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Elucidating mechanisms of interferon gamma that protect against Ebola virus infection

阐明干扰素γ预防埃博拉病毒感染的机制

基本信息

批准号：
10696250
负责人：
Wendy Jean Maury
金额：
$ 19.31万
依托单位：
UNIVERSITY OF IOWA
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-09-02 至 2024-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10696250
关键词：
Animal Model Antiviral Agents B-Lymphocytes CD8-Positive T-Lymphocytes Cells Cellular Immunity Clinical Research Developing Countries Development Disease Disease Outbreaks Dose Ebola Hemorrhagic Fever Ebola virus Epidemic FDA approved Family Filoviridae Infections Filovirus Frequencies Future Genes Goals Hour IFNGR1 gene Immune Immune response Immunity Immunologics In Vitro Infection Infection Control Innate Immune Response Innate Immune System Interferon Type I Interferon Type II Interferons Investigation Knowledge Macrophage Mediating Mus Natural Immunity Pathogenesis Pathogenicity Pathway interactions Peritoneal Peritoneal Macrophages Peritoneum Pharmaceutical Preparations Phenotype Population Production Property Role Series Severities T-Lymphocyte Testing Therapeutic Tissues Vaccines Viral Viral Pathogenesis Viral Proteins Viral load measurement Viremia Virus Virus Diseases Virus Replication Zaire Ebola virus adaptive immune response cellular targeting combat conditional knockout cost effective effective therapy in vivo insight mouse model pathogenic virus peripheral blood prevent recruit response side effect treatment response

项目摘要

Abstract Filovirus outbreaks/epidemics occur sporadically, but with increasing frequency and intensity. With no current approved filovirus therapeutics, the recent Ebola virus (EBOV) outbreaks emphasize the need for effective treatments against this highly pathogenic family of viruses. A better mechanistic understanding of effective early immune responses to EBOV will identify potential immunological approaches for controlling this infection and associated disease. Interferon gamma (IFN-γ) elicits production of antiviral proteins that control of virus replication and stimulates and activates cellular immune responses. In a series of recent studies, we demonstrated that IFN-γ profoundly inhibits EBOV infection of macrophages, an important early cellular target for the virus. We also showed that IFN-γ protects mice from EBOV challenge when mice were treated 24 hours prior to or after infection. These findings provide evidence that the immune responses elicited following IFN-γ stimulation effectively control EBOV infection and disease. Here, we will explore the contribution of both innate and cellular immunity to IFN-γ- mediated protection. In total, studies proposed here will provide critical mechanistic insights into the efficacy of this immune pathway to control filovirus infections.

摘要