The Ins and Outs of Viral Infection: Entry, Assembly, Exit and Spread

病毒感染的来龙去脉：进入、组装、退出和传播

基本信息

批准号：
8645272
负责人：
DAVID L. WOODLAND
金额：
$ 0.6万
依托单位：
KEYSTONE SYMPOSIA
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-02-01 至 2015-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8645272
关键词：
Address Adopted Affect Antiviral Agents Apoptosis Area Autophagocytosis Autophagosome Bacteriophages Bioinformatics Biological Assay Capsid Cell Communication Cell fusion Cell physiology Cells Cellular biology Collaborations Colorado Complex Cytolysis Drug resistance Endocytosis Epithelial Cells Generations Genome Gymnastics Human Virus Image Individual Knowledge Learning Life Mathematics Mediating Methodology Methods Molecular Multivesicular Body Outcome Pathway interactions Pharmaceutical Preparations Postdoctoral Fellow Process Research Research Personnel Schools Scientist Structural Biologist Structural Protein Structure Students Tight Junctions Tissues Training Translations Travel Viral Viral Pathogenesis Virus Virus Diseases Virus Receptors clinical practice deep sequencing drug resistant virus innovation interdisciplinary approach interest meetings novel programs public health relevance structural biology symposium virology

项目摘要

DESCRIPTION (provided by applicant): Support is requested for a Keystone Symposia meeting entitled The Ins and Outs of Viral Infection: Entry, Assembly, Exit and Spread, organized by Karla Kirkegaard, Mavis Agbandje-McKenna and Eric O. Freed. The meeting will be held in Breckenridge, Colorado from March 30 - April 4, 2014. Viruses can enter cells by mechanisms such as the classic virus-receptor interactions, cell-cell fusion and newly observed pathways that are currently being investigated. Similarly, viral exit from infected cells can follo the paradigms of cell lysis or viral budding, but new mechanisms such as unconventional secretion and exosome formation are emerging. Viruses in the process of entering or exiting cells should be especially vulnerable to antivirals because of their accessibility and because the formation of oligomeric structures that mix drug-susceptible and drug-resistant capsids can suppress the emergence of drug-resistant viruses. However, these steps are more difficult to target biochemically due to the lack of readily assayed enzymatic activity. This meeting will bring together structural biologists, geneticists, cell biologists and mathematic modelers to address the mechanisms and consequences of the different modes of viral travel. Thus, the program for this meeting is highly likely to attract a wide variety of investigators, many of whom might not otherwise interact.

描述（由申请人提供）：请求支持由 Karla Kirkegaard、Mavis Agbandje-McKenna 和 Eric O. Freed 组织的题为“病毒感染的来龙去脉：进入、装配、退出和传播”的 Keystone 研讨会。会议将于2014年3月30日至4月4日在科罗拉多州布雷肯里奇举行。病毒可以通过经典的病毒-受体相互作用、细胞-细胞融合以及目前正在研究的新观察到的途径等机制进入细胞。类似地，病毒从受感染细胞中排出可以遵循细胞裂解或病毒出芽的模式，但诸如非常规分泌和外泌体形成等新机制正在出现。病毒在进入或离开细胞的过程中应该特别容易受到抗病毒药物的影响，因为它们易于接近，而且混合药物敏感和耐药衣壳的寡聚结构的形成可以抑制耐药病毒的出现。然而，由于缺乏易于测定的酶活性，这些步骤更难以以生化方式靶向。本次会议将带来结构生物学家、遗传学家、细胞生物学家和数学建模师共同研究不同病毒传播模式的机制和后果。因此，这次会议的计划很可能会吸引各种各样的调查人员，其中许多人可能不会进行互动。