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

描述（由申请人提供）：要求对由Karla Kirkegaard、Mavis Agbandje-McKenna和Eric O.自由了会议将于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-细胞融合和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退出可以遵循细胞裂解或病毒出芽的范例，但新的机制如非常规分泌和外泌体形成正在出现。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攻击，因为它们的可及性，并且因为混合药物敏感和耐药衣壳的寡聚体结构的形成可以抑制耐药病毒的出现。然而，由于缺乏容易测定的酶活性，这些步骤更难以生物化学靶向。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一起解决病毒旅行的不同模式的机制和后果。因此，这次会议的计划很可能吸引各种各样的调查人员，其中许多人可能不会互动。

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.