Hepatitis B vims

Vaccines can be roughly categorized into killed vaccines and Hve vaccines. A killed vaccine can be (/) an inactivated, whole microorganism such as pertussis, (2) an inactivated toxin, called toxoid, such as diphtheria toxoid, or (J) one or more components of the microorganism commonly referred to as subunit vaccines. The examples are capsular polysaccharide of Streptococcus pneumoniae and the surface antigen protein for Hepatitis B vims vaccine. 

FIAC also strongly inhibits HCMV and Epstein-Barr vims (EBV) in vitro the two vimses known not to induce a specific viral thymidine kinase for their repHcation. However, HCMV may stimulate cellular kinases that can anabolize FIAC to its 5 -triphosphate, which specifically inhibits the HCMV-encoded DNA polymerase. This selective activity suggests that FIAC should be evaluated against HCMV infections. FIAC-ttiphosphate incorporated into DNA has shown strong in vitro activity against the DNA polymerases of human hepatitis B vims (HBV) and of woodchuck hepatitis vims (WHV) (37). 

A large and rapidly growing number of clinical trials (phase I and phase II) evaluating the potential of DNA vaccines to treat and prevent a variety of human diseases are currently being performed ( http // clinicaltrials.gov) however, there is yet no licensed DNA vaccine product available for use in humans. The clinical trials include the treatment of various types of cancers (e.g., melanoma, breast, renal, lymphoma, prostate, and pancreas) and also the prevention and therapy of infectious diseases (e.g., HIV/ABDS, malaria, Hepatitis B vims, Influenza vims, and Dengue vims). So far, no principally adverse effects have been reported from these trials. The main challenge for the development of DNA vaccines for use in humans is to improve the rather weak potency. DNA vaccines are already commercially available for veterinary medicine for prevention of West Nile Vims infections in horses and Infectious Hematopoetic Necrosis Vims in Salmon. 

A particle that spontaneously assembles from viral coat proteins in the absence of other viral components. Vims-like particles (VLPs) generated from recombinant coat proteins are used in vaccines against hepatitis B vims and papillomavirus. 

Hamasaki K, Nakao K, Matsumoto K, Ichikawa T, Ishikawa H, Eguchi K (2003) Short interfering RNA-directed inhibition of hepatitis B vims replication. EEBS Lett 543 51-54 He ML, Zheng B, Peng Y, Peiris IS, Poon LL, Yuen KY, Lin MC, Kung HP, Guan Y (2003) Inhibition of SARS-associated coronavims infection and replication by RNA interference. JAMA 290 2665-2666... 

Protzer U, Nassal M, Chiang PW, Kirschfink M, Schaller H (1999) Interferon gene transfer by a hepatitis B vims vector efficiently suppresses wild-type vims infection. Proc Natl Acad Sd USA 96 10818-10823... 

Hwang, S.-J., et al. (1996). Comparison of three different hybridization assays in the quantitative measurement of serum hepatitis B vims DNA. J. Virol. Methods 62,123-129. 

Kaneko, S., et al. (1990). Detection of hepatitis B vims DNA in semm by polymerase chain reaction. Application for clinical diagnosis. Gastrology 99,799-804. 

Other indications Household contacts and sex partners of persons with chronic hepatitis B vims (HBV) infection clients and staff members of institutions for persons with developmental disabilities international travelers to countries with high or intermediate prevalence of chronic HBV infection (a list of countries is available at wwwn.cdc.gov/travel/contentdiseases.aspx) and any adult seeking protection from HBV infection. 

Peghini PA, et al. In vitro inhibition of hepatitis B vims replication and pharmacokinetic properties of new lipophilic dinucleoside phosphate derivatives. Antivir Chem Chemother 1998 9 95. 

Blumberg BS (1997) Hepatitis B vims, the vaccine, and the control of primary cancer of the liver. Proc Natl Acad Sci USA, 94 7121-7125. 

Reactions with acid anhydrides (Scheme 110 <2003JA6462>) and acyl chlorides (Scheme 111 <2005S583>) occurred at room temperature in various solvents, and furnish acyl-azocanes in reportedly good to excellent yields (specific yields not given). Compounds of type 267 were studied as inhibitors of the Hepatitis B vims replications. Compound 269 was used as a chiral ligand for the enantioselective addition of diethyl zinc to aromatic aldehydes. 

Daub, H., Blencke, S., Habenberger, P., Kurtenbach, A., Dennenmoser, J., Wissing, J., Ullrich, A. and Gotten, M. (2002) Identification of SRPKl and SRPK2 as the major cellular protein kinases phosphorylating hepatitis B vims core protein. J. Virol. 76, 8124-8137. 

Hepatitis B vims (HBV) Since the detection of HBsAg by Blnmberg and the introdnction of HBsAg screening for donors of blood and plasma in aU developed countries, hepatitis B virns transmission throngh the use of blood and blood prodncts has been effectively prevented. Estimates of the risk of infection, based on the sensitivities of cnrrent tests for HBsAg and for anti-HBcAg, are in the order of 1 in 200000 per nnit (159). 

Ganem, B, N-butyldeoxynojirimycin is a novel inhibitor of glycoUpid biosynthesis. Secretion of human hepatitis B vims is inhibited by the imino sugar N-butyldeoxynojirimycin, Chemtracts Org. Chem., 1, 106-107, 1994. 

Jacquard, A.-C., Brunelle, M.-N., Pichoud, C., et al. (2006) In vitro characterization of the anti-hepatitis B vims activity and cross-resistance profile of 2, 3 -didcoxy-3 -fluoroguanosine. Antimicrob. Agents Chemother., 50, 955-961. 

Wu, T.-T., Coates, L., Aldrich, C., Summers, J., and Mason, W. S. (1990) In hepatocytes infected with duck hepatitis B vims, the template for viral RNA synthesis is amplified by an intracellular pathway. Virology 175, 255-261. 

Lin, E., Luscombe, C., Wang, Y-Y Shaw, T., and Locarnini, S. (1996) The guanine nucleoside analogue penciclovir is active against chronic duck hepatitis B vims infection in vivo. Antimicrob. Agents Chemother. 40,413—418. 

Bishop, N., Civitico, G., Wang, Y Guo, K., Gust, 1. D, and Locarnini, S. (1990) Antiviral strategies in chronic HBV infection I, Establishment of a suitable in vitro system using the duck hepatitis B vims model. /, Med. Virol. 31, 82-89. 

Jilbert, A., Freiman, J Burrell, C., Holmes, M Gowans, E, Roweand, R., Hall, P., and Cossart, Y. (1988) Virus-liver cell interactions in duck hepatitis B vims infection A study of virus dissemination within the liver. Gastroenterology 95, 1375-1382. 

Shaw, T., Mok, S. S., and Locamini, S. A. (1996) Inhibition of hepatitis B vims DNA polymerase by enantiomers of penciclovir triphosphate and metabolic basis for selective inhibition of HBV replication by penciclovir. Hepatology 24,996-1002. 

Hunt C, McGiU J, Allen M, Condreay L. Clinical relevance of hepatitis B vims mutations. Hepatology 2000 31 1037-44. 

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