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Hepatitis

Hepatitis

Hepatitis

Description:
 Hepatitis is inflammation of the liver. Several different viruses cause viral hepatitis. They are named the A, B, C, D, and E viruses. All of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong. Symptoms of viral hepatitis include jaundice (yellowing of the skin and eyes), fatigue, abdominal pain, loss of appetite, nausea, vomiting, diarrhea, low grade fever, and headache.

Who is at Risk?
 Risk groups depend on the type of hepatitis - A, B, C, D, or E. They include: people who have household contacts of infected persons, sex contacts of infected persons, persons traveling to countries where hepatitis is common, men who have sex with men, injecting and non-injecting drug users, persons with multiple sex partners or diagnosis of a sexually transmitted disease, infants born to infected mothers, health care and public safety workers, hemodialysis patients, recipients of clotting factors made before 1987, recipients of blood and/or solid organs before 1992, and people with undiagnosed liver problems.

Sources: National Institute of Diabetes and Digestive and Kidney Diseases, About, Inc.

TSRI Team Makes First Culture System
for Hepatitis C
 TSRI Professor Frank Chisari, M.D. and his colleagues have developed a way to produce the hepatitis C virus (HCV) in tissue culture. Their system will make it possible for the first time to understand all aspects of the life cycle of the virus, which in turn will lead to the development of antiviral drugs and vaccines. Until now, the inability to grow the pathogen in laboratories has delayed the development of more effective drugs and a vaccine. A liver-destroying pathogen, HCV infects 170 million people around the world and represents a growing public health burden. There are six major genetic families of HCV, and current treatments work better against some so-called genotypes than others. But a fundamental roadblock has stymied scientific progress: HCV has stubbornly refused to grow in laboratory cell cultures until now.

Chisari"s advance will finally enable researchers to study critical aspects of the pathogen"s life cycle, such as cell entry, replication, and packaging into new virus particles, each of which represents a novel drug target that has not been previously approachable. More precise targets, in turn, may yield drugs that are more effective than currently available agents, which are toxic and expensive, require a year of injections, and fail in some patients. Chisari"s other projects involve the discovery of how interferon cures hepatitis B infection by activating hepatocellular mechanisms that prevent the formation of replication competent HBV capsids and inhibit HBV replication; and how commonly used drugs that control serum cholesterol levels can also control hepatitis C virus replication by illustrating a complex cellular regulatory network that controls HCV RNA replication, presumably by modulating the trafficking and association of cellular and/or viral proteins with cellular membranes.

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Regulating Hepatitis B Gene Expression
 Hepatitis B Virus (HBV) is a worldwide health problem endemic in many regions of Asia and Africa. The HBV infection can be fatal. Although it can generally be prevented by vaccination with Hepatitis B surface antigen (HBsAg), chronic HBV infection remains a major clinical problem, with an estimated 200 to 500 million HBV chronic carriers in the world, for whom, to date, there is no reliable treatment. Understanding the viral life cycle in detail may reveal potential targets for antiviral therapy to control the liver disease associated with HBV infection. TSRI Associate Professor Alan McLachlan, Ph.D. and his colleagues are currently studying the regulation of HBV gene expression and its relationship to viral replication to reveal potential targets for antiviral therapy.

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Team Identifies Human Antibodies That Prevent Hepatitis C Virus Infection In Mouse Model
A team of researchers has found that certain antibodies can prevent hepatitis C virus infection in a "humanized" mouse model, opening the door to the use of antibodies as a human therapeutic and the development of a preventive vaccine for the disease. The study's authors, who include Scripps Research Professor Dennis Burton, Ph.D., University of Alberta Professor Norman Kneteman, and an international team of colleagues, identified a group of special antibodies that can broadly neutralize hepatitis C virus. Antibodies (proteins produced by the body's immune system in response to a foreign substance) are considered to be broadly neutralizing when they are effective against many different strains of a pathogen.

The findings that neutralizing human antibodies attack a region commonly found on the surface of many hepatitis C virus strains and that these antibodies protect against infection by the virus in an animal model provide proof of principle for the viability of passive immunotherapy against this extremely variable virus. The results also raise hopes for the development of an effective vaccine to prevent the disease from taking hold.

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Scientists Develop Process To Disrupt Hepatits C Virion Production
Scientists at The Scripps Research Institute's Scripps Florida facilities have discovered a method to disrupt the production of infectious virus particles that cause hepatitis C, a blood-borne liver disease. This discovery might be a first step in developing new and more effective therapies against the hepatitis C virus (HCV). Current anti-virals are ineffective for many patients infected with the viral strains most prevalent in the United States. HCV is a significant human pathogen, infecting more than three percent of the world's population. The incidence of infection in the United States has been estimated to be as high as 4 million cases. Timothy Tellinghuisen, Ph.D., an assistant professor in the Department of Infectology at Scripps Florida, and his colleagues used mutations of the viral NS5A phosphoprotein to disrupt virus particle production at an early stage of assembly. NS5A has long been proposed as a regulator of events in the HCV life cycle, but exactly how it orchestrates these events has been unclear.

The interesting thing about this mutant is that while it triggers totally normal RNA replication, it causes severe defects in the output of infectious virus - in fact, it releases no infectious virus that we can detect. And though this discovery isn't a cure for HCV, it is an important research tool that stops the assembly pathway. Total disruption of the replication process would be a cure for the disease and that's the team's long-term goal.

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