Hepatitis B
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| Hepatitis B Classification and external resources | |
| ICD-10 | B16., B18.0-B18.1 |
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| ICD-9 | 070.2-070.3 |
| OMIM | 610424 |
| DiseasesDB | 5765 |
| MedlinePlus | 000279 |
| eMedicine | med/992 ped/978 |
| MeSH | D006509 |
| Hepatitis B virus | ||||||||
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 Micrograph showing hepatitis B virions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753
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Overview
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.
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.
Epidemiology and Demographics
Hepatitis B is caused by a virus that attacks the liver. The virus, which is called hepatitis B virus (HBV), can cause lifelong infection, cirrhosis (scarring) of the liver, liver cancer, liver failure, and death. In 2003, an estimated 73,000 people were infected with HBV. People of all ages get hepatitis B and about 5,000 die per year of sickness caused by HBV. HBV is spread when blood from an infected person enters the body of a person who is not infected. Healthcare personnel who have received hepatitis B vaccine and developed immunity to the virus are at virtually no risk for infection. For a susceptible person, the risk from a single needlestick or cut exposure to HBV-infected blood ranges from 6-30%. The annual number of occupational infections has decreased 95% since hepatitis B vaccine became available in 1982, from >10,000 in 1983 to <400 in 2001.
References
http://www.cdc.gov/ncidod/dhqp/bp_hepatitisb.html
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 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]
Pathophysiology & Etiology
Hepatitis B is a serious disease caused by a virus that attacks the liver. The virus, which is called hepatitis B virus (HBV), can cause lifelong infection, cirrhosis (scarring) of the liver, liver cancer, liver failure, and death.
HBV is a 42-nm DNA virus classified in the Hepadnaviridae family. The liver is the primary site of HBV replication. After a susceptible person is exposed, the virus enters the liver via the bloodstream; no evidence exists indicating that the virus replicates at mucosal surfaces. HBV infection can produce either asymptomatic or symptomatic infection. The average incubation period is 90 days (range: 60--150 days) from exposure to onset of jaundice and 60 days (range: 40--90 days) from exposure to onset of abnormal serum alanine aminotransferase (ALT) levels.
For infants and children, the two primary sources of HBV infection are perinatal transmission from infected mothers and horizontal transmission from infected household contacts. Adolescents are at risk for HBV infection primarily through high-risk sexual activity (i.e., sex with more than one partner and male sexual activity with other males) and injection-drug use. Transmission of HBV via transfusion of blood and plasma-derived products is rare because of donor screening for HBsAg and viral inactivation procedures.
For a newborn infant whose mother is positive for both HBsAg and HBeAg, the risk for chronic HBV infection is 70%--90% by age 6 months in the absence of postexposure immunoprophylaxis. For infants of women who are HBsAg positive but HBeAg negative, the risk for chronic infection is <10% in the absence of postexposure immunoprophylaxis. Rare cases of fulminant hepatitis B among perinatally infected infants also have been reported. Studies suggest that breastfeeding by an HBsAg-positive mother does not increase the risk for acquisition of HBV infection in the infant.
Children who are not infected at birth remain at risk from long-term interpersonal contact with their infected mothers. In one study, 38% of infants who were born to HBsAg-positive mothers and who were not infected perinatally became infected by age 4 years. In addition, children living with any chronically infected persons are at risk for becoming infected through percutaneous or mucosal exposures to blood or infectious body fluids (e.g., sharing a toothbrush, contact with exudates from dermatologic lesions, contact with HBsAg-contaminated surfaces). HBV transmission rates to susceptible household contacts of chronically infected persons have varied (range: 14%--60%). High rates of infection also have been reported among unvaccinated long-term residents of institutions for the mentally handicapped, and, in rare instances, person-to-person transmission has been reported in child care settings.
References
http://www.cdc.gov/ncidod/diseases/hepatitis/index.htm
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5416a1.htm?s_cid=rr5416a1_e
Risk Factors
Individuals are at increased risk of HBV infection if they:
- have sex with someone infected with HBV
- have sex with more than one partner
- shoot drugs
- are a man and have sex with a man
- live in the same house with someone who has chronic (long-term) HBV infection
- have a job that involves contact with human blood
- are a client in a home for the developmentally disabled
- have hemophilia
- travel to areas where hepatitis B is common (country listing)
One out of 20 people in the United States will get infected with HBV some time during their lives.
Their risk is higher if their parents were born in Southeast Asia, Africa, the Amazon Basin in South America, the Pacific Islands, or the Middle East.
References
http://www.cdc.gov/ncidod/diseases/hepatitis/b/faqb.htm#gen
Further Risk Stratification and Prognosis
- Number of new infections per year has declined from an average of 260,000 in the 1980s to about 60,000 in 2004.
- Highest rate of disease occurs in 20-49-year-olds.
- Greatest decline has happened among children and adolescents due to routine hepatitis B vaccination.
- Estimated 1.25 million chronically infected Americans, of whom 20-30% acquired their infection in childhood.
References
http://www.cdc.gov/ncidod/diseases/hepatitis/b/fact.htm
Diagnosis
The tests, called 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.[11]
The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. 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. 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 serological evidence of disease.
Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the 'e' antigen, 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 afterwards. 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 IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG).[1] A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.
Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers.[12] Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.[13]
More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are called viral loads and are used to assess a person's infection status and to monitor treatment.[14]
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[15]) 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[16] | 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[17]) 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.
Symptoms and Signs
Sometimes a person with HBV infection has no symptoms at all. The older you are, the more apt you are to have symptoms. You might be infected with HBV (and be spreading the virus) and not know it.
Symptoms might include:
- yellow skin or yellowing of the whites of your eyes (jaundice)
- tiredness
- loss of appetite
- nausea and vomiting
- abdominal discomfort
- dark urine
- clay-colored bowel movements
- joint pain
References
http://www.cdc.gov/ncidod/diseases/hepatitis/b/faqb.htm#gen
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. 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.[18] 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.
Pathology
Click on the arrow to view the pathologic findings in viral hepatitis:
Differential Diagnosis
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,[19] 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.[20]
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.[21]
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.[22]
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.
As a summary:
There are no medications available for recently acquired (acute) HBV infection. Hepatitis B vaccine is available for the prevention of HBV infection. There are antiviral drugs available for the treatment of chronic HBV infection.
- HBV infected persons should be evaluated by their doctor for liver disease.
- Adefovir dipivoxil, interferon alfa-2b, pegylated interferon alfa-2a, lamivudine, entecavir, and telbivudine are six drugs used for the treatment of persons with chronic hepatitis B.
- These drugs should not be used by pregnant women.
- Drinking alcohol can make liver disease worse.
References
http://www.cdc.gov/ncidod/diseases/hepatitis/b/faqb.htm#gen
http://www.cdc.gov/ncidod/diseases/hepatitis/b/fact.htm
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.
Reactivation
Hepatitis B virus DNA persists in the body after infection and in some people the disease re-occurs.[23] Although rare, reactivation is seen most often in people with impaired immunity.[24]
Primary Prevention
- If you are having sex, but not with one steady partner, use latex condoms correctly and every time you have sex. The efficacy of latex condoms in preventing infection with HBV is unknown, but their proper use might reduce transmission.
- If you are pregnant, you should get a blood test for hepatitis B. Infants born to HBV-infected mothers should be given HBIG (hepatitis B immune globulin) and vaccine within 12 hours after birth.
- Do not shoot drugs; if you shoot drugs, stop and get into a treatment program; if you can't stop, never share drugs, needles, syringes, water, or "works", and get vaccinated against hepatitis A and B.
- Do not share personal care items that might have blood on them (razors, toothbrushes).
- Consider the risks if you are thinking about getting a tattoo or body piercing. You might get infected if the tools have someone else's blood on them or if the artist or piercer does not follow good health practices.
- If you have or had hepatitis B, do not donate blood, organs, or tissue.
- If you are a health-care or public safety worker, get vaccinated against hepatitis B, and always follow routine barrier precautions and safely handle needles and other sharps (view current post-exposure prophylaxis recommendations).
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.
Hepatitis B Vaccine
HBsAg is the antigen used for hepatitis B vaccination. Vaccine antigen can be purified from the plasma of persons with chronic HBV infection or produced by recombinant DNA technology. Vaccines available in the United States use recombinant DNA technology to express HBsAg in yeast, which is then purified from the cells by biochemical and biophysical separation techniques (81,82). Hepatitis B vaccines licensed in the United States are formulated to contain 10--40 µg of HBsAg protein/mL. Since March 2000, hepatitis B vaccines produced for distribution in the United States do not contain thimerosal as a preservative or contain only a trace amount (<1.0 mcg mercury/mL) from the manufacturing process (83,84).
Hepatitis B vaccine is available as a single-antigen formulation and also in fixed combination with other vaccines. Two single-antigen vaccines are available in the United States: Recombivax HB® (Merck & Co., Inc., Whitehouse Station, New Jersey) and Engerix-B® (GlaxoSmithKline Biologicals, Rixensart, Belgium). Of the three licensed combination vaccines, one (Twinrix® [GlaxoSmithKline Biologicals, Rixensart, Belgium]) is used for vaccination of adults, and two (Comvax® [Merck & Co., Inc., Whitehouse Station, New Jersey] and Pediarix® [GlaxoSmithKline Biologicals, Rixensart, Belgium]) are used for vaccination of infants and young children. Twinrix contains recombinant HBsAg and inactivated hepatitis A virus. Comvax contains recombinant HBsAg and Haemophilus influenzae type b (Hib) polyribosylribitol phosphate conjugated to Neisseria meningitidis outer membrane protein complex. Pediarix contains recombinant HBsAg, diphtheria and tetanus toxoids and acellular pertussis adsorbed (DTaP), and inactivated poliovirus (IPV).
HBIG
HBIG provides passively acquired anti-HBs and temporary protection (i.e., 3--6 months) when administered in standard doses. HBIG is typically used as an adjunct to hepatitis B vaccine for postexposure immunoprophylaxis to prevent HBV infection. HBIG administered alone is the primary means of protection after an HBV exposure for nonresponders to hepatitis B vaccination.
HBIG is prepared from the plasma of donors with high concentrations of anti-HBs. The plasma is screened to eliminate donors who are positive for HBsAg, antibodies to HIV and hepatitis C virus (HCV), and HCV RNA. In addition, proper manufacturing techniques for HBIG inactivate viruses (e.g., HBV, HCV, and HIV) from the final product. No evidence exists that HBV, HCV, or HIV ever has been transmitted by HBIG commercially available in the United States. HBIG that is commercially available in the United States does not contain thimerosal.
References
http://www.cdc.gov/ncidod/diseases/hepatitis/b/fact.htm
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5416a1.htm?s_cid=rr5416a1_e
See also
- Hepatitis A
- Hepatitis B in China
- Hepatitis C
- Hepatitis D
- Hepatitis E
- Hepatitis F
- Hepatitis G
- Maurice Hilleman
References
- ↑ 1.0 1.1 1.2 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.
- ↑ 2.0 2.1 Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, pp. 544–51. ISBN 0-8385-8529-9.
- ↑ 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.
- ↑ Hepatitis B MedlinePlus article
- ↑ Hepadnaviridae characteristics - ICTVdB
- ↑ 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.
- ↑ 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.
- ↑ Alter MJ (2003). "Epidemiology and prevention of hepatitis B". Semin. Liver Dis. 23 (1): 39-46. doi:10.1055/s-2003-37583. PMID 12616449.
- ↑ Iannacone M. et al (2006). "Pathogenetic and antiviral immune responses against hepatitis B virus". Future Virology 1 (2): 189-196.
- ↑ 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.
- ↑ Bonino F, Chiaberge E, Maran E, Piantino P (1987). "Serological markers of HBV infectivity". Ann. Ist. Super. Sanita 24 (2): 217–23. PMID 3331068.
- ↑ Lok AS, McMahon BJ (2007). "Chronic hepatitis B". Hepatology 45 (2): 507–39. doi:10.1002/hep.21513. PMID 17256718.
- ↑ Chu CM, Liaw YF (2007). "Predictive factors for reactivation of hepatitis B following hepatitis B e antigen seroconversion in chronic hepatitis B". Gastroenterology 133 (5): 1458–65. doi:10.1053/j.gastro.2007.08.039. PMID 17935720.
- ↑ Zoulim F (2006). "New nucleic acid diagnostic tests in viral hepatitis". Semin. Liver Dis. 26 (4): 309–17. doi:10.1055/s-2006-951602. PMID 17051445.
- ↑ MeSH HBsAg
- ↑ MeSH HBcAg
- ↑ MeSH HBeAg
- ↑ Lok A. Hepatitis D virus infection and liver transplantation. uptodate.com. Retrieved on September 11, 2007.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ October 27, 2006. FDA Approves Telbivudine for Treatment of Chronic Hepatitis B. hivandhepatitis.com. Retrieved on September 11, 2007.
- ↑ Vierling JM (November 2007). "The immunology of hepatitis B". Clin Liver Dis 11 (4): 727–59, vii–viii. doi:10.1016/j.cld.2007.08.001. PMID 17981227.
- ↑ Katz LH, Fraser A, Gafter-Gvili A, Leibovici L, Tur-Kaspa R (February 2008). "Lamivudine prevents reactivation of hepatitis B and reduces mortality in immunosuppressed patients: systematic review and meta-analysis". J. Viral Hepat. 15 (2): 89–102. doi:10.1111/j.1365-2893.2007.00902.x. PMID 18184191.
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
Acknowledgements
The content on this page was first contributed by: C. Michael Gibson M.S., M.D.
bg:Хепатит B ca:Hepatitis B de:Hepatitis Bko:B형 간염 id:Hepatitis B it:Epatite virale B ms:Hepatitis B nl:Hepatitis B no:Hepatitt B-virussr:Хепатитис Б
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
