Hepatitis B

Last updated: November 29, 2023

Summarytoggle arrow icon

Hepatitis B is a viral infection caused by the hepatitis B virus (HBV). It occurs worldwide and is transmitted sexually, parenterally, or vertically. After an incubation period of 1–6 months, most patients develop asymptomatic or mild inflammation of the liver, which usually resolves spontaneously within a few weeks or months. However, 5% of adult patients and 90% of infants infected perinatally develop chronic hepatitis B (CHB). Individuals with CHB may be asymptomatic carriers or develop ongoing hepatic inflammation with an increased risk of cirrhosis and hepatocellular carcinoma. Serologic testing initially includes measurement of hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), and hepatitis B core antibody (anti-HBc). A detectable serum anti‑HBs (indicating seroconversion) is a sign of recovery or successful immunization. CHB with persistent liver inflammation is characterized by detectable HBsAg and elevated HBV DNA and ALT. Treatment of acute hepatitis B consists of supportive measures. In patients with fulminant hepatitis, liver transplantation may be necessary. For chronic active hepatitis B, nucleoside or nucleotide analogs (e.g., tenofovir) are the preferred agents for reducing viral replication and infectivity. Prophylactic immunization with a recombinant vaccine is recommended for all age groups. Other preventive measures include postexposure prophylaxis for infants born to individuals with HBsAg positive or unknown status and for unvaccinated individuals with recent exposure to HBV.

See also “Acute liver failure.”

Epidemiologytoggle arrow icon

  • Prevalence: Following the introduction of the hepatitis B vaccine in 1991, rates of acute hepatitis B in the US have declined by approx. 82%. [1]
    • In 2016 there were an estimated 862,000 cases (∼ 0.3% of US population) in the US. [2][3]
    • In 2015, there were > 257 million cases worldwide (3.5% of the global population). [4]
    • The Western Pacific is the most affected region worldwide (6.2% of its population). [4]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon


Transmission [4]

Frequency and patterns of transmission vary worldwide.

Risk factors for HBV infection and groups at risk [6][7]

Pathophysiologytoggle arrow icon

Replication cycle of HBV [8][9][10]

HBV carries a DNA polymerase with both DNA and RNA-dependent functions, also known as reverse transcriptase (RT).

  1. After entering the host cell's nucleus, reverse transcriptase completes the positive strand of the virus's partially double-stranded relaxed circular DNA (rcDNA).
  2. The rcDNA is converted to covalently closed circular DNA (cccDNA) primarily by host enzymes in a process that is not entirely understood.
  3. The cccDNA is then transcribed into viral mRNA by host RNA polymerase.
  4. The viral mRNA leaves the nucleus and is translated into HBV core proteins and new reverse transcriptase in the cytoplasm.
  5. Viral mRNA and reverse transcriptase are packaged into a capsid, where viral mRNA is then reverse-transcribed into viral rcDNA.
  6. New viral DNA genomes are enveloped and leave the cell as progeny virions.

Acute infection [11]

Chronic infection [13]

Caused by viral persistence due to failing immune clearance, which promotes:

Clinical featurestoggle arrow icon

Acute hepatitis B virus infection

Acute HBV infection is defined as infection acquired in the past 6 months.

Chronic hepatitis B virus infection [15]

Chronic HBV infection is defined as infection persisting for more than 6 months with detection of HBsAg and, possibly, signs and symptoms of liver damage.

  • Most patients are inactive, noncontagious carriers. [17]
  • Potential reactivation of chronic inactive hepatitis can manifest variably in the following ways:
    • Asymptomatic
    • Unspecific symptoms
    • Similar to acute hepatitis
    • Hepatic failure
  • The younger when infected, the more likely a patient develops chronic HBV [18]
    • 90% of infants
    • ∼ 50% of children between 1 and 5 years
    • Only 5% of adults

Overview of HBV serologytoggle arrow icon

Overview of HBV antigens and their corresponding antibodies [5][19]
HBV antigen/DNA Description Corresponding antibodies

Hepatitis B surface antigen (HBsAg)

  • Protein on the surface of HBV
  • First evidence of infection [19]
  • Presence for ≥ 6 months indicates a chronic infection.

Hepatitis B core antigen (HBcAg)

  • Protein of the nucleocapsid
  • Not routinely measured in clinical practice
  • Anti‑HBc
    • Anti-HBc IgM: indicates recent infection with HBV (within ≤ 6 months) [5]
    • Anti-HBc IgG: indicates resolved or chronic infection

Hepatitis B e antigen (HBeAg) [20]

  • Protein secreted by infected hepatocytes into the bloodstream
  • Indicates active viral replication and thus high transmissibility and a poor prognosis
  • Anti‑HBe: indicates long-term clearance of HBV and thus low transmissibility

Screeningtoggle arrow icon

Indications for HBV screening [7][21][22]

Obtain initial HBV serology for the following individuals (see “Diagnostics” for interpretation of results):

Diagnosticstoggle arrow icon

Approach [22][25][26]

Suspected acute HBV infection

Chronic HBV infection

Patients with chronic hepatitis B infection require further evaluation to identify and manage risk factors for liver-related morbidity and to identify patients eligible for antiviral therapy.

HBV serology [7][22][26]

  • Indications
  • Initial tests ; [7][22][25]
  • Interpretation
  • Further disease markers: indicated to assess disease activity if initial tests are positive
    • HBeAg: marker of high HBV replication and transmissibility
    • Anti-HBe: An undetectable HBeAg with development of anti-HBe indicates immune clearance or an inactive carrier state.
    • HBV DNA: quantification of viral load

Interpretation of hepatitis B serology

Interpretation of hepatitis B serology [19][22][28]
HBsAg Anti-HBs Anti-HBc


Anti-HBe HBV DNA Transaminases
Acute infection Undetectable IgM Undetectable Undetectable or ↑ ↑ (ALT > AST)

Window period

Undetectable Undetectable IgM IgG Undetectable Undetectable or ↑ Undetectable or ↑ ↑ (ALT > AST)

Chronic infection

Active (high transmissibility)

Undetectable IgG Undetectable

HBV DNA > 2000 IU/mL

Normal or ↑

Inactive (low transmissibility)

Undetectable IgG


HBV DNA ≤ 2000 IU/mL Normal
Immunity Resolved infection Undetectable IgG Undetectable Undetectable Undetectable
HBV vaccination Undetectable Undetectable

HBeAg: BEware! Extremely infEctious.

During the window period, anti-HBc IgM and anti-HBe may be the only markers available to diagnose an acute HBV infection.

Seroconversion of HBsAg to anti‑HBs indicates resolution of acute hepatitis.

Additional laboratory studies [26][27]

Laboratory findings in chronic HBV infection are highly variable; liver function tests may be normal or only mildly abnormal.

Abdominal ultrasound [26][27][29]

Liver biopsy [27]

  • Indications
    • Diagnostic uncertainty when results will be used to guide treatment decisions
    • Exclusion of other possible causes of liver damage in chronic disease or severely affected individuals
    • Assessment of the severity of liver disease
  • Findings: See “Pathology of viral hepatitis.”

Pathologytoggle arrow icon

Active viral hepatitis [30][31]

Chronic viral hepatitis [30][31]

Ground glass hepatocytes are pathognomonic for HBV, whereas interface hepatitis, fibrous septa, and periportal infiltrates also occur in other types of chronic hepatitis.

Differential diagnosestoggle arrow icon

Differential diagnosis of viral hepatitis
Pathogen Hepatitis A virus (HAV) [34] Hepatitis B virus (HBV) [22] Hepatitis C virus (HCV) [35] Hepatitis D virus (HDV) [36] Hepatitis E virus (HEV) [37]
Route of transmission
  • Fecal-oral
  • Fecal-oral
Incubation period
  • 2–6 weeks
  • 1–6 months
  • 2 weeks–6 months
  • 2–8 weeks
Clinical features
Clinical course
  • 3 phases:
    1. Prodromal phase: ∼ 1-2 weeks
    2. Icteric phase: ∼ 2 weeks
    3. Resolution of symptoms: ∼ 2-4 weeks
  • Varies greatly across affected individuals
    • Asymptomatic in two thirds of cases
    • One third of individuals develop acute icteric hepatitis
  • Asymptomatic in 80% of cases
  • May manifest as acute hepatitis
  • Progression to chronic disease possible (previously asymptomatic individuals are especially affected)
Risk of chronification
  • No
  • Yes: risk increases with lower age of infection
  • Yes: high risk approx. 85% of affected individuals > 20 years will develop chronic HCV infection [39]
  • Yes: depends on type of infection [40]


Extrahepatic manifestations [43]
  • See extrahepatic manifestations of hepatitis B
  • Supportive
  • Not available
  • Not available
  • Full recovery within ∼ 3 months
  • Usually resolves after a few weeks, but can last up to 6 months
  • If symptoms persist for > 6 months, HBV infection is considered chronic.
  • Usually resolves after a few weeks, but can last up to 6 months
  • Without proper treatment, most infected individuals will develop chronic hepatitis C.
  • With proper treatment, > 90% are cured. [45]
  • See HBP prognosis
  • Superinfection is associated with a poor prognosis.
  • Usually resolves within ∼ 3 months on its own without complications

Vowels (A and E) are bowels (transmitted fecal-orally) and usually only cause AcutE hepatitis.

Recovery rates of hepatitis B infection in adults are very good, with less than 5% of cases progressing to chronic infection. In contrast, the risk of developing chronic hepatitis is considerably higher in infants infected perinatally (90%) and young children (20–50%).

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

Approach [22][26][27][28]

Most acute hepatitis B infections in adults are self-limited. Antiviral therapy is not routinely indicated.

Antiviral therapy for chronic hepatitis B [22][26][27]

Treatment decisions should be made by a specialist and based on the risk of liver-related morbidity and mortality. The following information applies to nonpregnant individuals; for pregnant individuals, see “Management of hepatitis B in pregnancy.”

Treatment goals include immunologic cure (i.e., clearance of HBsAg and sustained HBV DNA suppression) and reduction of liver-related morbidity and mortality.

Pegylated interferon is a pregnancy category C drug, and is contraindicated in patients who have decompensated cirrhosis or uncontrolled psychiatric conditions.

Supportive care and patient education

HBV can survive outside the body (e.g., in dried blood on a surface) for at least 7 days, and remains infectious during that time. [5]

Complicationstoggle arrow icon

Hepatitis D virus infection [47][48]

Remember the 3 D's of hepatitis D: Defective Deltavirus Dependent on HBV HBsAg coat for entry.

Acute liver failure

Long-term complications of hepatitis B [15]

We list the most important complications. The selection is not exhaustive.

Preventiontoggle arrow icon

Vaccination [5][52]

Infants and children who did not receive a dose of vaccine at birth should receive the first dose as soon as possible.

Hepatitis B postvaccination serology [5][24]



In infants, do not check postvaccination serology until they are least 9 months of age and their last HBV vaccine dose was at least 1 month ago. [55]

Follow up

Hepatitis B postexposure prophylaxis [5]

For perinatal postexposure prophylaxis recommendations, see “Infants born to individuals with HBsAg positive or unknown status.”

Occupational exposure (i.e., health care providers)

HBV PEP for occupational exposure [5]
HCP vaccination status Source patient
HBsAg negative HBsAg positive or unknown
Complete series Anti-HBs ≥ 10 mIU/mL
  • No intervention required
Anti-HBs < 10 mIU/mL
  • Administer 1 dose of HBV vaccine, PLUS 1 dose of HBIG, simultaneously at two different anatomical sites. For a known HBV vaccine nonresponder, administer 2 doses of HBIG 1 month apart.
  • Complete vaccine series, and measure anti-HBs 1–2 months after the final dose.
  • Test for HBV infection: Measure anti-HBc immediately and repeat anti-HBc PLUS HBsAg in 6 months.

Unvaccinated or incomplete series

Modification of work duties and sexual practices of HCPs following exposure to a patient with a positive or unknown HBsAg status is unnecessary during the 6-month follow-up period. Pregnancy and breastfeeding are safe during this time. [5]

HCPs exposed to a patient with a positive or unknown HBsAg status should not donate blood products, organs, tissue, and/or semen during the 6-month follow-up period. [5]

Nonoccupational exposure

  • Exposure types include needle sharing and high-risk sexual contact.
  • Obtain vaccination history and measure HBsAg, anti-HBs, and anti-HBc in unvaccinated exposed patients.
  • Do not withhold or delay vaccination for prevaccination testing.
HBV PEP following nonoccupational exposure [5][57]
Patient vaccination status Source individual
HBsAg unknown HBsAg positive
Complete series Anti-HBs ≥ 10 mIU/mL
  • No intervention required
Anti-HBs < 10 mIU/mL or unknown
  • No intervention required
Unvaccinated or incomplete series
  • Administer 1 dose of HBV vaccine PLUS 1 dose of HBIG, simultaneously at two different anatomical sites.
  • Complete vaccine series.

Perinatal hepatitis Btoggle arrow icon

Approach [5][7][58]

Hepatitis B in pregnancy [22][27][58]

The prevalence of HBV infection in pregnant individuals in the US is 0.9%. [59]

Screening for HBV infection in pregnancy [7][23][58]


Further management

Management of HBV infection in pregnancy [60][61]

During pregnancy

Antiviral treatment is recommended in pregnant individuals with an HBV viral load > 200,000 IU/mL to reduce the risk of vertical transmission. [58]

Pegylated interferon alfa is a pregnancy category C drug and is therefore not recommended as first-line therapy for HBV infection in pregnant individuals. [61]

During delivery

After delivery

  • Breastfeeding may be started immediately if there are no contraindications (e.g., cracked or bleeding nipples), regardless of whether individuals:
  • Continue close monitoring (e.g., of HBV DNA and ALT levels) for at least 6 months postpartum. [60]

Hepatitis B in infants [5][24][58]

Management of infants born to individuals with HBsAg positive or unknown status

These infants are at risk of acquiring perinatal HBV infection and developing complications.

  • Administer the birth dose of HBV vaccine to all infants within 12 hours of life.
  • If the birthing parent's HBsAg status is unknown, obtain test immediately.
  • Determine the need for HBIG.
    • This depends on the birthing parent's HBsAg status and infant's birth weight (see table).
    • If HBIG and HBV vaccine are administered concurrently, they should be given in different limbs.
  • Report case to state and local perinatal hepatitis B prevention programs (see “Tips and Links”).
Management of infants born to HBsAg-positive and HBsAg-unknown individuals [5][24][58]
Status of birthing parent at delivery HBIG [24] HBV vaccine
HBsAg-positive or other evidence of HBV infection
  • Within 12 hours of birth
HBsAg-unknown < 2000 g birth weight
  • Within 12 hours of birth, unless the birthing parent's HBsAg is confirmed negative
≥ 2000 g birth weight
  • Wait for results of birthing parent's HBsAg testing.
    • If negative: not indicated
    • If positive or remains unknown: Administer within 7 days of birth or at hospital discharge (whichever occurs first)

Infants born to HBsAg-positive individuals should receive 1 dose of HBIG and the first dose of HBV vaccine within 12 hours of birth. [5][24]

If birth weight is < 2000 g, the dose of HBV vaccine given at birth does not count towards the vaccine series. [5]

Infants with HBV infection

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