病毒和HIV的介绍 - David Baltimore P1
本视频由科普中国和生物医学大讲堂出品
David Baltimore (Caltech) Part 1: Introduction to Viruses and HIV
Lecture Overview:
In this set of lectures, I describe the threat facing the world from the human immunodeficiency virus (HIV) and a bold proposal on how we might meet the challenge of eliminating this disease by engineering the immune system.
In part 1, I provide a broad introduction to viruses, describing their basic properties and my own history of studying the replication of RNA viruses which led to the discovery of reverse transcriptase. I also illustrate the distinguishing features of equilibrium viruses (e.g. the common cold) that have adapted to co-exist with their host and non-equilibrium viruses (e.g. HIV) that have recently jumped from another species, are not adapted to the new host, and which can lead to disastrous outcomes (e.g. loss of immune function with potential lethality in the case of HIV).
In part 2, I describe the growing health problem that is facing the world with the spread of HIV and the limitations of current drug therapies and vaccine strategies. We need new ideas for tackling this problem. Here and in the next segment, I describe bold strategies of using gene therapy to conquer HIV, The approach that I describe in this segment involves gene therapy to produce short hairpin RNAs (siRNA) that target the destruction of a critical co-receptor of HIV, which the viruses that needs to infect cells. I discuss initial proof-of-principle experiments that suggest this approach might be feasible and the next steps needed to develop this idea into a real therapy.
In this last segment, I describe another gene therapy strategy for HIV in which we propose to develop antibody-like proteins that can be expressed by a patient's B cells and will target the HIV virus for destruction. To achieve this objective, hematopoietic (blood) stem cells must to be targeted with the gene, which will ultimately develop into B cells that express the therapeutic molecule. The ultimate goal is to produce a life-long supply of anti-HIV neutralizing antibodies. In this lecture, I describe the molecular methods underlying this strategy and a development path from proof-of-principle studies in mouse to safe trials in humans. This project receives funding from the Bill and Melinda Gates Foundation.
Speaker Bio:
After serving as President of the California Institute of Technology for nine years, in 2006 David Baltimore was appointed President Emeritus and the Robert Andrews Millikan Professor of Biology. Born in New York City, he received his B.A. in Chemistry from Swarthmore College in 1960 and a Ph.D. in 1964 from Rockefeller University, where he returned to serve as President from 1990-91 and faculty member until 1994.
For almost 30 years, Baltimore was a faculty member at Massachusetts Institute of Technology. While his early work was on poliovirus, in 1970 he identified the enzyme reverse transcriptase in tumor virus particles, thus providing strong evidence for a process of RNA to DNA conversion, the existence of which had been hypothesized some years earlier. Baltimore and Howard Temin (with Renato Dulbecco, for related research) shared the 1975 Nobel Prize in Physiology or Medicine for their discovery, which provided the key to understanding the life-cycle of HIV. In the following years, he has contributed widely to the understanding of cancer, AIDS and the molecular basis of the immune response. His present research focuses on control of inflammatory and immune responses as well as on the use of gene therapy methods to treat HIV and cancer in a program called "Engineering Immunity".
Baltimore played an important role in creating a consensus on national science policy regarding recombinant DNA research. He served as founding director of the Whitehead Institute for Biomedical Research at MIT from 1982 until 1990. He co-chaired the 1986 National Academy of Sciences committee on a National Strategy for AIDS and was appointed in 1996 to head the National Institutes of Health AIDS Vaccine Research Committee.
In addition to receiving the Nobel Prize, Baltimore's numerous honors include the 1999 National Medal of Science, election to the National Academy of Sciences in 1974, the Royal Society of London, and the French Academy of Sciences. For 2007/8, he is President of the AAAS. He has published more than 600 peer-reviewed articles.
病毒结构的一般原则 - Stephen Harrison P1
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 1: Virus structures: General principles
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
病毒的膜融合 - Stephen Harrison P2
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 2: Viral membrane fusion
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
非包膜病毒如何侵入细胞 - Stephen Harrison P3
本视频由科普中国和生物医学大讲堂出品
Stephen Harrison (Harvard) Part 3: Non-enveloped virus entry
Harrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses are symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins are correctly placed. This arrangement results in symmetrically shaped viruses.
In Part 1, Harrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the molecular mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in Part 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of Part 3. Using rotavirus as a model, Harrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
病毒与宿主细胞表面结合的方式 - Ari Helenius P1
本视频由科普中国和生物医学大讲堂出品
Ari Helenius (ETH Zurich) Part 1: Virus entry
Viruses are extremely simple and small yet they are responsible for many of the worlds diseases. A virus particle consists of only a genome, a protein coat or capsid, and sometimes a surrounding lipid envelope. To replicate, a virus must successfully enter a host cell, uncoat its genome, and appropriate the host cell machinery to replicate its genome and produce viral proteins. Part 1 of this lecture will discuss ways in which viruses bind to the surface of host cells. Simian Virus 40 which binds to specific cell surface glycolipids, and Human Papilloma Virus-16 which binds to sites on filoipodia, are examples of different binding mechanisms. Attachment of viruses to the plasma membrane activates cell signaling resulting in endocytosis of the viral particles. This lecture is appropriate for upper level undergraduate and graduate classes studying virology or endocytosis.
牛痘病毒如何进入细胞 - Ari Helenius P3
本视频由科普中国和生物医学大讲堂出品
Ari Helenius (ETH Zurich) Part 3: Open Sesame: Cell Entry and Vaccinia Virus
Part 3 focuses on a single virus, the Vaccinia virus, as a model for cell binding, signaling and endocytosis. Fluorescently labeled Vaccinia viruses bind to and surf along host cell filopodia. Helenius lab members noticed that when Vaccinia, unlike other viruses, reached the surface of the cell body it caused the plasma membrane to form blebs. Further experiments showed that the virus tricks the cell into thinking it is apoptotic debris. This induces blebbing and subsequent uptake of the virus by macropinocytosis. Additionally, automated high throughput siRNA screening was used to screen a large number of infected cells for host genes required for Vaccinia virus uptake. Analysis of the genes identified allowed host factors and processes critical to viral infection to be identified. Expansion of this technique may provide a new source of information on pathogen-host interactions.
病毒包膜的内吞和渗透作用 - Ari Helenius P2
本视频由科普中国和生物医学大讲堂出品
Ari Helenius (ETH Zurich) Part 2: Endocytosis and Penetration
In the second lecture, the next steps in viral infection are described. Endocytosis of plasma membrane bound viruses can occur via a number of mechanisms including caveolar, clathrin, non-clathrin, or lipid raft mediated pathways. The internalized virus is enclosed in an endosome that may undergo increasing acidification resulting in acid mediated fusion between the viral envelope and the vesicle membrane. Following membrane penetration, the virus, once again, makes use of cellular machinery such as microtubules and their motors, to transfer its genome to the nucleus. Helenius describes experiments from his lab and others that have deciphered these complex processes.
将RNAscope®技术应用于病毒学的研究
Advanced Cell Diagnostics邀请了美国加利福尼亚大学（Davis）微生物、免疫及病理学系教授Patricia Pesavento，为大家介绍应用RNAscope®技术在研究新发现的病毒及致病病因、病理方面的研究。引起疾病的病毒可以跨越种族感染，通过测序发现新型病毒，利用RNAscope®进行病毒病理学分析，以准确判断疾病及复杂的宿主病毒相互影响。在这一讲座中，Pesavento教授以乳头瘤病毒等举例，对病毒的潜伏、致瘤和急性裂解细胞分析，分享了病毒学的研究进展。
RNAscope®技术可以针对任一病毒（或亚型）序列设计特异性探针，通过原位定量检测获得病毒感染、潜伏及与宿主反应的研究信息。详细信息请访问ACD官网www.acdbio.com。更多中文资料请关注中国官方微信号（ACD_China）咨询。
RNAscope原位杂交技术助力新冠病毒检测及初步结果展示
RNAscope原位杂交技术助理新冠病毒检测及初步结果展示 1. RNAscope技术原理介绍 2. 在Zika，MERs-Cov，HIV等病毒研究中的应用实例 3. RNAscope应对新冠病毒研究的相关产品及结果展示
GE：层析技术在病毒性疫苗中的应用策略
内容主要会覆盖目前中国市场疫苗现状，为了提高疫苗的质量标准，大多数厂家都开始对传统疫苗工艺进行升级换代，又或是选择更高效安全的层析方式进行抗原纯化，尤其是病毒性疫苗又有着通用性的策略，从而达到简化工艺流程，缩短工艺时间，提高疫苗质量