There is a broad spectrum of clinical disease with HBV infection, from subclinical through to fulminant hepatitis. Persistent infection can lead to chronic liver disease, potentially causing cirrhosis or hepatocellular carcinoma (HCC).
The virus preferentially infects liver cells, multiplying there and releasing large amounts of HBsAg, which is present in the blood of people with active infection. The incubation period varies between 45 and 180 days, and is commonly 60 to 90 days.
HBV is not directly cytopathic; it is the host’s immune response that leads to death of the infected liver cell. Most infected people mount an effective immune response that leads to eradication of infection over a period of several months. Adults with acute infection may be asymptomatic (approximately 20 percent) or have symptomatic hepatitis (approximately 80 percent, but variable2).
The common symptoms of acute hepatitis B illness are fever, jaundice, malaise, anorexia, nausea, vomiting, myalgias and abdominal pain. Jaundice develops usually within two weeks of onset of the illness, and dark urine and/or clay coloured stools might appear up to five days before clinical jaundice. Clinical signs and symptoms of acute hepatitis B usually resolve one to three months later.1
There is a small risk of acute liver failure (less than 1 percent), of whom almost half will die or require emergency liver transplantation.
The main burden of HBV disease occurs in people with chronic HBV infection. These chronically infected people are identified by persistence of hepatitis B surface antigen (HBsAg) in their serum for at least six months. The age of acquisition of HBV is strongly associated with the risk of developing chronic HBV infection. Approximately 90 percent of those infected perinatally or in infancy develop chronic HBV infection, compared with 30 percent of children infected between ages 1 and 4 years and less than 5 percent of people infected as adults.
Infants seldom mount an immune response to HBV infection, and infection in infancy is often asymptomatic. This asymptomatic chronic infection stimulates persistent immune responses that may eventually (decades later) lead to cirrhosis, which itself increases the risk of development of hepatocellular carcinoma.
Chronically infected people can be an ongoing source of infection to susceptible individuals. In the early years of chronic infection, high rates of viral replication are common, and both HBeAg and high levels of HBV DNA are present in the blood. In later years the rate of viral replication is lower, HBeAg may be absent from the blood, and HBV DNA levels are usually lower. People who have cleared HBeAg and remain HBsAg positive are termed carriers; this is a subset of chronic HBV infection.
HBV is usually transmitted through contact with infected blood or body ﬂuids during childbirth, contact with broken skin, or during sexual intercourse or intravenous drug use. Although HBV can be found in all body ﬂuids, blood has the highest concentration and saliva the lowest. HBV in dried blood remains infective for at least one week.3
The primary source of HBV infection is perinatal exposure from mothers with chronic HBV infection. Transmission usually occurs at the time of birth. The in utero transmission of HBV is relatively rare,4 accounting for less than 2 percent of infections transmitted from mother to infant.
If no prophylaxis is given to the infant, the baby of an HBeAg-positive mother has a 70–90 percent risk of infection, while the baby of an HBeAg-negative, HBsAg-positive carrier mother has a 5–20 percent risk of infection. Over 90 percent of infants who acquire infection perinatally go on to become chronic carriers.
Non-sexual person-to-person transmission probably occurs from inadvertent percutaneous or mucosal contact with blood or infectious body fluids amongst people in close daily contact (household members).
The main sources of transmission are: