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Hepatitis B has a complex natural history and causes a wide spectrum of disease. There is a large reservoir of carriers of hepatitis B virus (HBV) in the human population. Low (less than 2% of the population), intermediate (2–8%), and high prevalence regions (more than 8%) are recognised. Population movements and immigration are changing the prevalence of the disease in several non-endemic countries in Europe and elsewhere. Treatment is indicated for chronic, progressive disease, although there is a role for rapidly acting nucleoside analogues in fulminant acute hepatitis or subacute hepatic necrosis. Substantial health care resources will be required for the worldwide burden of disease. In endemic areas the direct costs can total 3.2% of the national health care expenditure.1 2
Several difficulties remain in formulating treatments for HBV infection and thus areas of disagreement on the management of chronic hepatitis B exist. Choices of treatment depend on a number of factors predictive of treatment response, clinical circumstances and stage of disease, potency of different agents, the likelihood and consequences of resistance to treatment, as well as the personal choice of the patient and physician.3 Current guidelines are not always constant or agreed and will require rapid adjustment as new treatments become available.4–6 Thus this review summarises an overall view of treatment and points to areas of controversy.
REPLICATION OF HBV AND HOST IMMUNE RESPONSE
Key steps in the replication of HBV have been defined. After entry into the cell, the virus is uncoated, and translocated to the nucleus. Relaxed circular HBV DNA is converted into supercoiled, or covalently closed (cccDNA) from which a pregenomic RNA is transcribed. HBV replicates through transcription of HBV RNA to DNA. The crucial steps include encapsidation, minus strand (−) DNA strand synthesis, plus strand (+) DNA synthesis, and maturation and release of viral particles. cccDNA is …
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