HEPATITIS B

Hepatitis B

Hepatitis B is an infectious inflammatory illness of the liver caused by the hepatitis B virus (HBV) that affects hominoidea, including humans. Originally known as "serum hepatitis",^[1] the disease has caused epidemics in parts of Asia and Africa, and it is endemic in China.^[2] About a third of the world population has been infected at one point in their lives,^[3] including 350 million who are chronic carriers.

Hepatitis B virus is an hepadnavirus—hepa from hepatotropic (attracted to the liver) and dna because it is a DNA virus[12]—and it has a circular genome of partially double-stranded DNA. The viruses replicate through an RNA intermediate form by reverse transcription, which practice relates them to retroviruses.[13] Although replication takes place in the liver, the virus spreads to the blood where viral proteins and antibodies against them are found in infected people.

Signs and symptoms

Acute infection with hepatitis B virus is associated with acute viral hepatitis – an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have more severe liver disease (fulminant hepatic failure), and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of Membranous glomerulonephritis (MGN).

Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti-Crosti syndrome).^[17][18] The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice.^[19] The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B.^[20] About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers.^[21] HBV-associated nephropathy has been described in adults but is more common in children.^[22][23] Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.

Virology     -     Structure 

Hepatitis B virus (HBV) is a member of the Hepadnavirus family.^[12] The virus particle, (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. These virions are 42 nM in diameter and are sometimes referred to as "Dane particles". The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity. The outer envelope contains embedded proteins that are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses, but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigen (HBsAg), and is produced in excess during the life cycle of the virus.

Transmission

Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood. Possible forms of transmission include sexual contact, blood transfusions, re-use of contaminated needles & syringes, and vertical transmission from mother to child (MTCT) during childbirth. Without intervention, a mother who is positive for HBsAg confers a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for HBeAg. HBV can be transmitted between family members within households, possibly by contact of nonintact skin or mucous membrane with secretions or saliva containing HBV. However, at least 30% of reported hepatitis B among adults cannot be associated with an identifiable risk factor.And Shi et al. showed that breastfeeding after proper immunoprophylaxis did not contribute to MTCT of HBV.

Prevention

Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from people who had long-standing hepatitis B virus infection. However, it is made using a synthetic recombinant DNA technology that does not contain blood products. One cannot be infected with hepatitis B from this vaccine.

Treatment

The hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously. Early antiviral treatment may be required in fewer than 1% of people, whose infection takes a very aggressive course (fulminant hepatitis) or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy. Treatment lasts from six months to a year, depending on medication and genotype.^[

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Reactivation

Hepatitis B virus DNA persists in the body after infection, and in some people the disease recurs. Although rare, reactivation is seen most often in people with impaired immunity. HBV goes through cycles of replication and non-replication. Approximately 50% of people experience acute reactivation. Males with baseline ALT of 200 UL/L are three times more likely to develop a reactivation than people with lower levels. People who undergo chemotherapy are at risk for HBV reactivation. The current^[when?] view is that immunosuppressive drugs favor increased HBV replication while inhibiting cytotoxic T cell function in the liver.