Báo cáo y học: "Study of the early steps of the Hepatitis B Virus life cycle"

Tuyển tập các báo cáo nghiên cứu khoa học ngành y học tạp chí Medical Sciences dành cho các bạn sinh viên ngành y tham khảo đề tài: Study of the early steps of the Hepatitis B Virus life cycle. | Int. J. Med. Sci. 2004 1 1 21-33 21 Research paper Received Accepted Published Abstract Key words Author biography Corresponding address International Journal of Medical Sciences ISSN 1449-1907 2004 1 1 21-33 2004 Ivyspring International Publisher. All rights reserved Study of the early steps of the Hepatitis B Virus life cycle Xuanyong Lu Timothy Block Jefferson Center for Biomedical Research and Agricultural Medicine Department of Biochemistry and Molecular Pharmacology Thomas Jefferson University Philadelphia USA Hepatitis B virus HBV is a human pathogen causing the serious liver disease. Despite considerable advances in the understanding of the natural history of HBV disease most of the early steps in the virus life cycle remain unclear. Virus attachment to permissive cells fusion and penetration through cell membranes and subsequent genome release are largely a mystery. Current knowledge on the early steps of HBV life cycle has mostly come from molecular cloning expression of individual genes and studies of the infection of duck hepatitis B virus DHBV with duck primary duck hepatocytes. However considering of the difference of the surface protein of HBV and DHBV both in the composition and sequence the degree to which information from DHBV applies to human HBV attachment and entry may be limited. A major obstacle to the study HBV infection is the lack of a reliable and sensitive in vitro infection system. We have found that the digestion of HBV and woodchuck hepatitis virus WHBV by protease V8 led to the infection of HepG2 cell a cell line generally is refractory for their infection Lu et al. J Virol. 1996. 70. 2277-2285. Lu et al. Virus Research. 2001. 73 1 27-4 . Further studies showed that a serine protease inhibitor Kazal SPIK was over expressed in the HepG2 cells. Therefore it is possible that to silence the over expressed SPIK and thus to reinstate the activity of indispensable cellular proteases can result in

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