The disease is caused by hepatitis A virus, a nonenveloped, positive, single-stranded RNA virus, first identified by electron microscopy in 1973, classified within the genus Hepatovirus of the picornavirus family. Feces contain the highest concentration of viral particles and viral excretion is highest late in the incubation and early in the prodromal phase. Duration of viremia is short with limited transmission in urine or other body fluids.
The virus replicates exclusively in the cytoplasm of the infected hepatocytes by a mechanism involving an RNA-dependent RNA polymerase. The inflammation and necrosis observed during HAV infection does not appear to be a direct viral effect, but rather an effect of the immune cell response induced by the viral infection. The resulting inflammatory response leads to hepatitis and necrosis and appears to be T-cell mediated.[1, 2, 3] In most patients the process is reversible with the damaged hepatic tissue restored within 8-12 weeks.
There is practically no maternal fetal transmission of HAV and it poses a minimal risk to the fetus and newborn. No intervention is recommended.
Hepatitis B is caused by the hepatitis B virus, an enveloped virus containing a partially double stranded, circular DNA genome, and classified within the family hepadnavirus.[11, 24] The nucleocapsid core measures 27 nm in diameter and is where the hepatitis B core antigen (HbcAg) is derived. The core is surrounded by a lipoprotein coat or envelope, which is the hepatitis B surface antigen (HbsAg).[25, 26, 11, 27, 28] The envelope lipoprotein is produced in excessive amounts and released into the circulation as hepatitis B surface antigen (HBsAg).
The virus interferes with the functions of the liver while replicating in hepatocytes. The immune system is then activated to produce a specific reaction to combat and attempt to eradicate the virus. Intracellular HBV is not cytopathic.
The inflammatory response develops as a result of the immune response.
HBV does not cross the placenta because of its size and cannot infect the fetus unless there have been breaks in the maternal-fetal barrier such as those that occur during amniocentesis. Women who are infected can transmit HBV to the infant during the delivery. Unless adequate prophylaxis is provided, the newborn is at high risk to develop a chronic HBV infection, with its known long-term complications. Perinatal transmission from the mother to her newborn baby is the most important mode of infection. If a pregnant woman is an HBV carrier and is also HBeAg-positive, her newborn baby has a 90% likelihood of becoming infected. Approximately 25% of infected infants will become chronic carriers. Most hepatitis B surface antigen (HbsAg) carriers are asymptomatic and potentially infectious. HBV carriers are a constant source of new infections.
Less frequent, but important, modes of HBV transmission include transfer through percutaneous or parenteral contact with infected blood, body fluids, and by sexual intercourse.[11, 27] A break in the skin or mucosal barrier is required for transmission. HBV is able to remain on any surface it comes into contact with for about a week without losing infectivity.[26, 24] An affected individual’s blood is infective weeks before the onset of any symptoms and throughout the acute phase of the disease. The infectivity of chronically infected individuals varies from highly infectious (HBeAg positive) to rarely infectious (anti-HBe positive).