Hepatitis B Virus

Basic Virology and Epidemiology

Hepatitis B virus (HBV) is a member of the Hepadnavirus family. It is a large deoxyribonucleic acid (DNA) virus with a circular chromosome that undergoes an RNA stage in the host cell during its replicative cycle. It subsequently produces viral DNA, which ultimately leads to synthesis of the viral proteins. The major proteins involved in HBV infection are the surface antigen (HBsAg), core antigen (HBcAg), and the e antigen (HBeAg). The HBsAg is an element of the outer surface of the virus; HBcAg and HBeAg are different forms of the same polyprotein. HBcAg is made up of subunit proteins that form the genomic core of the full virus; HBeAg is a truncated form of this protein that is thought to play a role in signaling for viral replication (4).

HBV infection occurs only in humans and is passed from person to person by sexual and blood-borne contact, as well as vertical transmission. HBV is a worldwide public health concern. It is estimated that 350 million people are carriers of the virus, with prevalence rates in Africa and Asia of greater than 8%. In developing nations, the major route of acquisition of HBV is by vertical transmission from mother to child at birth; in the Western Hemisphere, most individuals acquire infection in adolescence and adulthood via sexual or parenteral routes (2-4).

Course of Infection

Incubation of HBV after exposure averages 70 days before the onset of symptoms. Acute HBV infection is subtle in most adult cases but may be symptomatic in about 30% of patients. Symptoms include fever, jaundice, malaise, and abdominal pain, with a clinical course identical to HAV. HBV may have some extrahepatic manifestations that are characteristic: Gianotti-Crosti skin eruption, also known as papular acrodermatitis of childhood, and acute glomerulonephritis. Symptoms appear after HBsAg levels have peaked in the bloodstream (4).

About 90% of patients with acute HBV infection will have spontaneous resolution of their infection. A very small percentage of patients develop fulminant hepatic failure after acute infection. Of patients, 5-10% develop a chronic carrier state in which the virus remains active at a low level. These carriers are at high risk for end-stage liver disease and, ultimately, hepatocellular carcinoma. Patients with chronic HBV infection may also present with glomerulonephritis secondary to immune complex deposition. In addition to their own morbidity, HBV carriers represent the largest reservoir for transmission of HBV (4).

Infection During Pregnancy

HBV can infect pregnant women but does not cause more severe disease than seen in the general population. Chronic carriers of the virus usually have uncomplicated pregnancies unless evidence of liver failure is present. The importance of HBV infection during pregnancy is the significant risk of transmission to the infant (2,3,5). If the mother is known to be HBV infected and is acutely infected or a chronic carrier, the infant is at risk not only for infection, but also to become a chronic HBV carrier.

Vertical Transmission

HBV can be passed from mother to infant during a maternal acute infection, or if the mother is a chronic carrier. The risk of transmission is greater in acute infections when the virus is acquired by the mother later in pregnancy, presumably because of lack of adequate protective antibody passed from mother to child. It has been estimated that 85% of transmission occurs during blood exposure at delivery, and only 15% of transmission is in utero. Mothers with evidence of active viral replication by detection of viral and immunologic markers have a much higher incidence of vertical transmission (2,3).

Breast-feeding in infected mothers has been studied and found not to pose a risk for transmission (8). Presumably, maternal antibody is transmitted in enough quantity to neutralize any virus present.

Prenatal Evaluation

Mothers who exhibit symptoms of acute hepatitis, including fever, jaundice, abdominal pain, and who by history engaged in high-risk behaviors for acquisition of HBV (e.g., promiscuous sexual practices, sex with a known HBV carrier, or intravenous drug use) should be screened for viral markers of infection. Most states require that all mothers be tested for laboratory evidence of hepatitis B infection.

HBsAg is a marker of either early acute infection or ongoing chronic replication. HBsAb is a marker of the immune response to the virus. Mothers who are HBsAg positive are at high risk for transmitting the virus to their offspring (7).

HBeAg is a marker used to estimate the amount of active viral replication. Studies have shown that patients who are HBeAg positive transmit the virus at a much higher rate (90%) to their offspring than do mothers who are HBeAg negative (40%) (3).

Postnatal Evaluation of the Infant

Physical examination of infants in the postnatal period will usually be unremarkable. HBV can cause symptoms at birth if the mother has active replication of HBV, including fulminant hepatic failure, but they are rare.

Infants born to mothers with active HBV infection or who are chronic carriers of the virus should receive prophylaxis with the hepatitis B immunoglobulin within the first 12 hours of life, as well as prompt initiation of the hepatitis B vaccine series.

Laboratory Evaluation of Mother and Infant

As discussed, the mother should have as part of her routine prenatal evaluation testing for HBsAg and HBsAb. If the mother is HBsAg positive, it is recommended that she should have further assessment with HBeAg for activity of her infection.

Babies receiving prophylaxis should have follow-up testing for HBsAg and HBsAb at 6 months to confirm that the infant has not developed a carrier state but rather is protected against HBV infection. If the HBsAg is negative and HbsAb is positive, the infant is considered immune, and no further testing is necessary (7).

Bacterial Vaginosis Facts

Bacterial Vaginosis Facts

This fact sheet is designed to provide you with information on Bacterial Vaginosis. Bacterial vaginosis is an abnormal vaginal condition that is characterized by vaginal discharge and results from an overgrowth of atypical bacteria in the vagina.

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