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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jolanta Marszalek, M.D. [2], Sara Mehrsefat, M.D. [3]

Overview

The first descriptions of hepatitis (epidemic jaundice), recorded in the 5th century BCE, are generally attributed to Hippocrates.[1] In 1885, the earliest identifiable occurrence of hepatitis B virus was documented by Lurman.[2] In 1947, the current nomenclature of hepatitis A (so-called infectious hepatitis) and hepatitis B (so-called serum hepatitis) was proposed by MacCallum and Bauer. Throughout the 20th century, advancements in the recognition, isolation, classification, and prevention of hepatitis B were achieved. Today, the focus around HBV remains on the spread of awareness and prevention across the world, especially in endemic areas that would benefit greatly from immunization programs.[3][4]

Historical Perspective

Early History

  • The first descriptions of hepatitis (epidemic jaundice), recorded in the 5th century BCE, are generally attributed to Hippocrates.[1]
  • In 1885, the earliest identifiable occurrence of hepatitis B virus was documented by Lurman. Lurman's paper, which is regarded as a classic example of an epidemiological study, definitively identified contaminated lymph as the source of hepatitis outbreak.[2] Lurman described a form of hepatitis that was transmitted by direct inoculation of blood or blood products during a smallpox outbreak in Bremen, Germany. Thousands of shipyard employees were vaccinated against smallpox with a preparation made from human lymph. Between several weeks and 8 months later, 15% of the workers became ill with jaundice, while unvaccinated workers remained healthy.[3]
  • During the early 20th century, similar outbreaks of jaundice occurring after longer incubation periods were documented in clinics treating patients with syphilis, diabetes, and tuberculosis.[3]
  • In the 1920s, reports from clinics in Germany and the United States referred to the treatment of syphilis with intravenous therapy.[5] At the time, the so-called "salvarsan icterus" was thought to be a direct effect of the treatment for syphilis, rather than an artifact of the use of contaminated needles and syringes.
  • In 1926, Flaum, Malmros, and Persson published a paper on the role of syringes and needles in the transmission of the disease, in which they documented the distinctive incubation period of the infection compared to the so-called spontaneous catarrhal jaundice (now known as Hepatitis A). In their paper, they introduced the possibility that two different viruses might cause hepatitis.[5] Further evidence supporting the notion of the existence of at least two separate etiological agents causing hepatitis came during World War II, when jaundice epidemics were clearly distinguished among United States military personnel based on differences in transmission and incubation periods.[2]
  • In 1947, the current nomenclature of hepatitis A (so-called infectious hepatitis) and hepatitis B (so-called serum hepatitis) was proposed by MacCallum and Bauer. By this time, it was already known that in comparison with hepatitis A, hepatitis B:[3]
    • Was transmitted by percutaneous exposure to blood products
    • Had a longer incubation period (2-6 months)
    • Occurred more often in adults
  • In the 1960’s and 1970’s, Krugman et al. performed studies confirming these previously observed differences as well as the occurrence of homologous immunity after infection with hepatitis B.[5]
  • In 1965, the hepatitis B virus was discovered by Baruch Blumberg. He identified the Australia antigen (later known to be hepatitis B surface antigen or HBsAg) in blood collected from Australian aborigines.[6] In 1970, the virus particle was identified with electron microscopy by D.S. Dane et al.[7]
  • In 1970, the virus particle was identified with electron microscopy by D.S. Dane et al.[7]
  • In 1972, hepatitis B virus was classified into four subtypes: adr, adw, ayr, and yaw. This initial classification was based on the envelope protein of the virus. The four subtypes were noted to have different geographical distributions, which helped trace the route of infections.[8][9]

Discovery and Vaccine

  • By the early 1980s the genome of the hepatitis B virus had been sequenced.
  • Since 1982, a vaccine against hepatitis B has been available.[6]
  • Recent discoveries have allowed hepatitis B virus to be classified not only according to serotype, but according to genotype. Today, HBV is classified into ten genotypes (A-J) according to the variation of the nucleotide sequence of the genome.[10]

Global Health

  • In 1992, the Global Advisory Group to the World Health Organization (WHO) recommended that hepatitis B vaccine be incorporated into national immunization programs in all countries by 1997.
  • Since 2007, World Hepatitis Day has taken place on July 28. The intention of the day is to raise global awareness of hepatitis B and hepatitis C and encourage prevention, diagnosis, and treatment. It has been led by the World Hepatitis Alliance.
  • On May 2010, the World Hepatitis Alliance received global endorsement from the World Health Organization.[11]

References

  1. 1.0 1.1 Center for Disease Control and Prevention.Epidemiology and Prevention of Vaccine Preventable Diseases 2012. http://www.cdc.gov/vaccines/pubs/pinkbook/hepa.html
  2. 2.0 2.1 2.2 Hussey, Hugh H. (1981). "The Hepatitis B Saga". JAMA: The Journal of the American Medical Association. 245 (13): 1317. doi:10.1001/jama.1981.03310380021018. ISSN 0098-7484.
  3. 3.0 3.1 3.2 3.3 Mahoney FJ (1999). "Update on diagnosis, management, and prevention of hepatitis B virus infection". Clin Microbiol Rev. 12 (2): 351–66. PMC 88921. PMID 10194463.
  4. Neefe, John R., Sydney S. Gellis, and Joseph Stokes. "Homologous serum hepatitis and infectious (epidemic) hepatitis: Studies in volunteers bearing on immunological and other characteristics of the etiological agents." The American journal of medicine 1.1 (1946): 3-22.
  5. 5.0 5.1 5.2 "Evolution of Concepts of Hepatitis".
  6. 6.0 6.1 Alter HJ, Blumberg BS (1966). "Further studies on a "new" human isoprecipitin system (Australia antigen)". Blood. 27 (3): 297–309. PMID 5930797. Retrieved 2012-02-08. Unknown parameter |month= ignored (help)
  7. 7.0 7.1 Dane DS, Cameron CH, Briggs M (1970). "Virus-like particles in serum of patients with Australia-antigen-associated hepatitis". Lancet. 1 (7649): 695–8. PMID 4190997. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  8. Mazzur S, Burgert S, Blumberg BS (1974). "Geographical distribution of Australia antigen determinants d, y and w." Nature. 247 (5435): 38–40. PMID 4128782.
  9. Yamanaka T, Akahane Y, Suzuki H, Okamoto H, Tsuda F, Miyakawa Y; et al. (1990). "Hepatitis B surface antigen particles with all four subtypic determinants: point mutations of hepatitis B virus DNA inducing phenotypic changes or double infection with viruses of different subtypes". Mol Immunol. 27 (5): 443–9. PMID 1694959.
  10. Enomoto M, Tamori A, Nishiguchi S (2006). "Hepatitis B virus genotypes and response to antiviral therapy". Clin Lab. 52 (1–2): 43–7. PMID 16506363.
  11. World Health Organization. Viral hepatitis (2010). http://apps.who.int/gb/ebwha/pdf_files/EB126/B126_R16-en.pdf Accessed on October 5th, 2016


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