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hepatitis B

 
American Heritage Dictionary:

hepatitis B

Home > Library > Literature & Language > Dictionary

n.
An infection of the liver that is caused by a DNA virus, is transmitted by contaminated blood or blood derivatives in transfusions, by sexual contact with an infected person, or by the use of contaminated needles and instruments. The disease has a long incubation and symptoms that may become severe or chronic, causing serious damage to the liver. Also called serum hepatitis.


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Gale Encyclopedia of Children's Health:

Hepatitis B

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Definition

Hepatitis B is a liver disease caused by the hepatitis B virus (HBV).

Description

Hepatitis B is a form of viral hepatitis that is also known as serum hepatitis, due to its ability to be spread through body fluids and blood. HBV can cause lifelong infection, cirrhosis (scarring) of the liver, liver cancer, liver failure, and death. Hepatitis B is a more severe liver disease than hepatitis A, and asymptomatic infections occur frequently. Chronic hepatitis B infection may take one of two forms: chronic persistent hepatitis, a condition characterized by persistence of the virus but in which liver damage is minimal; and chronic active hepatitis, in which there is aggressive destruction of liver tissue and rapid progression to cirrhosis or liver failure.

Transmission

Transmission of HBV occurs through blood and body fluid exposure such as blood, semen, vaginal secretions, or saliva. Hepatitis B is not spread through food or water or by casual contact. Infants may also develop the disease if they are born to a mother who has the virus. Infected children often spread the virus to other children if there is frequent contact or a child has many scrapes or cuts. The common modes of transmission of hepatitis B are as follows:

  • children born to mothers who have hepatitis B (the illness may present up to five years after the child is born)
  • children who are born to mothers who have emigrated from a country where hepatitis B is widespread such as southeast Asia and China
  • individuals who live in households where another member is infected with the virus
  • infection through intravenous (IV) drug use and/or unprotected heterosexual or homosexual sexual contact
  • infection through blood transfusions from infected donors

Demographics

Worldwide there are 450 million carriers of hepatitis B, 50 million of which are in Africa. Carriage rates vary markedly in different areas. In South Africa, infection is much more common in rural communities than in the cities.

According to the Centers for Disease Control (CDC), an estimated 78,000 persons in the United States were infected with HBV in 2001. People of all ages get hepatitis B, and about 5,000 die per year of sickness caused by HBV. An estimated 1.25 million Americans are chronically infected, of whom 20 to 30 percent acquired their infection in childhood. It is estimated that hepatitis B accounts for 20 to 25 percent of all acute viral hepatitis in children. Infected newborns rarely suffer but have 90 percent chance of becoming carriers. Twenty-five percent of all HAV positive newborns develop chronic liver disease by the third to fourth decade of life.

Causes and Symptoms

Hepatitis B is caused by HBV, also called Hepadna virus. The virus has an incubation period of two to five months. It replicates in the liver, and virus particles are shed in large amounts into the blood. The blood of infected individuals is thus highly infectious.

Hepatitis B has a wide range of symptoms. It can also be mild, without symptoms. When present, the symptoms are non-specific and usually include fever, tiredness, loss of appetite, nausea, abdominal discomfort, dark urine, clay-colored bowel movements, and jaundice (yellowing of the skin and eyes).

When to Call the Doctor

Parents should call the doctor immediately if any of the following occurs:

  • A child has changes in symptoms, is confused, is difficult to wake up, is lethargic (sluggish), or irritable.
  • A child is unable to drink fluids.
  • A child's skin becomes much more yellow in color.
  • A child has signs of dehydration such as no urine in over eight hours or a dry mouth.
  • A child starts to look very sick.

Diagnosis

A blood test is required to diagnose hepatitis B. The test detects one of the viral antigens called hepatitis B surface antigen (HBsAg) in the blood. Later on, HBsAg may no longer be present, in which case a test for antibodies to a different antigen, called hepatitis B core antigen, is used. If HBsAg can be detected in the blood for longer than six months, chronic hepatitis B is diagnosed.

Treatment

There is no cure for hepatitis B and no specific treatment is available. However, the following guidelines are often recommended:

  • Fluids and diet. The best treatment is to ensure that the child drinks a lot of fluids and eats well.
  • Rest. The child should rest while he or she has fever or jaundice. When fever and jaundice are gone, activity may be gradually increased as with the healthcare provider's approval.
  • Medications. There is no medicine that gets rid of HBV or heals the liver. There are medications available to treat chronic HBV-infection. These work for some people, but experience with children is limited. Three drugs are licensed, as of 2004, for the treatment of chronic hepatitis B: Adefovir dipivoxil, alpha interferon, and lamivudine.

Nutritional Concerns

Parents should ensure that their infected child has a well-balanced diet. Children with advanced liver disease need to follow specific diets issued by the treating physician. However, most children are not in this category, and no special diet is recommended for them, except that they should avoid eating fatty foods because the body has difficulty digesting fat when the liver is not working well.

However, adequate protein intake is important to regenerate liver cells. Children without liver cirrhosis require about 1–2 grams of protein per pound (2–3 grams per kilogram) of body weight. Children with cirrhosis need an individual nutrition plan from their pediatric specialist or nutritionist.

There is some evidence that iron can lower the response to interferon treatment in adults. Although no results have been reported for children, the issue of restricting iron intake should be discussed with the treating physician.

Prognosis

Viral hepatitis symptoms usually last three weeks to two months but may last up to six months. Children may return to daycare one week after symptoms first appear, with the doctor's permission. Most children with hepatitis get better naturally without liver problems later on in life. However, some children do have subsequent liver problems. Thus, it is important to keep in close touch with the treating physician and to keep all follow-up appointments. Chronic, or relapsing, infection occurs with hepatitis B in about 5–10 percent of cases.

Prevention

A vaccine for hepatitis B is as of 2004 widely used in the United States for routine childhood immunization. Children usually receive the first vaccine between birth and two months of age, the second vaccine at one to four months, and the third vaccine at six to 18 months. The vaccine is generally required for all children born on or after January 1, 1992, before they enter school. The vaccine is available for older children who may have not been immunized before 1992 and is recommended before age 11 or 12.

Parental Concerns

If mothers have HBV in their blood, they can give hepatitis B to their baby during childbirth. Babies who get HBV at birth may have the virus for the rest of their lives, can spread the disease, and can get cirrhosis of the liver or liver cancer. The CDC recommends that all pregnant women be tested for HBV early in their pregnancy. If the blood test is positive, the baby should receive vaccine along with hepatitis B immune globulin (HBIG) at birth. The second dose of vaccine should be given at one to two months of age and the third dose at six months of age.

See also Hepatitis A; Hepatitis B vaccine; Vaccination.

Resources

Books

Achord, James. Understanding Hepatitis. Jackson: University of Mississippi Press, 2002.

Berkman, Alan, and N. Bakalar. Hepatitis A to G: The Facts You Need to Know about All the Forms of This Dangerous Disease. Clayton, Australia: Warner Books, 2000.

Blumberg, Baruch S. Hepatitis B: The Hunt for a Killer Virus. Princeton, NJ: Princeton University Press, 2002.

Everson, Gregory T., et al. Living with Hepatitis B: A Survivor's Guide. Long Island City, NY: Hatherleigh Press, 2004.

Green, William F., and H. Conjeevaram. The First Year—Hepatitis B: An Essential Guide for the Newly Diagnosed. New York: Marlowe & Co., 2002.

Periodicals

Arya, G., and W. F. Balistreri. "Pediatric liver disease in the United States: Epidemiology and impact." Journal of Gastroenterology & Hepatology 17, no. 5 (May 2002): 521–25.

Helvaci, M., et al. "Efficacy of hepatitis B vaccination and interferon-[alpha]-2b combination therapy versus interferon-[alpha]-2b monotherapy in children with chronic hepatitis B." Journal of Gastroenterology & Hepatology 19, no. 7 (July 2004): 785–91.

Liberek, A., et al. "Tolerance of interferon-alpha therapy in children with chronic hepatitis B." Journal of Paediatrics & Child Health 63, no. 23 (2003): 2625–49.

Murdoch, David L. et al. "Combined Hepatitis A and B Vaccines: A Review of Their Immunogenicity and Tolerability." Drugs 40, no. 5–6 (May-June 2004): 265–69.

Shulman, Stanford T. "The History of Pediatric Infectious Diseases." Pediatric Research 55, no. 1 (January 2004): 163–176.

Sokal, Etienne. "Drug Treatment of Pediatric Chronic Hepatitis B." Pediatric Drugs 4, no. 6 (2002): 361–69.

Organizations

American Liver Foundation (ALF). 75 Maiden Lane, Suite 603, New York, NY 10038–4810. Web site: www.liverfoundation.org.

Hepatitis B Foundation. 700 East Butler Avenue, Doylestown, PA 18901–2697. Web site: www.hepb.org.

Hepatitis Foundation International (HFI). 504 Blick Drive, Silver Spring, MD 20904–2901. Web site: www.liverfoundation.org.

National Center for Infectious Diseases (NCID). Centers for Disease Control and Prevention, Mailstop C-14, 1600 Clifton Road, Atlanta, GA 30333. Web site: www.cdc.gov/ncidod.

Web Sites

"Viral Hepatitis B Homepage." NCID. Available online at www.cdc.gov/ncidod/diseases/hepatitis/b/index.htm (accessed October 22, 2004).

"What I need to know about Hepatitis B Homepage." NIHNDDIC. Available online at (accessed October 22, 2004).

[Article by: Monique Laberge, Ph.D.]


American Heritage Stedman's Medical Dictionary:

hepatitis B

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Home > Library > Health > Medical Dictionary

n.

A form of hepatitis caused by a DNA virus that persists in the blood serum and is transmitted by infected blood or blood derivatives, or by contaminated needles or other instruments. The disease has a long incubation period and symptoms that may become severe or chronic, causing serious damage to the liver. Also called serum hepatitis.

Random House Word Menu:

categories related to 'serum hepatitis'

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Random House Word Menu by Stephen Glazier
For a list of words related to serum hepatitis, see:
  • Diseases and Infestations - serum hepatitis: liver inflammation that causes fever and jaundice, transmitted by infected hypodermic needle or blood transfusion

Wikipedia on Answers.com:

Hepatitis B virus

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For the disease, see Hepatitis B.
Hepatitis B virus
TEM micrograph showing hepatitis B viruses
Virus classification
Group: Group VII (dsDNA-RT)
Order: Unassigned
Family: Hepadnaviridae
Genus: Orthohepadnavirus
Species: Hepatitis B virus

Hepatitis B virus, abbreviated HBV, is a species of the genus Orthohepadnavirus, which is likewise a part of the Hepadnaviridae family of viruses.[1] This virus causes the disease hepatitis B.[2]

Contents

Disease

Main article: Hepatitis B

In addition to causing hepatitis B, infection with HBV can lead to cirrhosis and hepatocellular carcinoma.[3]

It has also been suggested that it may increase the risk of pancreatic cancer.[2]

Classification

The hepatitis B virus is classified as the type species of the Orthohepadnavirus, which contains three other species: the Ground squirrel hepatitis virus, Woodchuck hepatitis virus, and the Woolly monkey hepatitis B virus. The genus is classified as part of the Hepadnaviridae family, which contains two other genera, the Avihepadnavirus and a second which has yet to be assigned. This family of viruses have not been assigned to a viral order.[4] Viruses similar to hepatitis B have been found in all the Old World apes (orangutan, gibbons, gorillas and chimpanzees) and from a New World woolly monkey suggesting an ancient origin for this virus in primates.

The virus is divided into four major serotypes (adr, adw, ayr, ayw) based on antigenic epitopes present on its envelope proteins, and into eight genotypes (A-H) according to overall nucleotide sequence variation of the genome. The genotypes have a distinct geographical distribution and are used in tracing the evolution and transmission of the virus. Differences between genotypes affect the disease severity, course and likelihood of complications, and response to treatment and possibly vaccination.[5][6]

Morphology

Structure

Hepatitis B virus is a member of the Hepadnavirus family.[7] The virus particle, (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity similar to retroviruses.[8] The outer envelope contains embedded proteins which are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses with a virion diameter of 42 nm, but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigen (HBsAg), and is produced in excess during the life cycle of the virus.[9]

Components

It consists of:

Hepatitis D virus requires HBV envelope particles to become virulent.[11]

Evolution

The early evolution of the Hepatitis B, like that of all viruses, is difficult to establish.

The divergence of orthohepadnavirus and avihepadnavirus occurred ~125,000 years ago (95% interval 78,297–313,500).[12] Both the Avihepadnavirus and Orthohepadna viruses began to diversify about 25,000 years ago.[12] The branching at this time lead to the emergence of the Orthohepadna genotypes A-H. Human strains have a most recent common ancestor dating back to 7,000 (95% interval: 5,287–9,270) to 10,000 (95% interval: 6,305–16,681) years ago.

The Avihepadnavirus lack a X protein but a vestigial X reading frame is present in the genome of duck hepadnavirus.[13] The X protein may have evolved from a DNA glycosylase.

The rate of nonsynonymous mutations in this virus has been estimated to be about 2×10−5 amino acid replacements per site per year.[14] The mean number of nucleotide substitutions/site/year is ~7.9 x 10-5.

A second estimate of the origin of this virus suggests a most recent common ancestor of the human strains evolved ~1500 years ago.[15] The most recent common ancestor of the avian strains was placed at 6000 years ago. The mutation rate was estimated to be ~10-6 substitutions/site/year.

Genome

The genome organisation of HBV. The genes overlap.

Size

The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase. The genome is 3020–3320 nucleotides long (for the full length strand) and 1700–2800 nucleotides long (for the short length strand).[16]

Encoding

The negative-sense, (non-coding), is complementary to the viral mRNA. The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the (+) sense strand and removal of a protein molecule from the (-) sense strand and a short sequence of RNA from the (+) sense strand. Non-coding bases are removed from the ends of the (-)sense strand and the ends are rejoined.

There are four known genes encoded by the genome called C, X, P, and S. The core protein is coded for by gene C (HBcAg), and its start codon is preceded by an upstream in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen (HBsAg). The HBsAg gene is one long open reading frame but contains three in frame "start" (ATG) codons that divide the gene into three sections, pre-S1, pre-S2, and S. Because of the multiple start codons, polypeptides of three different sizes called large, middle, and small (pre-S1 + pre-S2 + S, pre-S2 + S, or S) are produced.[17] The function of the protein coded for by gene X is not fully understood.[18]

Several non-coding RNA elements have been identified in the HBV genome. These include: HBV PREalpha, HBV PREbeta and HBV RNA encapsidation signal epsilon.[19][20]

Genotypes

There are eight known genotypes labeled A through H.[5] A possible new "I" genotype has been described,[21] but acceptance of this notation is not universal.[22] Different genotypes may respond to treatment in different ways.[23][24]

The genotypes differ by at least 8% of the sequence and have distinct geographical distributions and this has been associated with anthropological history. Type F which diverges from the other genomes by 14% is the most divergent type known. Type A is prevalent in Europe, Africa and South-east Asia, including the Philippines. Type B and C are predominant in Asia; type D is common in the Mediterranean area, the Middle East and India; type E is localized in sub-Saharan Africa; type F (or H) is restricted to Central and South America. Type G has been found in France and Germany. Genotypes A, D and F are predominant in Brazil and all genotypes occur in the United States with frequencies dependent on ethnicity.

The E and F strains appear to have originated in aboriginal populations of Africa and the New World, respectively.

Within genotypes 24 subtypes have been described which differ by 4-8% of the genome.

Type A has two subtypes: Aa (A1) in Africa/Asia and the Philippines and Ae (A2) in Europe/United States.

Type B has two distinct geographical distributions: Bj/B1 ('j' — Japan) and Ba/B2 ('a' — Asia). Type Ba has been further subdivided into four clades (B2 — B4).

Type C has two geographically subtypes: Cs (C1) in South-east Asia and Ce (C2) in East Asia. The C subtypes have been divided into five clades (C1 — C5). A sixth clade (C6) has been described in the Philippines but only in one isolate to date.[25] Type C1 is associated with Vietnam, Myanmar and Thailand; type C2 with Japan, Korea and China; type C3 with New Caledonia and Polynesia; C4 with Australia; and C5 with the Philippines. A further subtype has been described in Papua, Indonesia.[26]

Type D has been divided into 7 subtypes (D1 — D7).

Type F has been subdivided into 4 subtypes (F1 — F4). F1 has been further divided in to 1a and 1b. In Venezuela subtypes F1, F2, and F3 are found in East and West Amerindians. Among South Amerindians only F3 was found. Subtypes Ia, III, and IV exhibit a restricted geographic distribution (Central America, the North and the South of South America respectively) while clades Ib and II are found in all the Americas except in the Northern South America and North America respectively.

Life cycle

Hepatitis B virus replication .

The life cycle of hepatitis B virus is complex. Hepatitis B is one of a few known non-retroviral viruses which use reverse transcription as a part of its replication process.

Attachment 
The virus gains entry into the cell by binding to a receptor on the surface of the cell and enters it by endocytosis. The cell surface receptor has yet to be identified however it is suspected to be a member of the ovalbumin family of serine protease inhibitors.[1]
Penetration 
The virus membrane then fuses with the host cell's membrane releasing the DNA and core proteins into the cytoplasm.
Uncoating 
Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus by host proteins called chaperones. The core proteins dissociate from the partially double stranded viral DNA is then made fully double stranded and transformed into covalently closed circular DNA (cccDNA) that serves as a template for transcription of four viral mRNAs.
Replication 
The largest mRNA, (which is longer than the viral genome), is used to make the new copies of the genome and to make the capsid core protein and the viral DNA polymerase.
Assembly 
These four viral transcripts undergo additional processing and go on to form progeny virions which are released from the cell or returned to the nucleus and re-cycled to produce even more copies.[17][27]
Release 
The long mRNA is then transported back to the cytoplasm where the virion P protein synthesizes DNA via its reverse transcriptase activity.

See also

References

  1. ^ a b Hunt, Richard (2007-11-21). "Hepatitis viruses". University of Southern California, Department of Pathology and Microbiology. http://pathmicro.med.sc.edu/virol/hepatitis-virus.htm. Retrieved 2008-03-13. 
  2. ^ a b Hassan MM, Li D, El-Deeb AS, et al. (October 2008). "Association between hepatitis B virus and pancreatic cancer". J. Clin. Oncol. 26 (28): 4557–62. doi:10.1200/JCO.2008.17.3526. PMC 2562875. PMID 18824707. http://www.jco.org/cgi/pmidlookup?view=long&pmid=18824707. 
  3. ^ Schwalbe M, Ohlenschläger O, Marchanka A, et al. (March 2008). "Solution structure of stem-loop alpha of the hepatitis B virus post-transcriptional regulatory element". Nucleic Acids Res. 36 (5): 1681–9. doi:10.1093/nar/gkn006. PMC 2275152. PMID 18263618. http://nar.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=18263618. 
  4. ^ Mason, W.S., et al. (2008-07-08). "00.030. Hepadnaviridae". ICTVdB Index of Viruses. International Committee on Taxonomy of Viruses. http://www.ncbi.nlm.nih.gov/ICTVdb/Ictv/fs_hepad.htm. Retrieved 2009-03-13. 
  5. ^ a b Kramvis A, Kew M, François G (2005). "Hepatitis B virus genotypes". Vaccine 23 (19): 2409–23. doi:10.1016/j.vaccine.2004.10.045. PMID 15752827. 
  6. ^ Magnius LO, Norder H (1995). "Subtypes, genotypes and molecular epidemiology of the hepatitis B virus as reflected by sequence variability of the S-gene". Intervirology 38 (1–2): 24–34. PMID 8666521. 
  7. ^ Zuckerman AJ (1996). Hepatitis Viruses. In: Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.3738. 
  8. ^ Locarnini S (2004). "Molecular virology of hepatitis B virus". Semin. Liver Dis. 24 (Suppl 1): 3–10. doi:10.1055/s-2004-828672. PMID 15192795. 
  9. ^ Howard CR (1986). "The biology of hepadnaviruses". J. Gen. Virol. 67 (7): 1215–35. doi:10.1099/0022-1317-67-7-1215. PMID 3014045. 
  10. ^ Guo GH, Tan DM, Zhu PA, Liu F (February 2009). "Hepatitis B virus X protein promotes proliferation and upregulates TGF-beta1 and CTGF in human hepatic stellate cell line, LX-2". Hbpd Int 8 (1): 59–64. PMID 19208517. http://www.hbpdint.com/text.asp?id=1196. 
  11. ^ Chai N, Chang HE, Nicolas E, Han Z, Jarnik M, Taylor J (August 2008). "Properties of subviral particles of hepatitis B virus". J. Virol. 82 (16): 7812–7. doi:10.1128/JVI.00561-08. PMC 2519590. PMID 18524834. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=18524834. 
  12. ^ a b van Hemert FJ, van de Klundert MA, Lukashov VV, Kootstra NA, Berkhout B, Zaaijer HL (2011). "Protein X of hepatitis B virus: origin and structure similarity with the central domain of DNA glycosylase". PLoS ONE 6 (8): e23392. doi:10.1371/journal.pone.0023392. PMC 3153941. PMID 21850270. http://dx.plos.org/10.1371/journal.pone.0023392. 
  13. ^ Lin B, Anderson DA (2000). "A vestigial X open reading frame in duck hepatitis B virus". Intervirology 43 (3): 185–90. PMID 11044813. http://content.karger.com/produktedb/produkte.asp?DOI=25037&typ=pdf. 
  14. ^ Osiowy C, Giles E, Tanaka Y, Mizokami M, Minuk GY (November 2006). "Molecular evolution of hepatitis B virus over 25 years". J. Virol. 80 (21): 10307–14. doi:10.1128/JVI.00996-06. PMC 1641782. PMID 17041211. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=17041211. 
  15. ^ Zhou Y, Holmes EC (2007) Bayesian estimates of the evolutionary rate and age of hepatitis B virus. J Mol Evol 65(2):197-205
  16. ^ Kay A, Zoulim F (2007). "Hepatitis B virus genetic variability and evolution". Virus Res. 127 (2): 164–76. doi:10.1016/j.virusres.2007.02.021. PMID 17383765. 
  17. ^ a b Beck J, Nassal M (2007). "Hepatitis B virus replication". World J. Gastroenterol. 13 (1): 48–64. PMID 17206754. 
  18. ^ Bouchard MJ, Schneider RJ (2004). "The enigmatic X gene of hepatitis B virus". J. Virol. 78 (23): 12725–34. doi:10.1128/JVI.78.23.12725-12734.2004. PMC 524990. PMID 15542625. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=524990. 
  19. ^ Smith Gj, 3rd; Donello, JE; Lück, R; Steger, G; Hope, TJ (1998). "The hepatitis B virus post-transcriptional regulatory element contains two conserved RNA stem-loops which are required for function". Nucleic Acids Research 26 (21): 4818–27. doi:10.1093/nar/26.21.4818. PMC 147918. PMID 9776740. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=147918. 
  20. ^ Flodell S, Schleucher J, Cromsigt J, Ippel H, Kidd-Ljunggren K, Wijmenga S (November 2002). "The apical stem-loop of the hepatitis B virus encapsidation signal folds into a stable tri-loop with two underlying pyrimidine bulges". Nucleic Acids Res. 30 (21): 4803–11. doi:10.1093/nar/gkf603. PMC 135823. PMID 12409471. http://nar.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12409471. 
  21. ^ Olinger CM, Jutavijittum P, Hübschen JM, et al. (November 2008). "Possible new hepatitis B virus genotype, southeast Asia". Emerging Infect. Dis. 14 (11): 1777–80. doi:10.3201/eid1411.080437. PMC 2630741. PMID 18976569. http://www.cdc.gov/eid/content/14/11/1777.htm. 
  22. ^ Kurbanov F, Tanaka Y, Kramvis A, Simmonds P, Mizokami M (August 2008). "When should "I" consider a new hepatitis B virus genotype?". J. Virol. 82 (16): 8241–2. doi:10.1128/JVI.00793-08. PMC 2519592. PMID 18663008. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=18663008. 
  23. ^ Palumbo E (2007). "Hepatitis B genotypes and response to antiviral therapy: a review". Am J Ther 14 (3): 306–9. doi:10.1097/01.pap.0000249927.67907.eb. PMID 17515708. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00045391-200705000-00016. 
  24. ^ Mahtab MA, Rahman S, Khan M, Karim F (October 2008). "Hepatitis B virus genotypes: an overview". Hbpd Int 7 (5): 457–64. PMID 18842489. http://www.hbpdint.com/text.asp?id=1142. 
  25. ^ Cavinta L, Sun J, May A, et al. (June 2009). "A new isolate of hepatitis B virus from the Philippines possibly representing a new subgenotype C6". J. Med. Virol. 81 (6): 983–7. doi:10.1002/jmv.21475. PMID 19382274. 
  26. ^ Lusida M.I., Nugrahaputra V.E., Soetjipto Handajani R., Nagano-Fujii M., Sasayama M., Utsumi T., Hotta H. (2008). "Novel subgenotypes of hepatitis B virus genotypes C and D in Papua, Indonesia". J. Clin. Microbiol 46 (7): 2160–2166. doi:10.1128/JCM.01681-07. PMC 2446895. PMID 18463220. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2446895. 
  27. ^ Bruss V (2007). "Hepatitis B virus morphogenesis". World J. Gastroenterol. 13 (1): 65–73. PMID 17206755. 
Oncovirus
Immune disorders
Central
nervous system
Cardiovascular
Respiratory system/
acute viral nasopharyngitis/
viral pneumonia
Digestive system
DNA virus: HBV (B)
RNA virus: CBV · HAV (A) · HCV (C) · HDV (D) · HEV (E) · HGV (G)
Urogenital
DNA
Hepatitis B
EBNA-1 · EBNA-2 · EBNA-3 · LMP-1 · LMP-2 · EBER
RNA
VNPs: NSP1 · NSP2 · NSP4 · NSP5 · NSP6

VSPs: E1 · E2

VNPs: P7 · NS2 · NS3 · NS4 · NS5
RT
Fusion protein

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