Universal Hepatitis B Virus Vaccination Research Articles

Progress towards the comprehensive control of hepatitis B in Africa: a view from South Africa.

The carrier rate of hepatitis B virus (HBV) in black Africans averages 10.4% throughout the continent. Even within each country, however, there may be wide variations. HBV carriage in black Africans is largely established in early childhood, mostly through horizontal transmission. Perinatal transmission also occurs but to a much lesser extent than in the Far East. For unknown reasons, HBeAg positivity rates are much lower in black Africans of childbearing age than in women in the Far East. Universal HBV vaccination of infants in South Africa started in April 1995. Effective integration into the Expanded Programme on Vaccination will probably be necessary if administration of second and third doses is to be ensured. Fortunately, a natural process of urbanisation is also having a beneficial effect on the black carrier rate in South Africa, as urban carrier rates tend to be much lower than those in rural area. Within the next 20 years, therefore, there should be a great reduction in the numbers of acute HBV infections and new carriers. However, it will take much longer before there is any substantial impact on the burden of the longterm sequelae of HBV infection--that is, cirrhosis and hepatocellular carcinoma.

Clinical aspects of hepatitis B virus infection

Adults with a healthy immune system who are exposed to hepatitis B virus (HBV) usually suffer from a mild acute infection. The likelihood of chronicity is only 5%, but climbs as high as 90% in newborns and n the immunocompromised. Acute HBV infection can cause fulminant liver failure (case fatality rate of 80%). People with chronic infection tend to have no symptoms, normal liver enzymes, and normal or almost normal liver histology, making diagnosis difficult. Active viral replication occurs in most people with active liver disease. People with persistent active replication are at higher risk of death from liver disease or hepatocellular carcinoma (HCC) than those with inactive disease. HBV transmission occurs via sexual intercourse or blood or needle contact. In the US, iv drug use is the major risk factor for HBV infection in adults. Prevention of HBV infection is through patient education and vaccination. Some people advocate universal HBV vaccination because it is often difficult to vaccinate high risk populations and to identify risk factors. Universal vaccination is not cost effective in low risk areas, however, e.g., the US and Europe. Treatment for chronic HBV infection is limited. Response to interferon therapy depends on low HBV DNA levels, high transaminase levels, and a history of acute hepatitis. Short- and longterm response rates tend to be low, however ( 40% short term and much lower for longterm). Experimental drugs are thymosin and nucleoside analogues. Standard treatment for patients with end-stage chronic liver disease or fulminant hepatic failure is liver transplantation. High dose immune globulin is the best means to delay and prevent recurrent HBV infection in transplantation patients. Some problems with management of chronic HBV are prevention of HCC and recurrent HBV after transplantation. Variant viruses are mutations of the precore or of a surface gene. HIV/AIDS is often associated with HBV and hepatitis delta virus infection.