INHIBITION OF IRF7-MEDIATED INTERFERON SIGNAL TRANSDUCTION BY KSHV VIRF3

KSHV VIRF3 对 IRF7 介导的干扰素信号转导的抑制

• 批准号: 7715515
• 负责人: CHUL HYUN JOO
• 金额: $ 3.24万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-06-05 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715515
• 关键词: Acquired Immunodeficiency Syndrome; Computer Retrieval of Information on Scientific Projects Database; DNA Binding; DNA Binding Domain; Funding; Grant; Herpesviridae; Homologous Gene; Human; Human Herpesvirus 8; Immune; Immune response; Immune system; Immunity; Institution; Interferon Activation; Interferons; Life Cycle Stages; Mediating; Natural Immunity; Pathway interactions; Production; Reporting; Research; Research Personnel; Resources; Signal Transduction; Simplexvirus; Source; United States National Institutes of Health; Viral; Viral Physiology; Virus; Virus Diseases; novel; response; tumor; viral interferon regulatory factor-3

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. Upon viral infection, the major defense mounted by the host immune system is activation of the interferon (IFN)-mediated anti-viral pathway that is mediated by interferon regulatory factors (IRFs). In order to complete their life cycle, viruses must modulate host IFN-mediated immune response. Kaposi's sarcoma-associated herpesvirus (KSHV), a human tumor-inducing herpesvirus, has developed a unique mechanism for antagonizing cellular IFN-mediated anti-viral activity by incorporating viral homologs of the cellular IRFs, called vIRFs. Here, we report a novel immune evasion mechanism of KSHV vIRF3 to block cellular IRF7-mediated innate immunity in response to viral infection. KSHV vIRF3 specifically interacts with either the DNA binding domain or the central IRF association domain of IRF7 and this interaction leads to the inhibition of IRF7 DNA binding activity, thereof suppression of IFNalpha production and IFN-mediated immunity. AIDS related.

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