEFILIPPIS的其他文献

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{{ truncateString('VICTOR Robert DEFILIPPIS', 18)}}的其他基金

A Self-Adjuvanting Virus Like Particle Vaccine Platform for Emerging Viruses
针对新兴病毒的自我佐剂病毒样颗粒疫苗平台
  • 批准号:
    10711617
  • 财政年份:
    2023
  • 资助金额:
    $ 2.77万
  • 项目类别:
Anti-tumor efficacy of novel cGAS-STING pathway agonists
新型 cGAS-STING 通路激动剂的抗肿瘤功效
  • 批准号:
    10286612
  • 财政年份:
    2021
  • 资助金额:
    $ 2.77万
  • 项目类别:
Anti-tumor efficacy of novel cGAS-STING pathway agonists
新型 cGAS-STING 通路激动剂的抗肿瘤功效
  • 批准号:
    10430274
  • 财政年份:
    2021
  • 资助金额:
    $ 2.77万
  • 项目类别:
Mechanistic Exploration of cGAS-STING-Mediated Vaccine Enhancement
cGAS-STING 介导的疫苗增强机制探索
  • 批准号:
    10318966
  • 财政年份:
    2019
  • 资助金额:
    $ 2.77万
  • 项目类别:
Mechanistic Exploration of cGAS-STING-Mediated Vaccine Enhancement
cGAS-STING 介导的疫苗增强机制探索
  • 批准号:
    10534676
  • 财政年份:
    2019
  • 资助金额:
    $ 2.77万
  • 项目类别:
THE ROLE OF CYTOMEGALOVIRUS PHOSPHOPROTEIN 65 IN VIRUS REPLICATON IN VIVO
巨细胞病毒磷酸蛋白65在体内病毒复制中的作用
  • 批准号:
    7958465
  • 财政年份:
    2009
  • 资助金额:
    $ 2.77万
  • 项目类别:
THE ROLE OF CYTOMEGALOVIRUS PHOSPHOPROTEIN 65 IN VIRUS REPLICATON IN VIVO
巨细胞病毒磷酸蛋白65在体内病毒复制中的作用
  • 批准号:
    7561989
  • 财政年份:
    2007
  • 资助金额:
    $ 2.77万
  • 项目类别:

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