Hepatitis B

Definition

Hepatitis B is a potentially serious form of liver inflammation due to infection by the hepatitis B virus (HBV). It occurs in both rapidly developing (acute) and long-lasting (chronic) forms, and is one of the commonest chronic infectious diseases worldwide. An effective vaccine is available which will prevent the disease in those who are later exposed.

Description

Commonly called "serum hepatitis," hepatitis B ranges from mild to very severe. Some people who are infected by HBV develop no symptoms and are totally unaware of the fact, but they may carry HBV in their blood and pass the infection on to others. In its chronic form, HBV infection may destroy the liver through a scarring process, called cirrhosis, or it may lead to cancer of the liver.

When a person is infected by HBV, the virus enters the bloodstream and body fluids, and is able to pass through tiny breaks in the skin, mouth, or the male or female genital area. There are several ways of getting the infection:

• During birth, a mother with hepatitis B may pass HBV on to her infant.
• Contact with infected blood is a common means of transmitting hepatitis B. One way this may happen is by being stuck with a needle. Both healthcare workers and those who inject drugs into their veins are at risk in this way.
• Having sex with a person infected by HBV is an important risk factor (especially anal sex).

Although there are many ways of passing on HBV, the virus actually is not very easily transmitted. There is no need to worry that casual contact, such as shaking hands, will expose one to hepatitis B. There is no reason not to share a workplace or even a bathroom with an infected person.

More than 300 million persons throughout the world are infected by HBV. While most who become chronic carriers of the virus live in Asia and Africa, there are no fewer than 1.5 million carriers in the United States. Because carriers represent a constant threat of transmitting the infection, the risk of hepatitis B is always highest where there are many carriers. Such areas are said to be endemic for hepatitis B. When infants or young children living in an endemic area are infected, their chance of becoming a chronic hepatitis B carrier is at least 90%. This probably is because their bodies are not able to make the substances (antibodies) that destroy the virus. In contrast, no more than 5% of infected teenagers and adults develop chronic infection.

— David A. Cramer, MD

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.

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.]

"HBV" redirects here. For other uses, see HBV (disambiguation).

Hepatitis B
Classification & external resources

ICD-10	B16., B18.0-B18.1
ICD-9	070.2-070.3
OMIM	610424
DiseasesDB	5765
MedlinePlus	000279
eMedicine	med/992  ped/978
MeSH	D006509

Hepatitis B virus
Micrograph showing hepatitis B virions
Virus classification
Group: Group VII (dsDNA-RT) Family: Hepadnaviridae Genus: Orthohepadnavirus Species: Hepatitis B virus

Hepatitis B is an inflammation of the liver and is caused by the Hepatitis B virus (HBV), a member of the Hepadnavirus family^[1] and one of hundreds of unrelated viral species which cause viral hepatitis. It was originally known as "serum hepatitis" and has caused current epidemics in parts of Asia and Africa.^[2] Hepatitis B is recognized as endemic in China and various other parts of Asia.^[3] The proportion of the world's population currently infected with the virus is 3 to 6%, but up to a third have been exposed. Symptoms of the acute illness caused by the virus include liver inflammation, vomiting, jaundice, and rarely, death. Chronic hepatitis B may cause liver cirrhosis which may then lead to liver cancer, a fatal disease with very poor response to current chemotherapy.

Hepatitis B usually gets better on its own after a few months.^[4] It may, however, cause a more serious chronic infection.

Structure

Virions consist 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. The outer envelope contains embedded proteins which are involved in viral binding of, and release into, susceptible cells. Virion shape is generally spherical with a diameter of 40 - 48 nanometers (nm), but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These "subviral" particles are not infectious.^{[citation needed]}

The DNA genome is not segmented but rather partially double-stranded, containing a long and short segment which overlap approximately 240 nucleotides to form an open circle. The longer strand is 3020-3320 nucleotides long, and the shorter is 1700-2800 nucleotides long.^[5] The virus can be 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. Different genotypes have distinct geographic distributions. For example, genotypes B and C are prevalent in China and neighboring countries.

Replication

Hepatitis B is one of a few known non-retroviral viruses which employ reverse transcription as a part of its replication process. (HIV, a completely unrelated virus, also uses reverse transcription, but it is a retrovirus.) HBV invades hepatocytes by binding to surface receptors and becoming internalized. The viral core particles then migrate to the nucleus and the partially double-stranded, relaxed circular genomes (RC-DNA) are repaired to form a covalently closed circular DNA (cccDNA), which is the template for transcription of viral genomic and sub-genomic RNAs by cellular RNA polymerase II. Of these, the pregenomic RNA (pgRNA) is selectively packaged into progeny capsids and is then reverse-transcribed into new RC-DNA. The core can either bud into the endoplasmic reticulum to be enveloped and exported from the cell or recycled back into the nucleus for conversion to cccDNA.

Transmission

Transmission results from exposure to infectious blood or body fluids containing blood. Possible forms of transmission include (but are not limited to) unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, and vertical transmission from mother to child during childbirth. Without intervention, a mother who is positive for the hepatitis B surface antigen confers a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for the hepatitis B e antigen. HBV can also be transmitted between family members within households, possibly by contact of nonintact skin or mucous membrane with secretions or saliva containing HBV.^[6]

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, where less than 2% of the population is chronically infected, injection drug abuse and unprotected sex are the primary methods, although other factors may be important.^[7] In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2-7% of the population is chronically infected, the disease is predominantly spread among children. In high prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is also a significant factor.^[8] The prevalence of chronic HBV infection in areas of high endemicity is at least 8%.

Roughly 16-40% of unimmunized^{[citation needed]} sexual partners of individuals with hepatitis B will be infected through sexual contact. The risk of transmission is closely related to the rate of viral replication in the infected individual at the time of exposure.

Immunopathogenesis

During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. While the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to nearly all of the liver injury associated with HBV infection. By killing infected cells and by producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs also eliminate the virus.^[9] Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology and platelets may facilitate the accumulation of CTLs into the liver.^[10]

Symptoms and complications

Hepatitis B virus infection may either be acute (self-limited) or chronic (long-standing). Persons with self-limited infection clear the infection spontaneously within weeks to months.

Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus. However, only 5% of newborns that acquire the infection from their mother at birth will clear the infection. Of those infected between the age of one to six, 70% will clear the infection.^{[citation needed]} When the infection is not cleared, one becomes a chronic carrier of the virus.

Acute infection with hepatitis B virus is associated with acute viral hepatitis - an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, dark urine, and then progresses to development of jaundice. It has also been noted that itchy skin all over the body has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may also be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of liver cancer.

Hepatitis D infection usually only occurs with a concomitant infection with hepatitis B.^[11] Co-infection with hepatitis D increases the risk of liver cirrhosis and subsequently, liver cancer.

Polyarteritis nodosa is more common in people with hepatitis B infection.

Diagnosis

The original assays for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex. The table below is organized chronologically, from top to bottom:

Antigens	Antibodies
The hepatitis B surface antigen (HBsAg[12]) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection with this virus; however, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host.	-
The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg[13]	During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IGM) may be the only serologic evidence of disease.
Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg[14]) will appear.[2] Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication; however, some variants of the hepatitis B virus do not produce the 'e' antigen at all, so this rule does not always hold true.	During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterward. This conversion is usually associated with a dramatic decline in viral replication.
-	If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by antibodies to the hepatitis B surface antigen (anti-HBs).[1]

A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously. A number of persons who are positive for HBsAg may have very little viral multiplication, and hence may be at little risk of long-term complications or of transmitting infection to others.

More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are useful to assess a person's infection status and to monitor treatment.

Treatment

In the first few months of infection, hepatitis B does not usually get treated. Up to 95% of adults clear the infection spontaneously without treatment. Therapy in this stage of infection does not seem to further improve the chances of spontaneous cure. Early antiviral treatment may only be required in fewer than 1% of patients, whose hepatitis B takes a very aggressive course ("fulminant hepatitis").

There are currently several treatments for chronic hepatitis B. While none of the available drugs usually clear the infection, they can stop the virus from replicating, and prevent liver damage such as cirrhosis and/or liver cancer. Treatments are available in the form of antiviral drugs such as lamivudine, adefovir, entecavir or telbivudine, and immune system modulators such as interferon alpha (Uniferon) or peg-interferon alpha (PEGASYS). There are several other antivirals under investigation. However, some individuals are much more likely to respond than others. It does not appear that combination therapy offers any advantages,^[15] but may help in patients with resistant viruses, or in advanced liver disease where resistant viruses may lead to liver failure. In general, each treatment works by reducing the viral load by several orders of magnitude. In some patients, chronic hepatitis B takes a mild course and does not require immediate treatment. Treatment strategies should be individualized. Considerations include a person's risk for developing complications of persistent infection, a person's likelihood of adhering and responding to treatment, and potential risks such as side effects or development of viral resistance.

On March 29, 2005, the US Food and Drug Administration (FDA) approved Entecavir for the treatment of hepatitis B.^[16]

On February 25, 2005, the EU Commission approved PEGASYS for the treatment of hepatitis B making it the first pegylated interferon to be approved for hepatitis B.^[17]

On October 27, 2006, telbivudine gained FDA approval for treatment of chronic hepatitis B. It is marketed under the brand name Tyzeka in the US and Sebivo outside the US. It is already approved in Switzerland.^[18]

Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and hepatocellular carcinoma (liver cancer).

Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment also allows a mother to safely breastfeed her child.

An individual exposed to the virus who has never been vaccinated may be treated with HBIg immediately following the exposure. For instance, a health care worker accidentally stuck by a needle used in a hepatitis B carrier would qualify. Treatment must be soon after exposure, however.

Prevention

While abstinence is the only guaranteed way of preventing sexual transmission of hepatitis B., latex condoms, if used properly, greatly reduce the chances of transmission.

Vaccine

Main article Hepatitis B vaccine

Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from patients who had long-standing hepatitis B virus infection. However, currently, these are more often made using recombinant DNA technology, though plasma-derived vaccines continue to be used; the two types of vaccines are equally effective and safe.^{[citation needed]}

Missing Women Puzzle

Emily Oster argued that high Hepatitis B rates explain significant portion of the "missing women" first expounded in Amartya Sen's famous 1990 essay, "More Than 100 Million Women Are Missing.", and that the use of Hepatitis B vaccine in 1982 helped lower the male-to-female birth ratio.

See also

• Hepatitis A
• Hepatitis B in China
• Hepatitis C
• Hepatitis D
• Hepatitis E
• Hepatitis F
• Hepatitis G
• Maurice Hilleman
• Baruch S. Blumberg

References

1. ^ ^{a b} 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. 
2. ^ ^{a b} Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, pp. 544–51. ISBN 0-8385-8529-9. 
3. ^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). Molecular Biology of the Cell, 4th, Garland. (via NCBI Bookshelf) ISBN 0-8153-3218-1. 
4. ^ Hepatitis B MedlinePlus article
5. ^ Hepadnaviridae characteristics - ICTVdB
6. ^ Petersen NJ, Barrett DH, Bond WW, Berquist KR, Favero MS, Bender TR, Maynard JE (1976). "Hepatitis B surface antigen in saliva, impetiginous lesions, and the environment in two remote Alaskan villages". Appl. Environ. Microbiol. 32 (4): 572-574. PMID 791124. 
7. ^ Redd JT, Baumbach J, Kohn W, et al. (2007). "Patient-to-patient transmission of hepatitis B virus associated with oral surgery". J Infect Dis 195 (9): 1311–4. 
8. ^ Alter MJ (2003). "Epidemiology and prevention of hepatitis B". Semin. Liver Dis. 23 (1): 39-46. DOI:10.1055/s-2003-37583. PMID 12616449. 
9. ^ Iannacone M. et al (2006). "Pathogenetic and antiviral immune responses against hepatitis B virus". Future Virology 1 (2): 189-196. 
10. ^ Iannacone M, Sitia G, Isogawa M, Marchese P, Castro M, Lowenstein P, Chisari F, Ruggeri Z, Guidotti L (2005). "Platelets mediate cytotoxic T lymphocyte-induced liver damage". Nature Medicine 11 (11): 1167-1169. PMID 16258538. 
11. ^ Lok A. Hepatitis D virus infection and liver transplantation. uptodate.com. Retrieved on September 11, 2007.
12. ^ MeSH HBsAg
13. ^ MeSH HBcAg
14. ^ MeSH HBeAg
15. ^ Lau GKK et al (2005). "Peginterferon Alfa-2a, lamivudine, and the combination for HBeAg-positive chronic hepatitis B". N Engl J Med 352 (26): 2682-95. PMID 15987917. 
16. ^ U.S. Food and Drug Administration. March 30, 2005. FDA Talk Paper: FDA Approves New Treatment for Chronic Hepatitis B. fda.gov. Retrieved on September 11, 2007.
17. ^ February 25, 2005. Pegasys approved in the European Union for the treatment of chronic hepatitis B: Only pegylated interferon approved for the treatment of chronic hepatitis B. roche.com. Retrieved on September 11, 2007.
18. ^ October 27, 2006. FDA Approves Telbivudine for Treatment of Chronic Hepatitis B. hivandhepatitis.com. Retrieved on September 11, 2007.

External links

• NIH collection of links to relevant articles on Hepatitis B
• Hepatitis B Foundation, non-profit organization dedicated to the global problem of hepatitis B
• CDC webpage on Hepatitis B
• CDC fact sheet on Hepatitis B
• ThinkB: Hepatitis B information for Asians. Multiple language content available.
• Pediatric Hepatitis Report compiled by Parents of Kids with Infectious Diseases
• Asian Liver Center at Stanford University, non-profit organization to fight hepatitis B and liver cancer
• Advances in Hepatitis B Research: From Virology to Clinical Management
• Jade Ribbon Campaign, international campaign addressing the high prevalence of hepatitis B in Asian Pacific Islander communities
• An illustration of subunit vaccine development for Hepatitis B - Nova Online
• American Liver Foundation: Comprehensive information about Hepatitis B, including links to chapters for finding local resources

Sexually transmitted diseases and infections (STD/STI) (primarily A50-A64, 090-099)
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