Viral Hepatitis B:     Introduction    

Figure 1. Location of the liver in body.

“Viral hepatitis," refers to infections that affect the liver and are caused by viruses. It is a major public health issue in the United States and worldwide. Not only does viral hepatitis carry a high morbidity, but it also stresses medical resources and can have severe economic consequences. The majority of all viral hepatitis cases are preventable.

Viral hepatitis includes five distinct disease entities, which are caused by at least five different viruses. Hepatitis A and hepatitis B (infectious and serum hepatitis, respectively) are considered separate diseases and both can be diagnosed by a specific serologic test. Hepatitis C and E comprise a third category, each a distinct type, with Hepatitis C parenterally transmitted, and hepatitis E enterically transmitted. Hepatitis D, or delta hepatitis, is another distinct virus that is dependent upon hepatitis B infection. This form of hepatitis may occur as a super-infectionin a hepatitis B carrier or as a co-infection in an individual with acute hepatitis B. Hepatitis viruses most often found in the United States include A, B, C, and D.

Because fatality from hepatitis is relatively low, mortality figures are a poor indicator of the actual incidence of these diseases. The Centers for Disease Control and Prevention estimated that approximately 400,000–600,000 people were infected with viral hepatitis during the decade of the 1990s.

Hepatitis plagued mankind as early as the fifth century BC. It was referenced in early biblical literature and described as occurring in outbreaks, especially during times of war. Toward the end of the nineteenth century, hepatitis was thought to occur as a result of infection of the hepatic parenchyma. The infectious nature of hepatitis was established after World War II. In the mid-1960s, Blumberg and colleagues discovered the surface antigen and antibody of hepatitis B. This Nobel Prize-winning research opened the door to our appreciation of the morphological and immunochemical features of other forms of viral hepatitis.

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What is Hepatitis B?
Chronic hepatitis B virus (HBV) is the ninth leading cause of death, with approximately 300 million chronic carriers of HBV worldwide. In the United States there are an estimated 1.2 million chronic carriers, accounting for roughly 17,000 hospitalizations and 5,500 deaths each year. Hepatitis B belongs to the hepadnaviridae class of viruses. It is transmitted by direct percutaneous or permucosal exposure to infected blood. The hepatitis B infection occurs in adolescents and adults and can lead to acute hepatitis, subclinical infection, or the development of chronic infection. The incubation period ranges from 45–160 days, with an average of 75 days, followed by an insidious onset of acute disease (Figure 2).  

Figure 2. Morphology of hepatitis B virus. M, L, S, envelope proteins.

HBV is a small, partially double-stranded DNA genome (3.2 kb) encoding four genes—HBsAg (surface envelope glycoprotein), HBcAg (viral capsid protein), HBV Pol/RT (polymerase reverse transcriptase), and X gene (transcriptional activator) (Figure 3).  

Figure 3. Genomic organization of hepatitis B virus.

There are four major serologic types of hepatitis B virus (adw, ayw, adr, and ayr), with different geographic distributions. The clinical significance of the four types remains unclear. Common to all of these subtypes, however, is an immuno-dominant epitope, the “a” determinant, that is the target of a neutralizing antibody in hepatitis B viral infection (anti-HBsAg). Recently, mutations in the “a” determinant have been reported to be associated with recurrence of hepatitis B viremia in serum despite the presence of protective antibodies (anti-HBsAg).

The life cycle of the hepatitis B virus is depicted in the animation (Figure 4). 
  

Figure 5. Possible outcomes after hepatitis B infection; A, acute infection; B, chronic infection.

Early in the disease process, generally called the prodromal phase, some patients experience a serum-type sickness that may include fever, arthralgia , arthritis , rash, and angioneurotic edema . These symptoms usually occur 2–3 weeks before jaundice and generally subside before jaundice develops, although they may be concomitant with its appearance.

In the pre-icteric phase, patients may experience respiratory and gastrointestinal tract symptoms, including malaise, fatigue, myalgia, anorexia , nausea, and/or vomiting. They may also experience moderate weight loss, headache, coryza , fever, or pharyngitis and cough. Many patients complain of mid-epigastric pain, right upper quadrant discomfort, or diarrhea. Also characteristic of this phase is the development of dark urine and the lightening of stool color. This duration of this stage of the disease may range from 2–3 days to 2–3 weeks.

The icteric phase is signaled by the development of jaundice. General constitutional symptoms may subside. There may be worsening of anorexia, nausea, and vomiting along with scratching and irritated skin lesions related to pruritis.

 
 
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