Hepatitis B

Hepatitis B is a serious liver infection caused by the hepatitis B virus (HBV). For some people, the infection becomes chronic, leading to liver failure, liver cancer, or cirrhosis a condition that causes permanent scarring of the liver.

The hepatitis B virus is transmitted through contact with the blood and body fluids of someone who is infected. You're especially at risk if you are an intravenous (IV) drug user who shares needles or other paraphernalia, have unprotected sexual contact with an infected partner, or were born in or travel to parts of the world where hepatitis B is widespread. In addition, women with HBV can pass the infection to their babies during childbirth.

Most people infected as adults recover fully from hepatitis B, even if their signs and symptoms are severe. Infants and children are much more likely to develop a chronic infection. Although no cure exists for hepatitis B, a vaccine can prevent the disease. If you're already infected, taking certain precautions can help prevent spreading HBV to others.


Hepatitis B is a liver disease caused by infection with the hepatitis B virus (HBV). Hepatitis B is one of the most easily spread (contagious) forms of viral hepatitis, which includes hepatitis A, B, C, D, E and.G However, hepatitis has many other causes, including some medications, long-term alcohol use, fatty deposits in the liver, and exposure to certain industrial chemicals.

HBV is spread when blood, semen, or vaginal fluids (including menstrual blood) from an infected person enter another person's body, usually in one of the following ways:

  • Sexual contact. The hepatitis B virus can enter the body through a break in the lining of the rectum, vagina, urethra, or mouth. Sexual contact is the most important risk factor for the spread of HBV.

Sharing needles. People who share needles and other equipment (such as cotton, spoons, and water) used for injecting illegal drugs may inject HBV-infected blood into their veins.

  • Work-related exposure. People who handle blood or instruments used to draw blood may become infected with the virus. Health care workers are at risk of becoming infected with the virus if they are accidentally stuck with a used needle or other sharp instrument infected with an infected person's blood, or if blood splashes onto an exposed surface, such as the eyes, mouth, or a cut in the skin.

  • Childbirth. A newborn baby can get the virus from his or her mother during delivery when the baby comes in contact with the mother's body fluids in the birth canal (perinatal transmission). However, breast-feeding does not transmit the virus from a woman with HBV to her child.

  • Body piercings and tattoos. HBV can be spread when needles used for body piercing or tattooing are not properly cleaned (sterilized) and HBV-infected blood enters a person's skin.

  • Toiletries. Grooming items such as razors and toothbrushes can spread HBV if they carry blood from a person who is infected with the virus.

In the past, blood transfusions were a common means of spreading HBV. Today, all donated blood is screened for the virus, so it is extremely unlikely that you could become infected with the virus from a blood transfusion.

Signs and symptoms

Most infants and children with hepatitis B never develop signs and symptoms. The same is true for some adults. Signs and symptoms usually appear 12 weeks after you're infected and can range from mild to severe. They may include some or all of the following:

  • Loss of appetite

  • Nausea and vomiting

  • Weakness and fatigue

  • Abdominal pain, especially around your liver

  • Dark urine

  • Yellowing of your skin and the whites of your eyes (jaundice)

  • Joint pain

Hepatitis B can damage your liver — and spread to other people — even if you don't have any signs and symptoms. That's why it's important to be tested if you think you've been exposed to hepatitis B or if you engage in behavior that puts you at risk.

Self-Care at Home

The goals of self-care are to relieve symptoms and prevent worsening of the disease.

  • Drink plenty of fluids to prevent dehydration. Water is fine; broth, sports drinks, Jello, frozen ice treats (such as Popsicles), and fruit juices are even better because they provide calories.

  • Avoid medicines and substances that can cause harm to the liver, such as acetaminophen (Tylenol).

  • Avoid drinking alcohol until your health care provider OKs it. If your infection becomes chronic, you should avoid alcohol for the rest of your life.

  • Avoid using drugs, even legal drugs, without consulting your doctor. Hepatitis can change the way drugs affect you. If you take prescription medications, continue taking them unless your health care provider has told you to stop. Do not start any new medication (prescription or nonprescription), herbs, or supplements without first talking to your health care provider.

  • Try to eat enough for adequate nutrition. Eat foods that appeal to you, but try to maintain a balanced diet. Many people with hepatitis have the greatest urge to eat early in the day.

  • Take it easy. Your activity level should match your energy level.

  • Avoid prolonged, vigorous exercise until symptoms start to improve.

  • Call your health care provider for advice if your condition worsens or new symptoms appear.

Avoid any activity that may spread the infection to other people.

Risk Factors

A risk factor is something that increases your chance of getting a disease or condition. Coming in contact with the blood or other body fluids of someone infected with hepatitis B increases your risk for infection. Unlike hepatitis A virus, hepatitis B virus is not spread through contaminated food or water.

The following situations may increase your risk of getting hepatitis B:

  • Having sex with someone infected with hepatitis B or who is a carrier of hepatitis B

  • Injecting illicit drugs, especially with shared needles

  • Having more than one sexual partner

  • Being a man who has sex with men

  • Living in the same house with someone who is infected with hepatitis B

  • Having a job that involves contact with body fluids, such as:

    • First aid or emergency workers

    • Funeral directors

    • Medical personnel

    • Dentists

    • Dental assistants

    • Firefighters

    • Police personnel

  • Having a sexually transmitted disease at the time you come in contact with hepatitis B

  • Traveling to areas where hepatitis B is common, such as China, southeast Asia, and sub-Saharan Africa

  • Receiving a blood transfusion prior to 1992 (the year a more reliable test to screen blood was developed)

  • Receiving multiple transfusions of blood or blood products, as hemophiliacs do (risk is greatly reduced with modern blood screening techniques)

  • Working or being a patient in a hospital or long-term care facility

  • Working or being incarcerated in a prison

  • Being bitten so that the skin is broken by someone whose saliva contains the virus

  • Being a hemodialysis patient


How can you protect yourself from getting hepatitis B?

Although there is no cure for the HBV, there is a safe and effective vaccine that can prevent hepatitis B. This vaccine has been available since 1982 and is given in a series of three shots. It provides protection against hepatitis B in 90-95% of those vaccinated. Getting vaccinated is the best way to reduce your risk of getting hepatitis B.

It is recommended the vaccine be administered to:

  • Individuals who engage in high-risk behaviors (including unprotected sex, sex with multiple partners, and sharing needles)

  • All babies

  • Adolescents

  • Individuals who live with people infected with HBV

  • Individuals who live in areas with high rates of HBV infection

In addition, other ways to reduce your risk include:

  • Using latex or polyurethane condoms during sex (whenever there is a chance that a sex partner is susceptible to HBV, including unvaccinated or previously uninfected regular partners)

  • Limiting your number of sex partners

  • Avoiding sharing needles, IV drugs, and drug paraphernalia

  • Avoiding skin-piercing or tattoos

  • Practicing standard precautions if you are a health care worker

  • Using care when handling any items that may have HBV-infected blood on them (such as razors, toothbrushes, nail clippers, sanitary napkins, and tampons)


Having a chronic HBV infection eventually may lead to serious liver diseases such as cirrhosis and liver cancer. Having had HBV infection as an infant or child gives you a greater chance of developing these illnesses as an adult.

In addition, hepatitis B puts you at risk of acute liver failure — a condition in which all the vital functions of the liver shut down. When that occurs, a liver transplant is necessary to sustain life.

Anyone chronically infected with HBV is also susceptible to infection with another strain of viral hepatitis — hepatitis D. Formerly known as delta virus, the hepatitis D virus needs the outside coat of HBV in order to infect cells. You can't become infected with hepatitis D unless you're already infected with HBV.

Injection drug users with hepatitis B are most at risk, but you can also contract hepatitis D if you have unprotected sexual contact with an infected partner or live with someone infected with hepatitis D. Having both hepatitis B and hepatitis D makes it more likely you'll develop cirrhosis or liver cancer.


Hepatitis B is detected by a blood test that will show a positive reaction to antibodies. This reveals that your body is making antibodies to try and fight the hepatitis B virus.

Your GP may also request a liver function test. These are blood tests that measure certain enzymes and proteins in your bloodstream, which indicate whether your liver is damaged or inflamed. These will often show raised levels if you are infected with the hepatitis B virus.

The amount of liver damage can only be assessed by taking a liver biopsy. This involves a hollow fine needle being passed through the skin into your liver, to take a sample of tissue. The cells are then examined under a microscope to assess the amount of liver damage, inflammation, and cirrhosis (scarring).                                                   

Laboratory Diagnosis

A battery of ELISAs and RIAs are now available for the diagnosis of specific serological markers of HBV infection.


HBsAg HBeAg Anti-HBe IgM IgG Anti-HBs Interpretation

  +     +     -       -   -     -     Incubation period

  +     +     -       +   +     -     Acute hepatitis B or persistent carrier state

  +     +     -       -   +     -     Persistent carrier state

  +     -     +      +/-  +     -     Persistent carrier state

  -     -     +      +/-  +     +     Convalescence

  -     -     -       -   +     +     Recovery

  -     -     -       +   -     -     Infection with HBV without detectable HBsAg

  -     -     -       -   +     -     Recovery with loss of detectable anti-HBs

  -     -     -       -   -     +     Immunization without infection. Repeated exposure to antigen without infection, or recovery from infection with loss of detectable anti-HBc

During the incubation period, HBsAg is the first serological marker to appear. This occurs 2 to 8 weeks before biochemical evidence of liver dysfunction or the onset of jaundice. The antigen persists throughout the course of the illness and is usually cleared from the circulation during convalescence. Next to appear is the viral DNA polymerase and the e antigen. The e antigen is a distinct soluble antigen that is located within the core and correlates closely with the no, of virus particles and the relative infectivity. Anti-HBc is found in the serum 2 - 4 weeks after the appearance of the surface antigen and is always detectable during the acute early phase of the illness. Core IgM become undetectable several months after the onset of uncomplicated acute infection, but core IgG persists for many years, possibly for life. The next antibody to appear is the anti-e. In general, the presence of anti-e is associated with low infectivity of the serum. Anti-Hbs is the last marker to appear late during convalescence.

In general, detection of HBsAg is used for the diagnosis of acute infection and the screening for carrier status. HBeAg is used to assess the potential infectivity of carriers and antibodies to specific antigens indicate past infection and are of value in monitoring progress. Core IgM is of value in diagnosing recent infection in those who have lost detectable antigen and in whom antibodies have not become apparent (termed the diagnostic window). It is possible to get cases where anti-HBs has disappeared whilst anti-HBc persists. It is also possible to have a situation where anti-HBs is present with no anti-HBc with no history of immunization. This may occur in a situation when the person is continually exposed to minute amounts of HBV which is insufficient to set up an infection. In this manner, the patient becomes immune to HBV.

The presence in the serum gene products of the pre-S1 and pre-S2 regions has been found to be associated with high levels of replication. Pre-S proteins have also been found in the liver. The presence of pre-S1 proteins in the serum and in the liver correlates closely with HBV DNA and on cessation of viral replication, pre-S1 is no longer detectable. Antibodies to pre-S2 have been reported as markers of viral clearance and recovery. Furthermore anti-pre-S2 neutralize the infectivity of HBV. These antibodies may be important in the clearance of circulating HBV virions and the termination of infection ; their absence in patients with chronic active hepatitis may explain why infection persists. Other tests which may be of value include:

(1) The detection of HBsAg-IgM immune complexes - This has been shown to be of value in predicting the outcome of an acute HBV infection in the sense of whether the patient is likely or not to go onto becoming a carrier. HBsAg-IgM immune complexes should only be present for a few weeks after which they become undetectable. If HBsAg-IgM immune complexes persists for more than a few weeks, then the patient is likely to become a carrier.

(2) Serotyping of the HBsAg - This can be done by the use of monoclonal antibodies. Such typing may provide useful information on the epidemiology of a particular outbreak. However, its usefulness is limited by the low no. of strains of HBsAg so that typing of HBsAg will never provide as much information as phage typing for S.aureus.

A Guide to Common Blood Tests


Normal Range

Abnormal Range


Abnormal Range


Liver Enzymes




Aspartate aminotransferase (AST)

<40 IU/L

40-200 IU/L

>200 IU/lL

Alanine aminotransferase


<40 IU/L

40-200 IU/L

>200 IU/L

Gamma-glutamyl transferase (GGT)

<60 IU/L

60-200 IU/L

>200 IU/L

Alkaline phosphatase

<112 IU/L

112-300 IU/L

>300 IU/L

Liver Function Tests





<1.2 mg/dL

1.2-2.5 mg/dL

>2.5 mg/dL


3.5-4.5 g/dL

3.0-3.5 g/dL

<3.0 g/dL

Prothrombin time

<14 seconds

14-17 seconds

>17 seconds

Blood Count




White blood count





Hematocrit (HCT)












U= International Unit


























Blood and blood products are the main routes through which the virus is transmitted. Only a very small amount of blood is needed for transmission (down to 0.00004 ml intradermally). Any technique that allows the transfer of blood or serum from one individual to another is potentially likely to transmit HBV. HBV infection is especially common amongst IV drug abusers. Before the advent of screening, many cases occurred following blood transfusion. It is also particularly common amongst homosexuals where the practice of anal intercourse is particularly traumatic and frequently results in bleeding. Cases have been reported following acupuncture, tattooing and ear piercing.

HBV is a known occupational hazard. The risk to health workers following accidental inoculation is 6 - 20%. Health personnel in renal dialysis units are particularly vulnerable. It is striking that infected professionals often develop severe disease whereas their immunocompromised do not, suggesting that an immunopathological mechanism may be involved in the pathogenesis of the disease. Many infected health workers on the haemodialysis units do not recall any accidental inoculation.

It has become clear that HBV is not spread exclusively by blood and blood products. Under certain circumstances, the virus is infective by mouth. It is endemic in closed institutions such as homes for the mentally handicapped and prisons. The virus is also found in semen, vaginal discharges, breast milk and serous exudates such as the CSF and these have been implicated as possible vehicles of transmission. The presence of HBV antigens has been reported in urine, faeces, bile, sweat and tears but has not been confirmed. There have been cases of family outbreaks of hepatitis B where no known exchange of blood has occurred. The entrance of the virus through the membranes of the eye or mouth must be a possible route of transmission. All biological fluids from a HBV infected individual must be treated as potentially infectious. Although HBsAg has been detected in mosquitoes and bed bugs, there is no convincing evidence for replication of the virus in these insects. The role of arthropod vectors in uncertain although mechanical transmission of infection must be a possibility.

Clustering of HBV infection also occurs within family groups, but does not appear to be related to genetic factors and does not reflect maternal or venereal transmission. HBV does not normally infect the fetus but the baby is at risk of infection during the birth process. The perinatal transmission of HBV is an important factor in maintaining the high level of carriers and thus the prevalence of HBV infection in some regions, notably China and S.E Asia. The risk of transmission to the fetus may reach 50 - 60%, though it varies from country to country and appears to be related to ethnic groups. The risk is greatest if the mother has a history of transmission of infection to previous children or has a high titre of HBsAg or e antigen. There is also a substantial risk of perinatal infection if the mother had acute hepatitis B in the second or third trimester of pregnancy or within 2 months of delivery. Although HBV can infect the fetus in utero, this appears to be rare and is generally associated with antepartum hemorrhage and tears in the placenta. The mechanism of perinatal transmission is uncertain. It probably occurs during or shortly after birth as a result of a leak of maternal blood into the baby's circulation or of its ingestion or inadvertent inoculation. Most children infected during the perinatal period become persistent carriers. 70 - 90% of infants born to e +ve mothers become carriers.

Hepatitis B infection is found worldwide but the prevalence varies enormously between different countries. It is estimated that one-half of the world population has experienced infection and there are 350 million chronically infected individuals. Hepatitis B is responsible for 1.5 million deaths per year. Around 40% of chronically infected individuals will die as a result of their infection. The high carrier rate and the high rate of perinatal infection appears to be the mechanism for maintaining the high prevalence rate in some countries. In high prevalence areas, infection in infancy is very common, particularly acquired from the carrier mothers at birth. The earlier in life the infection, the more likely is persistent carriage to be the outcome. The result is that the carrier rate in the adult population is 10 - 20% and almost all the remainder of the population is immune. In areas of intermediate prevalence, infection is also common in childhood but is usually horizontal between children. This may be due to the fact African HBV carrier mothers are less likely to be e +ve than their Oriental counterparts and thus less likely to transfer HBV perinatally. The carrier rate in adults is 2 - 10% and a quarter to half the population is immune. In low prevalence areas, infection in childhood is rare, the carrier rate is low, 0.1 - 0.5% with a low prevalence of natural immunity in the general population being in order of 2 - 6%. The UK having one of the lowest rates.


                        N and W.Europe     Mediterranean     Parts of China

                        N.America USSR     SW.Asia             S.E.Asia

                        Australia               S.America          Tropical Africa

HBsAg                0.2 - 0.5%            2 - 7%              8 - 20%

Anti-HBs             4 - 6%                 20 - 55%           70 - 95%

The Carrier State

The carrier state is defined as persistence of the HBsAg in the circulation for more than 6 months. The carrier state may be lifelong and may be associated with mild liver damage varying from minor changes in liver function to chronic active hepatitis and cirrhosis and hepatocellular carcinoma. The carrier state is more likely to occur if the infection occurred earlier in childhood rather than adults. It is more frequent in males and more likely to occur in those with acquired or natural immune deficiencies. Approximately half the carriers are e antigen positive. A carrier state is established in 5 - 10% of infected adults. The e antigen is also more likely to be positive in younger carriers.


Infected hepatocytes are characteristically enlarged and their cytoplasm has a ground glass appearance. HBsAg is found associated with the endoplasmic reticulum, core particles containing HBcAg are present in the cell nuclei. Due to large antigenic load present in hepatocytes and in the serum, together with the knowledge is more likely to be asymptomatic or mild in the immunocompromised, it has been postulated that liver injury may result from immune mechanism. Necrosis of hepatocytes results in scattered focal inflammatory response with macrophage and lymphocyte infiltrations together with portal inflammation and endophlebitis of the central veins. In more severe cases, lines of necrosis extends from the portal tracts to the central veins and this often precedes chronic hepatitis and cirrhosis.

Those who become asymptomatic carriers may either have normal liver histology or may show chronic liver inflammation that is recognized as chronic persistent hepatitis. This normally resolves within months or years of acute infection. Some may develop chronic periportal hepatitis which correlates clinically with chronic active hepatitis and continuing patchy necrosis with fibrosis is likely to lead to the major disruption in liver architecture characteristic of cirrhosis. It takes around 4 to 5 years for cirrhosis to develop. Some carriers may go on to develop hepatocellular carcinoma.

Clinical Features

The incubation period for hepatitis B is 6 weeks to 6 months ie. 40 - 180 days (ave. 90 days or 3 months). As with hepatitis A the clinical picture is very variable, although the disease is on the whole more severe than hepatitis A. Asymptomatic and minor non-specific infections are common. The onset is insidious, with a non-specific prodrome consisting of fever, fatigue, nausea, diarrhoea, anorexia, chills, discomfort or pain in the right hypochondrium. The prodrome may be present for 1 - 3 weeks before the jaundice becomes apparent. Arthritis and urticaria are common and may sometimes precede the jaundice and these are thought to be due to circulating immune complexes. The onset of the jaundice is insidious and is accompanied by the darkening of urine and pale stools. In children, the onset of symptoms is more abrupt and the icteric phase shorter. GI disturbances predominate with vomiting, abdominal pain and ketoacidosis being usual. Although urticaria and arthritis are uncommon in children, other immune complex phenomena, particularly glomerulonephritis and papular acrodermatitis are relatively common. Recovery normally takes 6 to 12 weeks after the onset of illness. About 0.1% of patients presenting with acute hepatitis B develop fulminant hepatitis with death from liver failure. The mortality of acute HBV infection increases with age and also with the presence of other disorders.

The Immune Response And The Carrier State

Following HBV infection,the first marker to appear is HBsAg, which is evident 2 to 8 weeks before the appearance of the jaundice and biochemical evidence of liver damage. Next to appear are the markers of the virion, such as virus-specific DNA polymerase activity, the viral DNA and the soluble antigen, HBeAg. Although HBcAg is present, it is not detectable in the serum due to the early appearance of anti-HBc. Anti-HBc is found 2 - 4 weeks after the appearance of the surface antigen, at around the same time as the development of the signs and symptoms. In acute infections, clearance of the virus is marked by the disappearance of HBeAg and the appearance of anti-HBe. Later during convalescence, HBsAg also disappears with the appearance of anti-HBs. CMI to HBsAg appears near the end of the acute phase of hepatitis and appears to be mainly responsible for the disappearance of HBsAg. In contrast, anti-HBs does not appear until months after the termination of the clinical illness. It is noteworthy that in chronic HBsAg carriers specific CMI is generally decreased and circulating anti-HBs is not demonstrable. However, on electron microscopic examination of the patients' sera reveal HBsAg - anti-HBs immune complexes. An increase in anti-HBs is clearly correlated with immunity. In the case of approx. 10% of infected adults and a much larger percentage of perinatally infected children, the immune system fails to clear the infection and a carrier state develops (The carrier state is defined as the persistence of HBsAg in excess for more than 6 months). The carrier state may be divided into 2 phases:

(1) Virus replication continues and the patient is positive for HBeAg and the markers of the virion (viral DNA and DNA polymerase). Although HBeAg correlates with the presence of the virus and thus infectivity, in some cases, virus replication declines to very low levels and seroconversion to anti-HBe may occur. Therefore detection of viral DNA and DNA polymerase (by PCR or hybridization or the endogenous polymerase reaction) is a more reliable indicator of viral replication and infectivity. (It is not uncommon for HBV DNA to be detected in e -ve carriers nor is it uncommon for HBV DNA to be undetectable in e +ve carriers.) During this phase of chronicity, replicative forms of HBV DNA may be detected in the liver. Levels of virus replication may decline until this is eliminated with the development of anti-HBe. Rarely there will also be seroconversion to anti-HBs.

(2) In this second phase, HBsAg persists in the absence of active virus replication. HBV DNA is now integrated chromosomally in the hepatocytes. and HBsAg is produced following the transcription of this integrated DNA. This integration of the HBV DNA into the host cell chromosome may be a stage in the development of hepatocellular carcinoma. The integration of the HBV DNA is thought to occur at the time of seroconversion of e Ag.

In general e +ve carriers have a high infectivity whereas e -ve carriers have a much reduced or absent infectivity. Over a number of years, it is quite common to see e +ve carriers seroconvert with the development of anti-e Abs and then progress onwards to lose their HBsAg and develop anti-HBs. The rate for the reversion of the carriers to being naturally immune is around 2% per year. In chidren born to carrier mothers, girls are much more likely to seroconvert than boys although both sexes are just as likely to be infected and become carriers initially. It is not unusual for people who were naturally immune with anti-HBs to lose their anti-HBs and develop HBsAg in their blood (especially Haemophiliac patients with AIDS). It is not certain whether this is due to reinfection or the reactivation of the virus.

Chronic HBV carriage may take the form of chronic active hepatitis (CAH) or chronic persistent hepatitis (CPH) or minimal hepatitis. The distinction can only be made on histological examination of the liver. CAH is far more common in e +ve carriers as it is indicative of active viral replication. Cirrhosis and hepatocellular carcinoma (HCC) is thought to be more common in e -ve carriers. It was suggested that those e -ve carriers who had a prolonged e +ve stage are more prone to developing cirrhosis and HCC. It was reported that nuclear DNA is commonly detected alone in the late phase of HBV infection, which represents either integrated fragments or supercoiled HBV DNA, whereas cytoplasmic and nuclear HBV DNA is commonly detected in the early phase of the illness and CAH, which is indicative of active viral replication.

HBV is essentially hepatotropic but HBV DNA has been detected in other sites such as the peripheral leucocytes, the bone marrow and spleen. The viral DNA is usually in episomal form and is rarely integrated. These findings have implications for virus transmission and also for the possible recurrence of hepatitis B infection in patients who have cleared infection in the liver, in particular patients with AIDS who had had anti-HBs following an acute infection in the past but become HBsAg positive again. Individuals infected with both hepatitis B and hepatitis C are prone to prolonged disease, cirrhosis and hepatocellular carcinoma.


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Our Herbal formulation has the capacity of raising both the hemoglobin and interferon.