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:
- 金额:$ 0.6万
- 依托单位:
- 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:
- 关键词:AddressAdoptedAffectAntiviral AgentsApoptosisAreaAutophagocytosisAutophagosomeBacteriophagesBioinformaticsBiological AssayCapsidCell CommunicationCell fusionCell physiologyCellsCellular biologyCollaborationsColoradoComplexCytolysisDrug resistanceEndocytosisEpithelial CellsGenerationsGenomeGymnasticsHuman VirusImageIndividualKnowledgeLearningLifeMathematicsMediatingMethodologyMethodsMolecularMultivesicular BodyOutcomePathway interactionsPharmaceutical PreparationsPostdoctoral FellowProcessResearchResearch PersonnelSchoolsScientistStructural BiologistStructural ProteinStructureStudentsTight JunctionsTissuesTrainingTranslationsTravelViralViral PathogenesisVirusVirus DiseasesVirus Receptorsclinical practicedeep sequencingdrug resistant virusinnovationinterdisciplinary approachinterestmeetingsnovelprogramspublic health relevancestructural biologysymposiumvirology
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Keystone研讨会会议,标题为“病毒感染的Ins and Off:入境,组装,退出和扩散,由Karla Kirkegaard,Mavis Agbandje-McKenna和Eric O. Freed组织。该会议将于2014年3月30日至4月4日在科罗拉多州的布雷肯里奇举行。病毒可以通过诸如经典病毒 - 受体相互作用,细胞融合和当前正在研究的新观察的途径等机制进入细胞。同样,受感染细胞的病毒退出可以引起细胞裂解或病毒萌芽的范式,但是新机制(例如非常规分泌和外泌体形成)正在出现。在进入或退出细胞的过程中,病毒由于其可及性而尤其容易受到抗病毒药的影响,并且因为将药物敏感和耐药的衣壳混合在一起的寡聚结构的形成可以抑制耐药病毒的出现。但是,由于缺乏容易测定的酶促活性,这些步骤更难在生物化学上靶向。这次会议将带来
结构生物学家,遗传学家,细胞生物学家和数学建模者共同解决了病毒旅行模式的机制和后果。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互动。
项目成果
期刊论文数量(0)
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科研奖励数量(0)
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DAVID L. WOODLAND其他文献
DAVID L. WOODLAND的其他文献
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