GI-13000,吉利德的治疗性乙肝疫苗?

MP4

Strategic alliance with Gilead for chronic hepatitis B virus (HBV) infection. In November 2011, we licensed to Gilead Sciences, Inc. (Gilead) worldwide rights to our HBV Tarmogen program. Under the agreement, we granted Gilead exclusive worldwide rights to use our platform technology on Tarmogens to research, develop, and commercialize vaccine products directed at HBV. We will collaborate with Gilead on the development of our HBV Tarmogen product candidates in conjunction with Gilead’s drug, Viread® (tenofovir disoproxil fumarate), and other oral therapies for the treatment of chronic HBV infection.

GI-13000 is a series of Tarmogens expressing hepatitis B virus (HBV) antigens for the treatment of chronic HBV infection. GlobeImmune is developing GI-13000 in collaboration with Gilead Sciences, Inc.
HBV infection is the most common serious liver infection in the world. Worldwide, approximately 350 million people are chronic carriers of HBV, of whom more than 620,000 die from liver-related disease annually. In the United States, chronic HBV infection affects up to 1.4 million people. Vaccination has dramatically reduced the prevalence rates among children.  However, mother-to-newborn transmission, especially in Asia, remains a common source of new infection. There is currently no cure for the vast majority of chronically-infected patients.
Current treatment for HBV includes oral antiviral therapy to suppress virus replication. These antiviral products have been highly effective in controlling the disease but generally do not result in a long-term cure, thus requiring chronic suppressive therapy to control the disease. An important unmet need in HBV is a treatment that can effectively improve seroconversion rates or “cures” in chronically infected patients, allowing cessation of long-term antiviral therapy without relapse.


http://www.globeimmune.com/about/corporate-overview/
http://www.globeimmune.com/infectious-disease/gi-13000/

StephenW

                                        The Tarmogen platform is based on research conducted by the scientific founders of GlobeImmune, Drs. Donald Bellgrau, Richard Duke and Alex Franzusoff, in the late 1990s and early 2000s.
The discovery upon which the platform is based is that when animals are immunized with yeast expressing a recombinant protein, a cellular immune response is generated against the target recombinant protein and this immune response is capable of protecting the animal against diseased cells that express the same protein. While some antibody may be generated against the yeast, the antibody does not block the activity of the yeast, allowing for repeated administration and boosting of the immune response with additional administrations. The following graphics and corresponding captions describe the mechanism by which we believe Tarmogens work:
As shown in the graphic to the right, administration of Tarmogens initially results in binding of the yeast to white blood cells called antigen-presenting cells, the most important of which are known as dendritic cells, near the injection site. The dendritic cells are activated as a result of the Tarmogens binding to molecules called Toll-like receptors and other receptor molecules on the surface of the dendritic cell, resulting in the activation of immune signaling molecules called cytokines. The dendritic cell then engulfs the Tarmogen. Multiple Tarmogens may be taken up by the same dendritic cell.

The Tarmogen is processed by the dendritic cell in two ways. First, the Tarmogen is engulfed by subcellular bodies known as endosomes and the protein inside the endosome is cut into shorter fragments called peptides. These peptides are presented by Class II MHC molecules on the surface of the dendritic cell. In combination with IL-12, a cytokine that is produced by the dendritic cell, these MHC-peptide complexes on the surface of the dendritic cell are recognized by and activate cells involved in viral immunity called CD4+ helper T cells.

Dendritic cells also process Tarmogens by engulfing them with different subcellular bodies called phagosomes. This results in presentation of peptides, including the antigen from inside the Tarmogen, to cells, known as CD8+ killer T cells, via Class I MHC molecules on the surface of the dendritic cell, resulting in proliferation of identical antigen specific CD8+ T cells. CD4+ helper T cells are so named because one of their roles is to “help” activate killer T cells by expressing a cytokine called interferon gamma, IFNγ.

The newly activated CD8+ killer T cells move throughout the body and identify any other cell that expresses the same disease protein as the one recognized by the CD8+ killer T cells. Once the CD8+ killer T cell finds another cell in the body containing the target protein, it can kill the cell using multiple mechanisms.

                                                               

hata5

靠谱 我建议中国人联合起来找几个人去哪个研究所看看

9病成医

翻译一下呀，别让俺这不懂外文的干瞪眼。