清道夫受体 gp340 在粘膜 HIV-1 传播和抑制中的作用-猫眼课题宝

清道夫受体 gp340 在粘膜 HIV-1 传播和抑制中的作用

批准号：

8743609

负责人：

Min Lu

金额：

$49.23万

依托单位：

RBHS-NEW JERSEY MEDICAL SCHOOL

依托单位国家：

美国

项目类别：

财政年份：

2014

资助国家：

美国

项目状态：

已结题

起止时间：

2014-01-23 至 2016-01-22

来源：

https://reporter.nih.gov/project-details/8743609

关键词：

Acquired Immunodeficiency Syndrome Address Administrative Supplement Affinity Antiviral Agents Binding Binding Sites Biological Assay CCR5 gene CD209 gene CD4 Positive T Lymphocytes Cell Line Cell fusion Cell surface Cell-Matrix Junction Cells Cervical Chinese Hamster Ovary Cell Collaborations Competence Complement Complex Dentistry Development Disease Effectiveness Epithelial Epithelium Failure Female Funding Genital system Glycoproteins Goals Grant HIV Envelope Protein gp120 HIV-1 Human Hurricane Immunoglobulin Variable Region In Vitro Infection Inhibitory Concentration 50 Intervention Investigation Knowledge Lead Membrane Fusion Modeling Molecular Molecular Target Molecular Virology Multi-Drug Resistance Mus Mutation New Jersey New York North Carolina Oral Oryctolagus cuniculus Peptides Pharmaceutical Preparations Prevalence Process Production Property Proteins Reagent Receptor Cell Recombinants Research Research Project Grants Role SRCR proteins Saliva Specificity Structure Surface T-Lymphocyte Testing Tissues Toxic effect Universities Vagina Variant Viral Virus base biophysical chemistry biophysical techniques college combat cost design disulfide bond env Glycoproteins in vitro Model in vivo inhibitor/antagonist insight macrophage medical schools neutralizing antibody neutralizing monoclonal antibodies novel parent grant polyclonal antibody prevent programs receptor binding reproductive research study scavenger receptor structural biology syndecan synthetic peptide transcytosis transmission process vaginal transmission virucide

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中文摘要

翻译

本授权R01 AI094599行政补充中概述的研究涉及一个正在进行的

英文摘要

The research outlined in this Administrative Supplement to Grant R01 AI094599 involves an ongoing collaboration between Min Lu (Rutgers New Jersey Medical School) and Daniel Malamud (New York University College of Dentistry). Due to power failure during Hurricane Sandy, we lost all stable Chinese hamster ovary (CHO) cell lines expressing SRCR1 module fragments of the human scavenger receptor gp340, polyclonal antibodies raised in rabbits against a synthetic peptide derived from the SRCR1 module, and gp340 peptide and protein entry inhibitors. The supplemental funds are requested to reproduce these critical and proprietary research materials and reagents and to define the molecular target and mechanism of action of soluble gp340- based anti-HIV-1 agents. These studies could lead to discovery of novel entry inhibitors that target early infection to prevent mucosal HIV-1 transmission. Experiment 1: To generate stable CHO cell lines for high-level production of secreted SRCR1 module fragments. Experiment 2: To characterize the structural properties of the SRCR1 domain both free and bound to the V3 region of HIV-1 gp120. Our overall goal is to elucidate how HIV-1 envelope glycoprotein function in cell entry is modulated through the gp340-gp120 interaction; to use this knowledge to optimize SRCR1 entry inhibitors for antiviral potency; and to test these hypotheses in a humanized mouse vaginal transmission model, in collaboration with Dr. J. Victor Garcia-Martinez (University of North Carolina School of Medicine) in years 4 and 5. To achieve this goal, we will express and purify large quantities of recombinant gp340 fragments in CHO cells, and carry out a combined structural and physicochemical investigation of the SRCR1 domain in complex with the V3 region. These experiments will enable us to develop optimized SRCR1 entry inhibitors for evaluating their effectiveness to protect against mucosal HIV-1 infection in vivo. Fulfilling the central objective of the parent grant would not be possible without the with-cost extension of support that would significantly mitigate the impact of Sandy on this research project.

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