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'''Hepatitis B Virus (Draft)'''
{{Taxobox
| color=violet
| name = Hepatitis B virus
| image =  [[Image: hepB.jpg]]
| family = Hepadnaviridae
| genus = Orthohepadnavirus}}


'''Higher order taxa'''
==Classification==


Virus; Retro-transcribing viruses; Hepadnaviridae; Orthohepadnavirus


'''Species'''
===Higher order taxa===
Virus; Retro-transcribing viruses; Hepadnaviridae; Orthohepadnavirus [1]
 
===Species===


Hepatitis B virus
Hepatitis B virus


'''Description and significance'''


==Description and significance==
Hepatitis B virus (HBV) causes hepatitis B infection, also known as serum hepatitis. Hepatitis B is one of the most common infectious diseases in the world. Each year an estimated 300,000 people in the United States are infected with HBV. About 5,000 people die yearly from hepatitis-related cirrhosis and about 1,000 die from HBV-related liver cancer. Worldwide, HBV infects over 200 million people.
Hepatitis B virus (HBV) causes hepatitis B infection, also known as serum hepatitis. Hepatitis B is one of the most common infectious diseases in the world. Each year an estimated 300,000 people in the United States are infected with HBV. About 5,000 people die yearly from hepatitis-related cirrhosis and about 1,000 die from HBV-related liver cancer. Worldwide, HBV infects over 200 million people.
This virus is normally transmitted through blood transfusions, contaminated equipment, drug users' unsterile needles, or any body secretion (saliva, sweat, semen, breast milk, urine, feces). The virus also can pass from the blood of an infected mother through the placenta to infect the fetus.


Hepatitis B occurs in both acute and chronic forms and may range from mild to severe. Many people infected with HBV never develop any symptoms and may not even know they carry the virus in their bodies; nevertheless, they are still able to pass the virus on to other people. Such people are said to be carriers of the disease. About 1.5 million Americans are thought to be carriers of HBV.
Hepatitis B occurs in both acute and chronic forms and may range from mild to severe. Many people infected with HBV never develop any symptoms and may not even know they carry the virus in their bodies; nevertheless, they are still able to pass the virus on to other people. Such people are said to be carriers of the disease. About 1.5 million Americans are thought to be carriers of HBV.


'''Genome structure'''
==Cell structure ==
The hepatitis B virus is a complex virus with a central core and a protein coat.
The virions of Hepatitis B virus are 42nm in diameter and have an isometric nucleocapsid core of 27nm in diameter. This core structure is surrounded by an outer shell that is approximately 4 nm in thickness. The protein of the virion coat is known as the "surface antigen", or HBsAg, that is sometimes extended as a tubular tail on one side of the virus particle. This antigen is commonly produced in vast excesses, and can be seen in the blood of infected individuals in the form of filamentous and spherical particles. Filamentous particles are identical to the virion tails in that they vary in length and have a mean diameter of about 22nm. They sometimes display regular, non-helical transverse striations.


HBV is a mostly double-stranded DNA virus classified as Orthohepadnavirus within the Hepadnaviridae family. HBV causes hepatitis in human and related viruses in this family cause hepatitis in ducks, ground squirrels and woodchucks.
Note: an image will soon be uploaded for this section.
The HBV genome has four genes: pol, env, pre-core and X that respectively encode the viral DNA-polymerase, envelope protein, pre-core protein (which is processed to viral capsid) and protein X. The function of protein X is not clear but it may be involved in the activation of host cell genes and the development of cancer.


'''Cell structure and metabolism'''
==Genome structure==
HBV is a mostly double-stranded DNA virus classified as Orthohepadnavirus within the Hepadnaviridae family. HBV causes hepatitis in human and related viruses in this family cause hepatitis in ducks, ground squirrels and woodchucks.
The HBV genome has four genes: pol, env, pre-core and X that respectively encode the viral DNA-polymerase, envelope protein, pre-core protein (which is processed to viral capsid) and protein X. The specific function of protein X is not clear but it may be involved in the activation of host cell genes and the development of malignant cells.


The hepatitis B virus is a complex virus with a central core and a protein coat.
==Ecology and Transmission==
The virions of Hepatitis B virus are 42 nm in diameter and possess an isometric nucleocapsid, the core, of 27nm in diameter, surrounded by an outer coat approximately 4 nm thick. The protein of the virion coat is known as "surface antigen" or HBsAg. The surface antigen is sometimes extended as a tubular tail on one side of the virus particle. Produced generally in vast excesses, it is found in the blood of infected individuals in the form of filamentous and spherical particles. Filamentous particles are identical to the virion tails in that they vary in length and have a mean diameter of about 22nm. They sometimes display regular, non-helical transverse striations.
Hepatitis B virus is normally transmitted through blood transfusions, contaminated equipment, drug users' unsterile needles, or any body secretion (saliva, sweat, semen, breast milk, urine, feces). The virus also can pass from the blood of an infected mother through the placenta to infect the fetus.


'''Ecology'''
Note: an image will soon be uploaded for this section. Also, a section about the life cycle of HBV will be added.
 
'''Pathology'''


==Pathology==
HBV may cause acute and chronic hepatitis, cirrhosis, hepatocellular carcinoma, immune complex disease, polyarteritis, glomerulonephritis, infantile papular acrodermatitis and aplastic anemia. An asymptomatic carrier state with high viremia may develop particularly after perinatal infection or under immune suppression.
HBV may cause acute and chronic hepatitis, cirrhosis, hepatocellular carcinoma, immune complex disease, polyarteritis, glomerulonephritis, infantile papular acrodermatitis and aplastic anemia. An asymptomatic carrier state with high viremia may develop particularly after perinatal infection or under immune suppression.


HBV causes acute and chronic hepatitis. The chances of becoming chronically infected depends upon age. About 90% of infected neonates and 50% of infected young children will become chronically infected. In contrast, only about 5% to 10% of immunocompetent adults infected with HBV develop chronic hepatitis B. In some individuals who become chronically infected, especially neonates and children, the acute infection will not be clinically apparent.
The chances of becoming chronically infected depends upon age. About 90% of infected neonates and 50% of infected young children will become chronically infected. In contrast, only about 5% to 10% of immunocompetent adults infected with HBV develop chronic hepatitis B. In some individuals who become chronically infected, especially neonates and children, the acute infection will not be clinically apparent.


Acute hepatitis B can range from subclinical disease to fulminant hepatic failure in about 2% of cases. Many acutely infected individuals develop clinically apparent acute hepatitis with loss of appetite, nausea, vomiting, fever, abdominal pain and jaundice. In cases of fulminant hepatic failure from acute HBV infection, orthotopic liver transplantation can be life-saving. About 90% to 95% of acutely infected adults recover without sequelae. About 5% to 10% of acutely infected adults become chronically infected.
Acute hepatitis B can range from subclinical disease to fulminant hepatic failure in about 2% of cases. Many acutely infected individuals develop clinically apparent acute hepatitis with loss of appetite, nausea, vomiting, fever, abdominal pain and jaundice. In cases of fulminant hepatic failure from acute HBV infection, orthotopic liver transplantation can be life-saving. About 90% to 95% of acutely infected adults recover without sequelae. About 5% to 10% of acutely infected adults become chronically infected.
The natural history of chronic HBV infection can vary dramatically between individuals. Some will develop a condition commonly referred to as a chronic carrier state. These patients, who are still potentially infectious, have no symptoms and no abnormalities on laboratory testing. Nonetheless, some of these patients will have evidence of hepatitis on liver biopsy.
The natural history of chronic HBV infection can vary dramatically between individuals. Some will develop a condition commonly referred to as a chronic carrier state. These patients, who are still potentially infectious, have no symptoms and no abnormalities on laboratory testing. Nonetheless, some of these patients will have evidence of hepatitis on liver biopsy.


Some individuals with chronic hepatitis B will have clinically insignificant or minimal liver disease and never develop complications. Others will have clinically apparent chronic hepatitis. Some will go on to develop cirrhosis. Individuals with chronic hepatitis B, especially those with cirrhosis but even so-called chronic carriers, are at an increased risk of developing hepatocellular carcinoma (primary liver cancer). Although this type of cancer is relatively rare in the United States, it is the leading cause of cancer death in the world, primarily because HBV infection is endemic in the East.
Some individuals with chronic hepatitis B will have clinically insignificant or minimal liver disease and never develop complications. Others will have clinically apparent chronic hepatitis. Some will go on to develop cirrhosis. Individuals with chronic hepatitis B, especially those with cirrhosis but even so-called chronic carriers, are at an increased risk of developing hepatocellular carcinoma (primary liver cancer). Although this type of cancer is relatively rare in the United States, it is the leading cause of cancer death in the world, primarily because HBV infection is endemic in the East.
Chronic infection with HBV can be either "replicative" or "non-replicative." In non-replicative infection, the rate of viral replication in the liver is low and serum HBV DNA concentration is generally low and hepatitis Be antigen (HBeAg) is not detected. HBeAg is an alternatively processed protein of the pre-core gene that is only synthesized under conditions of high viral replication. In "replicative" infection, the patient usually has a relatively high serum concentration of viral DNA and detectable HBeAg. Patients with chronic hepatitis B and "replicative" infection defined by the presence of detectable HBeAg have a generally worse prognosis and a greater chance of developing cirrhosis and/or hepatocellular carcinoma than those without HBeAg. In rare strains of HBV with mutations in the pre-core gene, "replicative" infection can occur in the absence of detectable serum HBeAg.


Chronic infection with HBV can be either "replicative" or "non-replicative." In non-replicative infection, the rate of viral replication in the liver is low and serum HBV DNA concentration is generally low and hepatitis Be antigen (HBeAg) is not detected. HBeAg is an alternatively processed protein of the pre-core gene that is only synthesized under conditions of high viral replication. In "replicative" infection, the patient usually has a relatively high serum concentration of viral DNA and detectable HBeAg. Patients with chronic hepatitis B and "replicative" infection defined by the presence of detectable HBeAg have a generally worse prognosis and a greater chance of developing cirrhosis and/or hepatocellular carcinoma than those without HBeAg. In rare strains of HBV with mutations in the pre-core gene, "replicative" infection can occur in the absence of detectable serum HBeAg.
In its most serious forms, hepatitis B can be a life-threatening disease. The virus causes severe scarring of the liver. The scarring process is called cirrhosis (pronounced suh-RO-suss) of the liver. Cirrhosis damages the liver so badly that it may no longer be able to function normally. It can cause the death of the patient. Cirrhosis can also lead to liver cancer (see cancer entry).
In its most serious forms, hepatitis B can be a life-threatening disease. The virus causes severe scarring of the liver. The scarring process is called cirrhosis (pronounced suh-RO-suss) of the liver. Cirrhosis damages the liver so badly that it may no longer be able to function normally. It can cause the death of the patient. Cirrhosis can also lead to liver cancer (see cancer entry).


'''Application to Biotechnology'''
==Current research==
 
 
October 2002, Vol 92, No. 10 | American Journal of Public Health 1619-1628
Chinese Herbal Medicine and Interferon in the Treatment of Chronic Hepatitis B: A Meta-Analysis of Randomized, Controlled Trials
 
A study conducted by the University of California at Berkley showed that a new Chinese-herbal treatment may be beneficial to treatment of chronic hepatitis B.
The researchers compared changes in three markers of infection (HBsAg, HBeAg, and HBV) as a result of three types of treatments: Chinese herbal medicine alone, Chinese herbal treatment in conjugation with interferon alfa, and interferon alfa alone. The results showed that combination of Chinese herbal treatments with interferon alfa were 1.5 to 2 times more effective as interferon alfa in reducing the hepatitis B viral load to undetectable level for all three measure of infection.
The herbal treatments used for this study included mixtures of bufotoxin (an extract from the skin of the toad bufo gargarizans) and kurorinone (an extract from the root of the pant sophorae flavescentis).
Although the quality of this studty was poor, these data suggest that further trials of Chinese Herbal Medicine and interferon in chronic hepatitis B infection are justified.
 
==References==
 
<references/>
 
[1] http://www.uniprot.org/taxonomy/489460
 
http://phene.cpmc.columbia.edu/ICTVdB/00.030.0.01.003.htm
 
http://www.comeunity.com/adoption/health/hepatitis/smith.html
 
http://www.nlm.nih.gov/medlineplus/ency/imagepages/1031.htm
 
http://pathmicro.med.sc.edu/virol/hepatitis-virus.htm
 
http://www.faqs.org/health/Sick-V2/Hepatitis.html


'''Current Research'''
http://www.ajph.org/cgi/content/full/92/10/1619


'''References'''
* Please note, all sections will be further modified.

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Hepatitis B virus
[[image:File:HepB.jpg|200px|]]
Scientific classification
Genus: Orthohepadnavirus

Classification

Higher order taxa

Virus; Retro-transcribing viruses; Hepadnaviridae; Orthohepadnavirus [1]

Species

Hepatitis B virus


Description and significance

Hepatitis B virus (HBV) causes hepatitis B infection, also known as serum hepatitis. Hepatitis B is one of the most common infectious diseases in the world. Each year an estimated 300,000 people in the United States are infected with HBV. About 5,000 people die yearly from hepatitis-related cirrhosis and about 1,000 die from HBV-related liver cancer. Worldwide, HBV infects over 200 million people.

Hepatitis B occurs in both acute and chronic forms and may range from mild to severe. Many people infected with HBV never develop any symptoms and may not even know they carry the virus in their bodies; nevertheless, they are still able to pass the virus on to other people. Such people are said to be carriers of the disease. About 1.5 million Americans are thought to be carriers of HBV.

Cell structure

The hepatitis B virus is a complex virus with a central core and a protein coat. The virions of Hepatitis B virus are 42nm in diameter and have an isometric nucleocapsid core of 27nm in diameter. This core structure is surrounded by an outer shell that is approximately 4 nm in thickness. The protein of the virion coat is known as the "surface antigen", or HBsAg, that is sometimes extended as a tubular tail on one side of the virus particle. This antigen is commonly produced in vast excesses, and can be seen in the blood of infected individuals in the form of filamentous and spherical particles. Filamentous particles are identical to the virion tails in that they vary in length and have a mean diameter of about 22nm. They sometimes display regular, non-helical transverse striations.

Note: an image will soon be uploaded for this section.

Genome structure

HBV is a mostly double-stranded DNA virus classified as Orthohepadnavirus within the Hepadnaviridae family. HBV causes hepatitis in human and related viruses in this family cause hepatitis in ducks, ground squirrels and woodchucks.

The HBV genome has four genes: pol, env, pre-core and X that respectively encode the viral DNA-polymerase, envelope protein, pre-core protein (which is processed to viral capsid) and protein X. The specific function of protein X is not clear but it may be involved in the activation of host cell genes and the development of malignant cells.

Ecology and Transmission

Hepatitis B virus is normally transmitted through blood transfusions, contaminated equipment, drug users' unsterile needles, or any body secretion (saliva, sweat, semen, breast milk, urine, feces). The virus also can pass from the blood of an infected mother through the placenta to infect the fetus.

Note: an image will soon be uploaded for this section. Also, a section about the life cycle of HBV will be added.

Pathology

HBV may cause acute and chronic hepatitis, cirrhosis, hepatocellular carcinoma, immune complex disease, polyarteritis, glomerulonephritis, infantile papular acrodermatitis and aplastic anemia. An asymptomatic carrier state with high viremia may develop particularly after perinatal infection or under immune suppression.

The chances of becoming chronically infected depends upon age. About 90% of infected neonates and 50% of infected young children will become chronically infected. In contrast, only about 5% to 10% of immunocompetent adults infected with HBV develop chronic hepatitis B. In some individuals who become chronically infected, especially neonates and children, the acute infection will not be clinically apparent.

Acute hepatitis B can range from subclinical disease to fulminant hepatic failure in about 2% of cases. Many acutely infected individuals develop clinically apparent acute hepatitis with loss of appetite, nausea, vomiting, fever, abdominal pain and jaundice. In cases of fulminant hepatic failure from acute HBV infection, orthotopic liver transplantation can be life-saving. About 90% to 95% of acutely infected adults recover without sequelae. About 5% to 10% of acutely infected adults become chronically infected.

The natural history of chronic HBV infection can vary dramatically between individuals. Some will develop a condition commonly referred to as a chronic carrier state. These patients, who are still potentially infectious, have no symptoms and no abnormalities on laboratory testing. Nonetheless, some of these patients will have evidence of hepatitis on liver biopsy.

Some individuals with chronic hepatitis B will have clinically insignificant or minimal liver disease and never develop complications. Others will have clinically apparent chronic hepatitis. Some will go on to develop cirrhosis. Individuals with chronic hepatitis B, especially those with cirrhosis but even so-called chronic carriers, are at an increased risk of developing hepatocellular carcinoma (primary liver cancer). Although this type of cancer is relatively rare in the United States, it is the leading cause of cancer death in the world, primarily because HBV infection is endemic in the East.

Chronic infection with HBV can be either "replicative" or "non-replicative." In non-replicative infection, the rate of viral replication in the liver is low and serum HBV DNA concentration is generally low and hepatitis Be antigen (HBeAg) is not detected. HBeAg is an alternatively processed protein of the pre-core gene that is only synthesized under conditions of high viral replication. In "replicative" infection, the patient usually has a relatively high serum concentration of viral DNA and detectable HBeAg. Patients with chronic hepatitis B and "replicative" infection defined by the presence of detectable HBeAg have a generally worse prognosis and a greater chance of developing cirrhosis and/or hepatocellular carcinoma than those without HBeAg. In rare strains of HBV with mutations in the pre-core gene, "replicative" infection can occur in the absence of detectable serum HBeAg.

In its most serious forms, hepatitis B can be a life-threatening disease. The virus causes severe scarring of the liver. The scarring process is called cirrhosis (pronounced suh-RO-suss) of the liver. Cirrhosis damages the liver so badly that it may no longer be able to function normally. It can cause the death of the patient. Cirrhosis can also lead to liver cancer (see cancer entry).

Current research

October 2002, Vol 92, No. 10 | American Journal of Public Health 1619-1628 Chinese Herbal Medicine and Interferon in the Treatment of Chronic Hepatitis B: A Meta-Analysis of Randomized, Controlled Trials

A study conducted by the University of California at Berkley showed that a new Chinese-herbal treatment may be beneficial to treatment of chronic hepatitis B. The researchers compared changes in three markers of infection (HBsAg, HBeAg, and HBV) as a result of three types of treatments: Chinese herbal medicine alone, Chinese herbal treatment in conjugation with interferon alfa, and interferon alfa alone. The results showed that combination of Chinese herbal treatments with interferon alfa were 1.5 to 2 times more effective as interferon alfa in reducing the hepatitis B viral load to undetectable level for all three measure of infection. The herbal treatments used for this study included mixtures of bufotoxin (an extract from the skin of the toad bufo gargarizans) and kurorinone (an extract from the root of the pant sophorae flavescentis). Although the quality of this studty was poor, these data suggest that further trials of Chinese Herbal Medicine and interferon in chronic hepatitis B infection are justified.

References


[1] http://www.uniprot.org/taxonomy/489460

http://phene.cpmc.columbia.edu/ICTVdB/00.030.0.01.003.htm

http://www.comeunity.com/adoption/health/hepatitis/smith.html

http://www.nlm.nih.gov/medlineplus/ency/imagepages/1031.htm

http://pathmicro.med.sc.edu/virol/hepatitis-virus.htm

http://www.faqs.org/health/Sick-V2/Hepatitis.html

http://www.ajph.org/cgi/content/full/92/10/1619

  • Please note, all sections will be further modified.
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