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BAREILLY PGI offers latest treatment of Hepatitis B and C following latest national and international protocols and guidelines.It also offers complete workup for the stage of disease and monitoring of its progression or regression. Hepatitis B and C are no longer incurable diseases, but require advanced knowledge of pathogenesis and life cycleof the viruses to be able to determine the optimum line of treatment . Consult your hepatologist for your ideal treatment for Hepatitis B and C.

Hepatitis B. Infection with the hepatitis B virus (HBV) may result in three different clinical states: acute hepatitis, chronic hepatitis, and the asymptomatic carrier state. HBV causes much of the morbidity and mortality from acute and chronic liver disease worldwide. HBV is spread by the parenteral route and by intimate contact. In addition to chronic liver disease, it is also implicated in the pathogenesis of hepatocellular carcinoma.

  • HBV is a medium-sized DNA virus belonging to a new class of animal viruses called hepadna viruses. These viruses are hepatotropic, tend to cause persistent infections, and have been associated with the development of hepatocellular carcinoma. HBV is unique among human viruses in its genomic and antigenic structure and its replicative cycle.

It consists of an outer shell made up of a protein designated as the hepatitis B surface antigen (HBsAg) and a complex inner core called the hepatitis B core antigen (HBcAg). This core particle consists of a partially double-stranded circular DNA molecule and a DNA polymerase (DNAP). The genome is composed of circular DNA with a complete negative strand and an incomplete positive strand. The negative strand contains overlapping genes that encode structural proteins (surface proteins and their derivatives and core) and two replicative proteins (polymerase and X). HBV is unique among DNA viruses in that it replicates in a way similar to that of the RNA retroviruses such as the human immunodeficiency virus (HIV) via an RNA intermediate. Following entry of HBV into a hepatocyte, viral replication is initiated by the synthesis of an intermediary RNA molecule using host enzymes. Viral genomic DNA is produced by reverse transcription using DNA polymerase of the virus.

  • Pathogenesis:- At the entry of HBV and its invasion of hepatocytes, viral proteins are expressed on the hepatitis membrane. These proteins are recognized by the host immune systems, both the humoral and the cellular arms. If the host immune response to the infected hepatocytes is strong enough to destroy all the involved cells, hepatits is results in clearance of the virus. However, if the immune response is inadequate to completely obliterate the infected hepatocytes, an ongoing viral infection ensues with varying degrees of hepatic inflammatory response.
  • Serology:- Infection with HBV results in an overproduction of HBsAg outnumbering the intact virus by 10 million to 1.

Hepatitis B e antigen (HBeAg) is an internal antigen of HBcAg particles that can be detected in the serum of patients with high levels of circulating HBV. HBeAg is found only in HBsAg-positive serum and signals active ongoing infection and infectivity. HBcAg is found only within the infected hepatocytes and not in the serum. The hepatitis B antibody (Ab) is described in the following sections.



  • Epidemiology. Hepatitis C virus (HCV), identified in 1988, is an RNA virus that appears to be responsible for most instances of parenterally transmitted non-A, non-B hepatitis. The virus seems to mutate frequently and appear in many subtypes. HCV is associated with transfusions of contaminated blood and blood products such as plasma, factor VIII, factor IX, fibrinogen, cryoprecipitate, and immune globulin.

HCV is also transmitted by IV drug abuse, hemodialysis, and organ transplantation. It appears to be transmitted rarely by familial, sexual, or maternal-infant exposure. Heterosexual transmission seems to be much less frequent than homosexual transmission of the virus.

Health-care workers exposed to a patient or the blood of a patient infected with HCV may acquire hepatitis C either from an accidental needle stick or without such an incident; however, the risk in such cases seems to be less than 10%. This occurrence has been documented in dialysis and oncology units and in plasmapheresis centers. Sporadic instances of hepatitis C occur and may account for 6% to 36% of the sporadic cases of hepatitis seen in urban areas. There may be unnoted percutaneous exposure among such patients. However, hepatitis C may also be transmitted by nonpercutaneous mechanisms. The epidemiology of hepatitis C has not been completely defined.

The disease is found worldwide and appears to be almost as common in economically developed countries as it is in underdeveloped countries.