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Hepatitis B

Last updated: October 8, 2021

Summarytoggle arrow icon

Hepatitis B is a viral infection caused by the hepatitis B virus (HBV), which occurs worldwide and can be transmitted sexually, parenterally, or perinatally. 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 all adult patients and 90% of infants born to a hepatitis B-positive mother develop chronic hepatitis. Chronically infected individuals may be asymptomatic carriers or develop ongoing hepatic inflammation with an increased risk of liver cirrhosis and hepatocellular carcinoma. Serologic testing, which is decisive for diagnosing HBV, initially involves measurement of HBs antigen. An increase in serum anti‑HBs (indicating seroconversion) is a sign of recovery or successful immunization. Chronic hepatitis with persistent liver inflammation is characterized by persistently elevated HBs antigen, HBV DNA, and transaminase levels. Treatment of acute hepatitis B consists of supportive measures. In the case of fulminant hepatitis, liver transplantation may be necessary. For chronic hepatitis B, pegylated interferon alpha and nucleoside/nucleotide analogues (e.g., tenofovir) are used to reduce viral replication and infectivity. Prophylactic immunization with a recombinant vaccine is recommended for all age groups. Other preventative measures include postexposure prophylaxis for newborns of hepatitis B-positive mothers and unvaccinated individuals with recent exposure to those who are hepatitis B-positive.

See also “Acute liver failure.”

  • 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.

Virus

Transmission [4]

Frequency and patterns of transmission vary worldwide. The following routes of transmission are possible and put a number of different groups at high risk for HBV infection:

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:

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
      • Fatigue, malaise
      • Nausea, poor appetite
      • Unspecific abdominal pain
    • 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

Diagnostically relevant virus antigens, DNA, and antibodies [19]

Overview of HBV antigens and their corresponding antibodies
HBV antigen/DNA Description Corresponding antibodies

Hepatitis B surface antigen (HBsAg)
  • Protein on the surface of HBV
  • First evidence of infection
  • Continued presence indicates a carrier state

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 (≤ 6 months)
    • Anti-HBc IgG: indicates resolved or chronic infection

Hepatitis B envelope antigen (HBeAg)
  • 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

HBV DNA
  • N/A

Hepatitis B serology

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

HBeAg

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

Window period

 undetectable undetectable undetectable undetectable or ↑ ↑ IgM, followed by ↑ IgG undetectable or ↑ ↑ (ALT > AST)
Resolved prior infection undetectable ↑ undetectable ↑ ↑ IgG undetectable undetectable

Virus persistence (chronic infection)

Active chronic infection (high transmissibility)

↑ undetectable ↑ undetectable ↑ IgG

HBV DNA > 2000 IU/mL

 Normal or ↑

Inactive chronic infection (low transmissibility)

 ↑ undetectable

undetectable

 ↑ ↑ IgG HBV DNA ≤ 2000 IU/mL Normal
Vaccination undetectable ↑ undetectable undetectable undetectable undetectable undetectable

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

HBEAg indicates highly Enfectious.

Testing algorithm

  1. Screening: measure HBsAg : and anti‑HBc IgM
  2. If HBsAg is positive: measure HBeAg: and HBV DNA to determine transmissibility

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 immune clearance of HBV.

Additional tests

Laboratory studies

Abdominal ultrasound [20]

Liver biopsy

  • A biopsy is indicated in the following cases:
    • Diagnosis is uncertain.
    • Exclusion of other possible causes of liver damage in chronic disease or severely affected individuals
    • Assessment of disease severity in patients with active chronic liver disease (i.e., ↑ AST/ALT and detectable levels of HBV DNA)
  • See “Pathology” below.

Test of common coinfections [21][22]

Coinfection with hepatitis C, hepatitis D, syphilis, and HIV is common and should be tested for accordingly.

Active viral hepatitis [23][24]

Chronic viral hepatitis [23][24]

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

Differential diagnosis of viral hepatitis
Pathogen Hepatitis A virus (HAV) [27] Hepatitis B virus (HBV) [28] Hepatitis C virus (HCV) [29] Hepatitis D virus (HDV) [30] Hepatitis E virus (HEV) [31]
Route of transmission
  • Fecal-oral
  • Fecal-oral
Incubation period
  • 2–6 weeks
  • 1–6 months
  • 2 weeks–6 months
  • 2–8 weeks
Clinical features
  • May be asymptomatic (especially children)
  • Fever, malaise
  • Loss of appetite, nausea, vomiting, change in bowel habits
  • RUQ pain, tender hepatomegaly, jaundice
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 [33]
  • Yes: depends on type of infection [34]

Serology
  • Anti-HEV IgM: active infection
  • Anti-HEV IgG: past detection
  • HEV RNA PCR
Extrahepatic manifestations [37]
Treatment
  • Supportive
Immunization
  • Not available
  • Not available
Prognosis
  • 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. [39]
  • 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.

Lifestyle changes

Antiviral treatment

Acute hepatitis B

  • Pharmacological treatment is generally not indicated, and supportive care suffices.
  • For treatment of acute liver failure, see “Complications” below. [28]

Chronic hepatitis B [28]

Liver transplantation indications

Special populations [28]

Treatment of HBV in special patient groups
Patient group Substances Guidance statements
Coinfection with HIV
Coinfection with hepatitis C
  • HCV DAA therapy may increase HBV DNA levels in HBsAg-positive individuals (HBV DNA levels should be closely monitored during treatment)
  • HBV antiviral therapy and hepatitis C DAA therapy should be started concurrently.
Coinfection with hepatitis D
Hepatitis B in pregnancy
  • Maternal screening (HBsAg) for all women at the first prenatal visit
  • HBsAg-positive pregnant women
    • Should receive additional testing
    • Indication for antiviral treatment should be evaluated
  • Initiate therapy if ≥ 1 of the following criteria are met:
  • Spontaneous vaginal delivery is safe. [43]
  • Breastfeeding is safe. [43]
  • HBV-infected newborns should receive 1 dose of HBIG and first shot of hepatitis B vaccine within 12 hours of birth. [44]

Hepatitis D virus infection [45][46]

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

Acute hepatic failure

Long-term complications of hepatitis B [15]

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

Screening [2]

  • The CDC recommends screening for the following population groups:
  • Individuals who test positive should be provided with counseling and referral to a medical specialist that can conduct a thorough clinical evaluation and provide appropriate care.

Hepatitis B preexposure prophylaxis

General lifestyle measures [51]

  • Regular, thorough hand-washing
  • Condom use
  • Covering wounds and cuts carefully to minimize the risk of contact.
  • Cleaning up spilled possibly infectious blood with a mixture of water and bleach solution (9 parts water, 1 part bleach)
  • Avoiding illegal street drugs (especially IV drugs) or making sure to use new, fresh, sterile equipment
  • Making sure that procedures like body piercings, tattoos, and acupuncture are done with sterile needles
  • Not sharing sharp items such as razors, toothbrushes, nail clippers, and earrings or body rings
  • Discarding tampons and sanitary napkins into plastic bags

Recommendations for active hepatitis B immunization [7]

Hepatitis B postexposure prophylaxis [7]

Exposure is defined as percutaneous or mucosal contact with blood or body fluids.

Administration

PEP recommendations differ for HBV exposure in health care personnel (HCP) and general population.

  • HCP
    • Completely vaccinated individuals with documented response do not require any intervention.
    • Unvaccinated/partly vaccinated individuals will receive 1 dose of HBIG and active immunization if exposed to bodily fluids of a patient with unknown or positive HBsAg status.
    • A completely vaccinated HCP with unknown response and patient should receive postexposure testing, regardless of source patient HBsAg status.
  • General population
    • Completely vaccinated individuals with documented response do not require any intervention.
    • Previously vaccinated and unvaccinated individuals should receive active immunization if exposed to a source with unknown HBsAg status.
    • When source is HBsAg positive, exposed unvaccinated/previously vaccinated individuals should receive full vaccine series with simultaneous administration of HBIG.
  1. Daniels D, Grytdal S, Wasley A, Centers for Disease Control and Prevention (CDC).. Surveillance for acute viral hepatitis - United States, 2007.. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002). 2009; 58 (3): p.1-27.
  2. Hepatitis B Questions and Answers for Health Professionals. https://www.cdc.gov/hepatitis/hbv/hbvfaq.htm#overview. Updated: March 16, 2020. Accessed: July 23, 2020.
  3. Hyun Kim B, Ray Kim W. Epidemiology of Hepatitis B Virus Infection in the United States. Clinical Liver Disease. 2018; 12 (1): p.1-4. doi: 10.1002/cld.732 . | Open in Read by QxMD
  4. Hepatitis B. http://www.who.int/mediacentre/factsheets/fs204/en/. Updated: July 1, 2016. Accessed: March 25, 2017.
  5. Teo EK, SF Lok ASF. Epidemiology, Transmission, and Prevention of Hepatitis B Virus Infection. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/epidemiology-transmission-and-prevention-of-hepatitis-b-virus-infection.Last updated: October 31, 2016. Accessed: March 25, 2017.
  6. Exposure to Blood - What Healthcare Personnel Need to Know.
  7. Schillie S, Vellozzi C, Reingold A, et al. Prevention of Hepatitis B Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices. MMWR. Recommendations and Reports. 2018; 67 (1): p.1-31. doi: 10.15585/mmwr.rr6701a1 . | Open in Read by QxMD
  8. Köck J, Schlicht HJ. Analysis of the earliest steps of hepadnavirus replication: genome repair after infectious entry into hepatocytes does not depend on viral polymerase activity.. J Virol. 1993; 67 (8): p.4867-74.
  9. Datta S, Chatterjee S, Veer V, Chakravarty R. Molecular Biology of the Hepatitis B Virus for Clinicians. Journal of Clinical and Experimental Hepatology. 2012; 2 (4): p.353-365. doi: 10.1016/j.jceh.2012.10.003 . | Open in Read by QxMD
  10. Urban S, Schulze A, Dandri M, Petersen J. The replication cycle of hepatitis B virus. J Hepatol. 2009; 52 (2): p.282-284. doi: 10.1016/j.jhep.2009.10.031 . | Open in Read by QxMD
  11. Beck J, Nassal M. Hepatitis B virus replication. World J Gastroenterol. 2007; 13 (1): p.48-64.
  12. Balmasova IP. Immunopathogenesis of chronic hepatitis B. World Journal of Gastroenterology. 2014; 20 (39): p.14156. doi: 10.3748/wjg.v20.i39.14156 . | Open in Read by QxMD
  13. Hai H, Tamori A, Kawada N. Role of hepatitis B virus DNA integration in human hepatocarcinogenesis. World J Gastroenterol. 2014; 20 (20): p.6236-43. doi: 10.3748/wjg.v20.i20.6236 . | Open in Read by QxMD
  14. Burns GS, Thompson AJ. Viral Hepatitis B: Clinical and Epidemiological Characteristics. Cold Spring Harbor Perspectives in Medicine. 2014; 4 (12): p.a024935-a024935. doi: 10.1101/cshperspect.a024935 . | Open in Read by QxMD
  15. Lok ASF. Clinical Manifestations and Natural History of Hepatitis B Virus Infection. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/clinical-manifestations-and-natural-history-of-hepatitis-b-virus-infection.Last updated: May 4, 2015. Accessed: March 25, 2017.
  16. Wener MH. Serum Sickness and Serum Sickness-Like Reactions. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/serum-sickness-and-serum-sickness-like-reactions.Last updated: October 19, 2015. Accessed: February 16, 2017.
  17. Sharma SK, Saini N, Chwla Y. Hepatitis B virus: inactive carriers. Virol J. 2005; 2 : p.82. doi: 10.1186/1743-422X-2-82 . | Open in Read by QxMD
  18. Fattovich G, Bortolotti F, Donato F. Natural history of chronic hepatitis B: Special emphasis on disease progression and prognostic factors. J Hepatol. 2008; 48 (2): p.335-352. doi: 10.1016/j.jhep.2007.11.011 . | Open in Read by QxMD
  19. Epidemiology and Prevention of Vaccine-Preventable Diseases - Hepatitis B.
  20. Kurtz AB, Rubin CS, Cooper HS, et al. Ultrasound findings in hepatitis. Radiology. 1980; 136 (3): p.717-723. doi: 10.1148/radiology.136.3.7403553 . | Open in Read by QxMD
  21. 2014 Sexually Transmitted Diseases Surveillance: Chlamydia. https://www.cdc.gov/std/stats14/chlamydia.htm. Updated: November 17, 2015. Accessed: September 25, 2016.
  22. Marrazzo J. Clinical manifestations and diagnosis of Chlamydia trachomatis infections. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-chlamydia-trachomatis-infections?source=machineLearning&search=chlamydia&selectedTitle=2%7E150&anchor=H22688563§ionRank=3#H22688563.Last updated: November 5, 2015. Accessed: September 5, 2016.
  23. Rubin E, Reisner HM. Essentials of Rubin's Pathology. Lippincott Williams & Wilkins ; 2009
  24. Ferrell L. Liver pathology: cirrhosis, hepatitis, and primary liver tumors: Update and diagnostic problems. Mod Pathol. 2000; 13 (6): p.679-704. doi: 10.1038/modpathol.3880119 . | Open in Read by QxMD
  25. Liver and Intrahepatic Bile Ducts - Nontumor - Hepatitis (Acute and Chronic) - Chronic Hepatitis - General. http://www.pathologyoutlines.com/topic/liverchronichepgeneral.html. Updated: October 31, 2017. Accessed: April 6, 2018.
  26. Cohen C. "Ground-glass" hepatocytes. S Afr Med J. 1975; 49 (34): p.1401-1403.
  27. Hepatitis A and the Vaccine (Shot) to Prevent It. https://www.cdc.gov/vaccines/parents/diseases/child/hepa.html. Updated: November 10, 2014. Accessed: March 25, 2017.
  28. Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Hepatology. 2018; 67 (4): p.1560-1599. doi: 10.1002/hep.29800 . | Open in Read by QxMD
  29. Ghany MG, Morgan TR. Hepatitis C Guidance 2019 Update: American Association for the Study of Liver Diseases–Infectious Diseases Society of America Recommendations for Testing, Managing, and Treating Hepatitis C Virus Infection. Hepatology. 2020; 71 (2): p.686-721. doi: 10.1002/hep.31060 . | Open in Read by QxMD
  30. Hepatitis D Infection Fact Sheet. http://www.health.state.mn.us/divs/idepc/diseases/hepatitis/hepdfact.html. Updated: March 25, 2017. Accessed: March 25, 2017.
  31. Kamar N, Izopet J, Dalton HR. Chronic Hepatitis E Virus Infection and Treatment. Journal of Clinical and Experimental Hepatology. 2014; 3 (2): p.134-140. doi: 10.1016/j.jceh.2013.05.003 . | Open in Read by QxMD
  32. Negro F. Hepatitis D Virus Coinfection and Superinfection. Cold Spring Harbor Perspectives in Medicine. 2014; 4 (11): p.a021550-a021550. doi: 10.1101/cshperspect.a021550 . | Open in Read by QxMD
  33. Jafri S, Gordon SC. Epidemiology of Hepatitis C. Clinical Liver Disease. 2018; 12 (5): p.140-142. doi: 10.1002/cld.783 . | Open in Read by QxMD
  34. Farci P, Niro G. Clinical Features of Hepatitis D. Semin Liver Dis. 2012; 32 (03): p.228-236. doi: 10.1055/s-0032-1323628 . | Open in Read by QxMD
  35. Wedemeyer H, Pischke S, Manns MP. Pathogenesis and Treatment of Hepatitis E Virus Infection. Gastroenterology. 2012; 142 (6): p.1388-1397.e1. doi: 10.1053/j.gastro.2012.02.014 . | Open in Read by QxMD
  36. Choi M, Hofmann J, Köhler A, et al. Prevalence and Clinical Correlates of Chronic Hepatitis E Infection in German Renal Transplant Recipients With Elevated Liver Enzymes. Transplantation Direct. 2018; 4 (2): p.e341. doi: 10.1097/txd.0000000000000758 . | Open in Read by QxMD
  37. Amarapurkar DN, Amarapurkar AD. Extrahepatic manifestations of viral hepatitis. Annals of Hepatology. 2002; 1 (4): p.192-195. doi: 10.1016/s1665-2681(19)32165-9 . | Open in Read by QxMD
  38. Guillevin L, Mahr A, Callard P, et al. Hepatitis B Virus-Associated Polyarteritis Nodosa. Medicine. 2005; 84 (5): p.313-322. doi: 10.1097/01.md.0000180792.80212.5e . | Open in Read by QxMD
  39. HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. https://www.hcvguidelines.org/sites/default/files/full-guidance-pdf/AASLD-IDSA_HCVGuidance_August_27_2020.pdf. Updated: August 27, 2020. Accessed: December 3, 2020.
  40. El- Kader SMA, Al-Dahr MHS. Impact of weight reduction program on serum alanine aminotransferase activity and immunologic response in obese hepatitis B patients. Afr Health Sci. 2016; 16 (1): p.128. doi: 10.4314/ahs.v16i1.17 . | Open in Read by QxMD
  41. Lok ASF. Standard and Pegylated Interferon for Chronic Hepatitis B Virus Infection. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/standard-and-pegylated-interferon-for-chronic-hepatitis-b-virus-infection.Last updated: November 28, 2016. Accessed: March 25, 2017.
  42. Davoodi L, Masoum B, Moosazadeh M, Jafarpour H, Haghshenas M, Mousavi T. Psychiatric side effects of pegylated interferon‑α and ribavirin therapy in Iranian patients with chronic hepatitis C: A meta‑analysis. Experimental and Therapeutic Medicine. 2018 . doi: 10.3892/etm.2018.6255 . | Open in Read by QxMD
  43. Hepatitis B and Hepatitis C in Pregnancy. https://www.acog.org/patient-resources/faqs/pregnancy/hepatitis-b-and-hepatitis-c-in-pregnancy. Updated: September 1, 2019. Accessed: August 12, 2020.
  44. Lee C, Gong Y, Brok J, Boxall EH, Gluud C. Effect of hepatitis B immunisation in newborn infants of mothers positive for hepatitis B surface antigen: systematic review and meta-analysis. BMJ. 2006; 332 (7537): p.328-336. doi: 10.1136/bmj.38719.435833.7c . | Open in Read by QxMD
  45. Review of Pathology of the Liver: Viral Hepatitis D.
  46. Hepatitis D. http://www.who.int/mediacentre/factsheets/hepatitis-d/en/. Updated: July 1, 2017. Accessed: April 6, 2018.
  47. Manka P, Verheyen J, Gerken G, Canbay A. Liver Failure due to Acute Viral Hepatitis (A-E). Visceral Medicine. 2016; 32 (2): p.80-85. doi: 10.1159/000444915 . | Open in Read by QxMD
  48. Xie Y. Hepatitis B virus-associated hepatocellular carcinoma. Springer Singapore ; 2017 : p. 11-21
  49. Cacoub P, Terrier B. Hepatitis B-Related Autoimmune Manifestations. Rheumatic Disease Clinics of North America. 2009; 35 (1): p.125-137. doi: 10.1016/j.rdc.2009.03.006 . | Open in Read by QxMD
  50. Epidemiological estimates of viral hepatitis. https://www.who.int/westernpacific/health-topics/hepatitis/regional-hepatitis-data. Updated: July 23, 2018. Accessed: July 23, 2020.
  51. Prevention Tips for Hepatitis B. https://www.hepb.org/prevention-and-diagnosis/prevention-tips/. . Accessed: July 27, 2020.
  52. Patel DM, Butler J, Feldman S, Graves GR, Rhodes PG. Immunogenicity of hepatitis B vaccine in healthy very low birth weight infants. J Pediatr. 1997; 131 (4): p.641-643. doi: 10.1016/s0022-3476(97)70078-7 . | Open in Read by QxMD
  53. Herold G. Internal Medicine. Herold G ; 2014
  54. Hepatitis E FAQs for Health Professionals. https://www.cdc.gov/hepatitis/hev/hevfaq.htm. Updated: May 31, 2015. Accessed: March 24, 2017.
  55. Franco E. Hepatitis A: Epidemiology and prevention in developing countries. World Journal of Hepatology. 2012; 4 (3): p.68. doi: 10.4254/wjh.v4.i3.68 . | Open in Read by QxMD
  56. MacLachlan JH, Cowie BC. Hepatitis B Virus Epidemiology. Cold Spring Harbor Perspectives in Medicine. 2015; 5 (5): p.a021410-a021410. doi: 10.1101/cshperspect.a021410 . | Open in Read by QxMD
  57. Mirazo S, Ramos N, Mainardi V, Arbiza J, Gerona S. Transmission, diagnosis, and management of hepatitis E: an update. Hepatic Medicine: Evidence and Research. 2014 : p.45. doi: 10.2147/hmer.s63417 . | Open in Read by QxMD
  58. Matheny SC, Kingery JE. Hepatitis A.. Am Fam Physician. 2012; 86 (11): p.1027-34; quiz 1010-2.
  59. Guan R, Lui HF. Treatment of Hepatitis B in Decompensated Liver Cirrhosis. International Journal of Hepatology. 2011; 2011 : p.1-11. doi: 10.4061/2011/918017 . | Open in Read by QxMD
  60. Harris AM, Iqbal K, Schillie S, et al. Increases in Acute Hepatitis B Virus Infections — Kentucky, Tennessee, and West Virginia, 2006–2013. MMWR Morb Mortal Wkly Rep. 2016; 65 (3): p.47-50. doi: 10.15585/mmwr.mm6503a2 . | Open in Read by QxMD
  61. Surveillance for Viral Hepatitis – United States, 2017. https://www.cdc.gov/hepatitis/statistics/2017surveillance/index.htm. Updated: November 14, 2019. Accessed: July 28, 2020.