(See also Causes of Hepatitis, Overview of Acute Viral Hepatitis, and Chronic Hepatitis B.)
Hepatitis B virus (HBV) is the most thoroughly characterized and complex hepatitis virus. The infective particle consists of a viral core plus an outer surface coat. The core contains circular double-stranded DNA and DNA polymerase, and it replicates within the nuclei of infected hepatocytes. A surface coat is added in the cytoplasm and, for unknown reasons, is produced in great excess.
HBV is the second most common cause of acute viral hepatitis after hepatitis A. Prior unrecognized infection is common but is much less widespread than that with hepatitis A virus. In the United States, 2045 cases of acute hepatitis B infection were reported in 2021. However, because many cases are not recognized or not reported, the Centers for Disease Control and Prevention (CDC) estimates that the actual number of acute hepatitis B infections was about 13,300 in 2021 (1).
HBV is sometimes associated with several primarily extrahepatic disorders, including polyarteritis nodosa, other systemic rheumatic diseases, membranous glomerulonephritis, and essential mixed cryoglobulinemia. The pathogenic role of HBV in these disorders is unclear, but autoimmune mechanisms are suggested.
Occasionally, coinfection with hepatitis D occurs.
Transmission of hepatitis B
HBV is often transmitted parenterally, typically via contaminated blood or blood products. Routine screening of donor blood for hepatitis B surface antigen (HBsAg) has nearly eliminated the previously common posttransfusion transmission, but transmission through needles shared by drug users remains common. Risk of HBV is increased for patients on dialysis and in oncology units, and for hospital personnel in contact with blood.
Infants born to infected mothers have a 70 to 90% risk of acquiring hepatitis B during delivery (see Neonatal Hepatitis B Virus Infectionvaccinated immediately after delivery. Earlier transplacental transmission can occur but is rare. The risk of vertical transmission of HBV is also mitigated by treating actively infected pregnant women with high viral loads in their third trimester with tenofovir.
The virus may be spread through mucosal contact with other body fluids (eg, between sex partners, both heterosexual and homosexual; in closed institutions, such as mental health institutions and prisons), but infectivity is far lower than that of hepatitis A virus, and the means of transmission is often unknown.
The role of insect bites in transmission is unclear. Many cases of acute hepatitis B occur sporadically without a known source.
Chronic HBV carriers provide a worldwide reservoir of infection. Prevalence varies widely according to several factors, including geography (eg, < 0.5% in North America and northern Europe, > 10% in some regions of the Far East and Africa).
General reference
1. Centers for Disease Control and Prevention (CDC): Hepatitis B Surveillance 2021. Accessed June 14, 2024.
Symptoms and Signs of Acute Hepatitis B
Hepatitis B infection causes a wide spectrum of liver diseases, from a subclinical carrier state to severe hepatitis or acute liver failure (fulminant hepatitis).
Most patients have typical manifestations of viral hepatitis, including anorexia, malaise, fever, nausea, and vomiting, followed by jaundice. Symptoms persist from a few weeks up to 6 months.
Five to 10% of all patients with acute HBV infection develop chronic hepatitis B. The younger the age that acute hepatitis B occurs, the higher the risk of developing chronic hepatitis B. For immunocompetent people, risk of developing chronic hepatitis B infection is as follows:
For infants: 90%
For children aged 1 to 5 years: 25 to 50%
For adults: About 5%
If hepatitis B becomes chronic, cirrhosis can develop, and hepatocellular carcinoma can ultimately develop, even without being preceded by cirrhosis.
Diagnosis of Acute Hepatitis B
Serologic testing
In the initial diagnosis of acute hepatitis, viral hepatitis should be differentiated from other disorders causing jaundice (see figure Simplified Diagnostic Approach to Possible Acute Viral Hepatitis).
If acute viral hepatitis is suspected, the following tests are done to screen for hepatitis viruses A, B, and C:
IgM antibody to HAV (IgM anti-HAV)
Hepatitis B surface antigen (HBsAg)
IgM antibody to hepatitis B core (IgM anti-HBc)
Antibody to hepatitis C virus (anti-HCV) and hepatitis C RNA (HCV-RNA) polymerase chain reaction
If any of the hepatitis B tests are positive, further serologic testing may be necessary to differentiate acute from past or chronic infection (see table Hepatitis B Serology). If serology suggests hepatitis B, testing for hepatitis B e antigen (HBeAg) and antibody to hepatitis B e antigen (anti-HBe) is usually done to help determine the prognosis and to guide antiviral therapy. If serologically confirmed HBV infection is severe, antibody to hepatitis D virus (anti-HDV) is measured.
Hepatitis B has at least 3 distinct antigen-antibody systems that can be tested:
HBsAg
Hepatitis B core antibody (HBcAb)
HBeAg
HBsAg characteristically appears during the incubation period, usually 1 to 6 weeks before clinical or biochemical illness develops, and implies infectivity of the blood. It disappears during convalescence. However, HBsAg is occasionally transient. The corresponding protective antibody (anti-HBs) appears weeks or months later, after clinical recovery, and usually persists for life; thus, its detection indicates past HBV infection and relative immunity. In 5 to 10% of patients, HBsAg persists and antibodies do not develop; these patients develop chronic hepatitis B.
HBcAb reflects antibody to the viral core. Hepatitis B core antigen (HBcAg) is detectable in infected liver cells but not in serum except by special techniques. Antibody to HBcAg (anti-HBc, or HBcAb) usually appears at the onset of clinical illness; thereafter, titers gradually diminish, usually over years or life. Its presence with anti-HBs indicates recovery from previous HBV infection. Anti-HBc is also present in chronic HBsAg carriers, who do not mount an anti-HBs response. In acute infection, anti-HBc is mainly of the IgM class, whereas in chronic infection, IgG anti-HBc predominates. IgM anti-HBc is a sensitive marker of acute HBV infection and occasionally is the only marker of recent infection, reflecting a window between disappearance of HBsAg and appearance of anti-HBs.
HBeAg is a protein derived from the viral core (not to be confused with hepatitis E virus). Present only in HBsAg-positive serum, HBeAg tends to suggest more active viral replication and greater infectivity. In contrast, presence of the corresponding antibody (anti-HBe) suggests lower infectivity. Thus, e antigen markers are more helpful in prognosis than in diagnosis. Chronic liver disease develops more often among patients with HBeAg and less often among patients with anti-HBe.
HBV-DNA can be detected in the serum of patients with active HBV infection.
Hepatitis B Serology*
Marker | Acute HBV Infection | Chronic HBV Infection | Prior HBV Infection† | Prior HBV Vaccination |
|---|---|---|---|---|
HBsAg | + | + | − | - |
Anti-HBs | − | − | + | + |
IgM anti-HBc | + | − | − | - |
IgG anti-HBc | − | + | ± | - |
HBeAg | ± | ± | − | - |
Anti-HBe | − | ± | ± | - |
HBV-DNA | + | + | − | - |
* Antibody to hepatitis D virus (anti-HDV) levels should be measured if serologic tests confirm HBV and infection is severe. | ||||
† Patients have had HBV infection and recovered. | ||||
Anti-HBc = antibody to hepatitis B core; anti-HBe = antibody to HBeAg; anti-HBs = antibody to HBsAg; HBeAg = hepatitis B e antigen; HBsAg = hepatitis B surface antigen; HBV = hepatitis B virus. | ||||
Other tests
Liver tests are needed if they were not previously done; they include serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase.
Treatment of Acute Hepatitis B
Supportive care
For fulminant hepatitis B, antivirals and liver transplantation
No treatments attenuate acute viral hepatitis, including hepatitis B. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis.
If fulminant hepatitis occurs, treatment with oral nucleoside or nucleotide analogsliver transplantation provides the best hope for survival. Survival in adults is uncommon without transplantation; children tend to do better.
Viral hepatitis should be reported to the local or state health department.
Prevention of Acute Hepatitis B
Patients should be advised to avoid high-risk behavior (eg, sharing needles to inject drugs, having multiple sex partners).
Blood and other body fluids (eg, saliva, semen) are considered infectious. Spills should be cleaned up using dilute bleach. Barrier protection is recommended, but isolation of patients is of no value.
Posttransfusion infection is minimized by avoiding unnecessary transfusions and screening all donors for hepatitis B and C. Screening has decreased the incidence of posttransfusion hepatitis B and hepatitis C, which are now extremely rare in the United States.
Vaccination
(See also Hepatitis B [HepB] vaccine.)
Hepatitis B vaccination in endemic areas has dramatically reduced local prevalence.
Preexposure immunization has long been recommended for people at high risk. However, selective vaccination of high-risk groups in the United States and other nonendemic areas has not substantially decreased the incidence of HBV infection; thus, vaccination is now recommended for all US residents ≤ 18 years old beginning at birth (see Centers for Disease Control and Prevention [CDC]: Child and Adolescent Immunization Schedule by Age). Universal worldwide vaccination is desirable but is too expensive to be feasible.
Adults at high risk of HBV infection should be screened and vaccinated if they are not already immune or infected (see also the CDC's Adult Immunization Schedule). These high-risk groups include
Men who have sex with men
People with a sexually transmitted infection
People who are sexually active but not in mutually monogamous relationship
Health care and public safety workers potentially exposed to blood or other infectious body fluids
People who currently or have recently injected illicit drugs
People with end-stage kidney disease who receive dialysis or have HIV infection, chronic liver disease, or hepatitis C
Household contacts and sex partners of people who are HBsAg-positive
Clients and staff members of institutions and nonresidential day care facilities for people with developmental disabilities
People in correctional facilities or facilities providing services to injection-drug users
International travelers to regions with high or intermediate HBV endemicity
For people 60 years of age and older with diabetes, the decision to receive the HepB vaccine should be based on shared clinical decision-making.
Postexposure prophylaxis
For infants born to HBsAg-positive mothers, an initial dose of vaccine plus 0.5 mL of HBIG is given IM in the thigh immediately after birth.
For anyone having sexual contact with an HBsAg-positive person or percutaneous or mucous membrane exposure to HBsAg-positive blood, 0.06 mL/kg of HBIG is given IM within days, along with vaccine.
Any previously vaccinated patient sustaining a percutaneous HBsAg-positive exposure is tested for anti-HBs; if titers are < 10 mIU/mL, a booster dose of vaccine is given.
Key Points
Hepatitis B is often transmitted by parenteral contact with contaminated blood but can result from mucosal contact with other body fluids.
Diagnose by testing for hepatitis B surface antigen and other serologic markers.
Treat supportively.
Chronic infection develops in 5 to 10% of patients with acute hepatitis B and often leads to cirrhosis and/or hepatocellular carcinoma.
Routine vaccination beginning at birth is recommended for all.
Postexposure prophylaxis consists of HBIG and vaccine; HBIG probably does not prevent infection but may prevent or attenuate clinical hepatitis.
More Information
The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.
