Info@livershield.net
For video click the link below:
The Hepatitis B (HBV) is a single molecule of DNA or RNA in a protein coat .It is a microscopic organism that cannot perform any function (living or reproductive) on its own until it infects a host liver cell. It has to get pass the immune system to infect a liver cell. During the Second World War, yellow fever vaccines given to army recruits were mistakenly contaminated with viruses that elicited jaundice. Further investigations found the viruses to be hepatitis. The HBV was discovered by Dr Baruch Blumberg – a Nobel Prize winner in 1965 while studying the genetic correlation to diseases and how antibodies react to antigens. Dr Blumberg did his test by collecting blood samples from different indigenous tribes worldwide. He observed that antibodies from some people from the Australian Aborigine reacted against an antigen. In 1966 he corroborated his findings with virologist Alfred Prince of the New York Blood Center who was doing some work on transfusion Hepatitis. Prince believed that the Australian antigen Blumberg had discovered was related to the HBV and in 1967; The Australian Antigen was confirmed to be the HBV.
It was initially called the AU or Australian antigen. In 1986 the HBV was first observed under an electron microscope and the first samples were grown in test tubes. (Green, 2002).It was determined that the Australian antigen was a surface antigen for the Hepatitis B virus (HBsAg) and till date it is still the most commonly used test to determine Hepatitis B. This surface antigen is a protein synthesized by the virus DNA genetic material and is an important element on the virus coat.In1972, the FDA mandated all blood banks to screen blood received for the HBV virus. In 1973, the American association of blood banks followed the FDAs line. Since 1975 more sensitive tests were introduced and individual who received blood transfusions before 1975 may have come in contact with the HBV.
HOW WIDESPREAD IS HBV VIRUS IN USA?
HOW GLOBAL IS HBV EPIDEMIC?
The world Health Organization states that:
HBV is transmitted through body fluids including blood, semen, vaginal secretions and saliva, any break in the skin and mucous membranes.
HBV mode of transmission is:
Since the Hepatitis B virus can stay alive for up to 10 days even on a dry surface, it is important not to torch any blood even if it is dry. All blood should be cleaned with a solution of 1 part of household bleach to 10 parts of water.
You cannot get Hepatitis B from the following routes
You are at risk of contracting Hepatitis B if:
WHAT DOES HBV LOOK LIKE?
Hepatitis B is a DNA virus a member of the hepadnaviridae family of viruses that have affinity for the liver cells. The infectious (“Dane”) particle comprises of an inner core plus an outer surface coat. The outer shell is composed of several proteins called HBs (surface proteins). The outer surface coat surround an inner protein shell composed of HBc (core proteins). The inner shell is called the core particle (capsid). The core particle surrounds the Viral DNA and the enzyme DNA polymerase. The entire virion is known as a Dane particle. The HBV genome encodes a DNA polymerase that also acts as a reverse transcriptase. After the viron enters the liver cells, it is uncoated and its genome is delivered into its nucleus and it releases its contents of DNA and DNA polymerase into the liver cell nucleus. There the viral genome is converted into covalently closed circular DNA (cccDNA) –a mitochromosome that serves as the viral transcription template.
RNA serves as a pre-genomic template for reverse transcription to negative-strand DNA, which in turn becomes the template for transcription of positively strand DNA. The mRNA transcribes viral proteins as well as pre-genomic RNA that is reverse transcribed into the HBV DNA of new virons. Without the reverse transcriptase, new virons cannot be produced and replication ceases.The significance of this explicative strategy led to the development of drugs called nucleoside analogues that can block viral multiplication. The HBV (like most viruses) is a microscopic single molecule of DNA or RNA wrapped in a protein coat. It is an invisible parasite that cannot perform any function (living or reproductive) on its own until it infects a host cell. It has to get pass the immune system to infect a liver cell. It ultimately is an unwelcomed guest.
WHAT HAPPENS WHEN ONE COMES IN CONTACT WITH HBV?
When the “Lifeless” Hepatitis B virus get past the immune system to incorporate itself into the host cell and uses the DNA materials of the liver cells to replicate itself, it comes “alive”. In the process the host cells become infected. Like an intruder using your house as it’s staging ground, once the virus attack a host cell; they take over the machinery the cell uses to multiply them. In the case of the liver cells, the virus causes the liver cell’s DNA or RNA to reproduce it instead of the liver cells. A parasitic relationship now exists that benefit the HBV. The virus uses the livers DNA as a template to replicate itself. The liver cells making the virus are referred to as “host infected cells” The thousands and millions of copies of the virus cells burst from the host liver cell killing the liver cells. Each new virus contaminates another host cell to make more copies. This explains how the virus moves around the liver. When the virus enters the body of a new host its initial response, if it gets past the immune system, then it infects the liver cells.
knowing your laboratory terminologies:
Seroconversion as the name implies is the conversion in the blood serum of the antigens and/or antibodies from one form to another. The forms can be positive or negative. This manifestation is used to access the progression of the disease or its response to remedies. It may involve loosing an antibody or gaining an antigen. When one looses antigens and gains antibodies in the serum it indicates, it is indicative of a favorable prognosis. In serological testing various relationships between the antibodies and the antigens are used as prognostic tools to follow the progression of hepatitis and response to treatment by the doctor. This is often referred to as lab based approach.
The antigens (Ag) are protein signals or indicators on the surface of intruding virus cells that host immune system recognizes. They elicit immunological responses from the host they are invading since the immune system them as foreign.
The antibodies- Ab are proteins produced by the white blood cells to fight antigens. Antigens are our foes and antibodies are our friend.
The “e” antigen is a peptide discovered in 1973 that assist the HBV to higher levels of contagiousness. It is not a favorable presence. It is a protective coat that protects the infected liver cells from the immune system so the liver cells can house the HBV for longer period of time. It presence means HBV is actively multiplying. Remedies that can help the host to lose the “e” antigen are most beneficial. Losing the “e” antigen is a favorable prognosis.
The “e” antigens and Core antigens are produced by the virus during viral replications. Their presence indicates there is replication or multiplication of the virus.
The Core antigen is part of the virus that stimulates immunological response from the host liver cells. These responses are called core antibodies.
DNA polymerase is an enzyme that helps the release of the Hepatitis B DNA needed or the multiplication of Hepatitis B viruses. They are part of the virus’s DNA and are released during active infection and replication of the virus. It can be used to monitor response to antiviral therapy
The “e” antigen and antibody. Written as HBeAg and HBeAb are antigens and antibodies seen in chronic and acute phases of Hepatitis B infections.
The surface antigens and antibody (S for surface) – HBsAg and HbsAb. They are the first indicators of initial infection but their presence does not tell whether the infection is acute or chronic.
The HBsAg – surface antigen to the Hepatitis B virus indicates the liver is infected with HBV and the liver is producing the antigen. It indicates that the host is contagious.
Core antigen and antibody (C for core because they are found in the core of the Hepatitis B virus) –HBcAg and HBcAb. They are also known to as IgM anti HBc and IgG anti –HBc. They are usually not part of routine testing in most hospitals and labs.
The core proteins are part of the virus particle and constitute part of the viral coat that covers its nuclear material. When the virus establishes itself in the liver cells this core protein is produced and the immune system responds to their presence by producing core antibodies. The presence of antibodies to core antigens in the blood as used as lab indicators to differentiate an acute from a chronic infection.
WHAT ARE IMMUNOGLOBULINS?
During encounters with the host immune system with the invading viruses, the host antibodies lock on to the virus surface antigens to form antigen -antibody complexes. This “tying up” of the virus antigens enable the immune system to take it’s time to organize the response needed to dispose the virus. These antibodies that lock onto to the antigens are called immunoglobulins or Ig for short. In HBV infections the IgG and IgM indicate the presence of antibodies that indicate ongoing or previous infections. People with IgG and surface antibodies for the HBV indicate the infection is resolved in them. Similarly individuals with IgG with no surface antibodies for the HBV have chronic HBV and are considered contagious. IgM are indicators of acute infections.
Does your child need hepatitis B vaccine? How safe is it? When Your Doctor Is Wrong… scrutinizes reportable data on the virus and the vaccine as it follows one child through the terrible maze of adversely reacting to this shot. His recovery is a must read for all families touched by autism, while the alarming news of the shot’s inappropriateness for infants and children will inform all parents. When Your Doctor Is Wrong… gives parents facts they need to vaccinate more safely. "A well written and arresting account that parents and the medical community need to see. This could be a breakthrough book about autism." - Randall Neustaedter, OMD, author, The Vaccine Guide Judy Converse, MPH, RD is a licensed registered dietitian specializing in dietary intervention for autism. Her practice assists agencies and hospitals serving those with autism and provides therapeutic diets for affected children. She holds graduate and undergraduate degrees in nutrition and has worked in cardiac nutrition, diabetes, and infant/toddler nutrition. A vaccine safety advocate, she has testified before state and federal legislators on infant hepatitis B vaccination. She lives with husband Chris and son Ben, who survived a nearly fatal hepatitis B vaccine adverse reaction at birth.
WHAT IS FLUMINANT HEPATITIS B?
It is a rare type of hepatitis B that manifest as sudden liver failure, bleeding propensities, jaundice and encephalopathy coma. It is a progressive degenerative type of hepatitis B and fatal in about 85% of cases. It requires immediate liver transplant. Co-infection with other types of Hepatitis is a risk factor for Fluminant Hepatitis B (Palmer, 2004).
WILL I OVERCOME HEPATITIS B INFECTION?
About 90% of adults will get rid of the virus while 10 % will become chronic carriers. This is unlike the Hepatitis C virus, the Hepatitis B virus does not mutate rapidly so anti-viral and the immune system can launch a coordinated war against the virus. About 40% of young children will get rid of the virus and about 60% will end up as chronic carriers. About 90% of infants will become chronic carriers and about 10 % of infants will be able to get rid of the virus
WHAT ARE THE PHASES OF HBV?
The immune system may accommodate the HBV virus in host’s blood. This occurs mostly in congenital cases or in teenagers because the immune system is developing or maturing and does not know what to do with the virus. This immune tolerance phase may last into the adult years. This stage is followed by the immune clearance phase. This stage is characterized by the maturing immune system waking up from ignorance and recognizing that it has a tiger on its back. It makes efforts to clear the virus if it can. Favorable seroconversions can occur and if not the illness progresses to more chronic manifestations.
WHAT HAPPENS DURING ACUTE HBV INFECTION?
The disruption of the host’s liver cells functions leads to acute symptoms of nausea, vomiting, fever, pain in the liver area, fatigue, dark urine, light stools and jaundice. Infected cells leak their contents which are read in laboratory test as elevated liver enzymes. The HBV infection usually takes an average of two to eight weeks before the liver enzymes (ALT and AST) are elevated. The HBV virus infection is acute as long as the host immune system clears the virus and develops antibodies against the virus. Viral and immune indicators are detectable in the blood and the antibody-antigen markers are used to characterize the patterns of HBV infection.
The hepatitis B virus’s surface antigens (HBsAg) (the surface protein of the HBV) also known as anti-HBs are found in the sweat, blood, saliva, semen, vaginal fluids, breast milk, tears, and nasal secretions also appears in the blood about 1-6 weeks after initial infection and even before symptoms manifests. They are the first detectable viral marker of the illness. A positive test for the presence of these surface antigens is the standard test for an ongoing infection. Their presence indicates that there is HBV in the body of the individual. The Hepatitis B viral infection has an incubation period of between 45 days to 160 days.
The average incubation period is 100 days. The HBsAg is followed by the HBeAg and HBV DNA. When the core of HBV disintegrates in the blood serum the antigen is formed and detected by lab tests. This is found in acute stage and resolves when the acute infection is over. If these antigens appear in the blood for more than six month, it indicates chronic infection. The titers are usually high during the incubation period but gradually levels off. The Hepatitis B viral DNA and Hepatitis ‘e’ antigen may continue to drop. During active infections, these immune-globulins (Ig) fuse with the Hepatitis B surface antibody (HBsAb) to neutralize HBV infection. The presence of immunoglobulins in the blood and the time intervals between the disappearance of Hepatitis B surface antigen (HBsAg) and the appearance of the antibodies-Anti-HBs is the standard marker for an acute infection. This time interval is referred to as the window period.
The most sensitive indicator of HBV replication is HBeAg. Laboratory test that indicate the presence of HBsAg and IgM core antibody or core antibody alone during the window period is diagnostic of an acute infection. The loss of HbsAg and the presence of HbsAb imply recovery from the acute illness and development of immunity. Immunity against HBV confers protection from Hepatitis D but not Hepatitis A and C. During stages of rapid replication of the HBV virus, short forms of hepatitis B core antigen (HBeAg) are also found in the blood. HBV “e” antigen is derived from the core or a portion of the core of the HBV. The Hepatitis B surface antibodies (HBsAb) to the virus is produced by the immune-globulins i.e. secreted by the body’s B lymphocytes in response to the presence of HBeAb) i.e. the Hepatitis antigen. It appears after the HBeAg turns negative signifying resolution of infection. And the presence of antibodies to Hepatitis ‘e’ (HBeAb) indicates a favorable prognosis.
WHEN HBV INFECTION BECOMES CHRONIC?
The presence of HBsAg in the blood for more than six months indicates a chronic infection. The presence of IgG core antibodies Chronic HBV carriers are divided into two distinguishable states of HBV infection. The presence and absence of Hepatitis B e Antigen (HbeAg) in the blood. In most cases of chronic infection, HBeAg is not detected in the blood, i.e. the virus switched from high explicative detectable state to low explicative undetectable state. I.e. it becomes an “occult illness”
WHEN IS HBV CONTAGIOUS?
When HBsAg (hepatitis B surface antigen) in the blood is positive, this indicates contagiousness. When anti-HBc (antibody to Hepatitis B core antigen) is positive in the blood, it implies recent or previous infection. In other cases, HBsAg is positive but the “e” antigen and Hepatitis BDNA is negative- this indicates that no replication is going on but the individual is still contagious. If the “e” antigen and HBDNA are negative contagiousness is reduced. High viral loads and antigen “e” positive indicates a serious contagious phase. When tests indicate the presence of the e antigen with HBV actively in the blood stream, the individual is still contagious. If tests indicate antigen e negative and undetectable HBV in the blood, the individual is not contagious. But could be infectious to some degree due to probability of seroconversion.
Individuals with HBsAg and HBeAg are highly contagious. They are undergoing active viral replication and are considered highly infective Individuals are HBeAg negative and HBeAb are less contagious. Individuals with HBeAg negative, HB DNA negative and HBeAb positive are not contagious. Inactive chronic carriers have HBeAb i.e. antibodies to the e antigens in their blood. Most people who are chronically infected are infected as infants because the immune systems of infants do not produce enough antibodies to eradicate the virus.
WHO ARE HEALTHY HBV CARRIERS?
About 10% of HBV patients who could not eradicate the virus after six months of infection and about 80% of congenital HBV sufferers are chronic carriers. Inactive healthy carriers are persons infected with HBV with no clinical evidence.They have detectable hepatitis B surface antigens (HBsAg) in their blood but no manifestations of liver disease i.e. no signs or symptoms. They show no signs of viral replication. They have laboratory evidence of HBV infection but no physical manifestation of the disease. ‘About 75% of chronic carriers will have no evidence of inflammation on liver biopsy.
They are referred to as true carriers. About 25% of chronic carriers show evidence of liver inflammation on liver biopsy. They are not true carriers. They have chronic hepatitis despite normal laboratory tests and no visible symptoms. They may exhibit liver cirrhosis on liver biopsy. They may develop clinically apparent hepatitis later in life’ (Worman, 1999). Since one in four chronic carriers will die from complications of liver cirrhosis or liver cancer, early detection is crucial to prevention of these complications.
WHO IS A SILENT CARRIER?
Hepatitis B virus is referred to as “silent infection” because chronically infected people can be infected for a long time and not even aware of it and do not display any apparent symptoms of the disease. Such people often show up in the doctor’s office with end stage liver disease. Silent carriers have laboratory markers that indicate HBsAg positive with near normal liver enzymes, with low or no viral loads and no symptoms of the disease.
The presence of HBeAg in the blood indicates an ongoing inflammation, high infective state and higher chances of progression to cirrhosis and cancer if the inflammation becomes uncontrollably chronic. Since 1987, the rate of acute HBV infection has dropped because of the introduction of immunization of neonates, vaccinations of occupationally exposed persons, refinements in the screenings of blood donors, and the use of virus inactivated blood products for patients with bleeding disorders as well as changes of lifestyles among high risk groups.
HOW DO I KNOW IF I HAVE RECOVERED FROM HBV INFECTION?
Individuals who clear the HBV virus loose the HbsAg and the lab results show the presence of Hepatitis B surface antibodies –HBsAb or anti-HBs. They develop lifelong immunity. The presence of anti-HBsAb and anti-HBcAb (IgG) indicate recovery and immunity in a previously infected person or have acquired immunity by receiving antibodies from their mother as infants. Vaccinations can cause the HBsAb i.e. the Hepatitis B surface antibody marker to be positive which can exist in the body for a long period of time.
WILL I GET CURED FROM CHRONIC HEPATITIS?
From a conventional point of view, cure is the reduction of the viral load to undetectable with anti-viral and/or interferon therapy. Like all other viruses that exist in the body it is impossible to completely eliminate them from the organs. Available test that indicate undetectable in the blood and body fluids cannot test their presence in the body tissues. In most instances they go into low explicative phase and are not picked up by the most sensitive lab tests. This is why HBV is called an occult illness.
From a holistic point of view, involvement with religion, lifestyles chances with nutrition, botanical supplements and stress reduction that help improve the quality of life, strengthen the terrains of the human body against viral onslaught, arrest inflammation with active involvement of the host ultimately leads to healing. Conventional and/or alternative can sometimes lead to seroconverion in chronic hepatitis B individuals. In those situations, individual involved will need to monitor their blood work periodically as indicated by their physician for the rest of their lives to ensure that they remain non- contagious.
Developing antibodies (HBsAb) to the Hepatitis B virus either through vaccination or through warding off acute infection confers lifelong immunity for the Hepatitis B viral infection. Doctors Health advisory: Individuals with HBV need to check for the presence of HIV, HCV and HDV as co-infections. Individuals who continue to actively replicate the HBV virus with high levels of HBV DNA and HBeAg in their blood have progressive liver diseases which have a higher probability of progressing to cirrhosis, end stage liver diseases and hepatocellular carcinoma. The loss of the HBeAg does not mean permanent resolution of the problems associated with Hepatitis B infection. Flare ups should be expected.
WHAT ARE THE CONVENTIONAL TREATMENTS FOR CHRONIC HEPATITIS B?
The use of synthetic drugs kills our incentives to find the root cause of our diminished immunity that made hepatitis B infective in addition to adding to our toxic loads. While antiviral treat the problem and not the person; botanical supplements treats both the person and the problem (virus). We liken antiviral to spraying your pantry for ants and leaving the sugar jaw on the shelf. Other ants will always come back for the sugar. Antibiotics are not used against viral infections because viruses like the HBV live inside their host’s cell .For antibiotics to get to the virus they has to first destroy the liver cells which is often too much collateral damage.
Drugs used in the management of hepatitis B with drugs falls into two categories:
Immune modulators namely-Recombinant Interferon Alfa-2b: The synthetic interferon alfa-2b was approved in the United States in 1992, as a therapy for chronic HBV. Their mode of action is to mimic natural interferons.
Exogenous Alpha interferon fail to resolve chronic HBV in many patients and the therapy is often fraught with a variety of adverse reactions like other synthetic drugs which includes low neutrophil and platelet counts. The platelet the body needs to fight infections is lowered by synthetic Alpha interferon. In the short term they are tolerated in less than 30% of Hepatitis B patients. The majority of these patients relapse with discontinuation of interferon.
To help ameliorate adverse reactions associated with interferon’s, physicians generally recommend Acetaminophen (Tylenol). Liver damage from excessive use of acetaminophen is responsible for majority of liver transplants in the United States. Exogenous interferon aggravates diabetes and thyroid disorders. It interferes with the nervous system causing tingling in the hands, feet, arms and legs. It causes depression, anxiety, irritability, confusion, nervousness, impaired concentration, insomnia and suicidal tendencies. Other more frequent side effects include back pain, dry mouth, diarrhea and inflammation at injection site. Hence artificial interferon’s always produce artificial reactions.
Inhibitors of HBV replication(Lamivudine -Epivir and Adefovoif Dipivoxil -Hepsera. These prevent viral multiplication in the liver cells. They are aimed to prevent viral replication and prevent end-stage liver disease. The markers of successful treatment with these drugs are HBeAg seroconversion, reduced or undetectable HBV DNA and lack of disease progression.
HOW DO SYNTHETIC ANTIVIRALS WORK?
When the HBV enters the host cell and takes control of the DNA it is converted to covalently closed circular DNA. This serves as a template for a series of reverse transcriptions. From a clinical point of view, this reverse transcription strategy is what currently available antiviral drugs disrupt. While they disrupt viral replication in infected liver cells, like a sledge hammer, they also indiscriminately disrupt the enzymes systems of healthy liver cells causing serious adverse reactions. The severity, the types and amount of these adverse reactions are unpredictable. We want you to know that all Hepatitis antiviral drugs cause Hepatitis.
Lamivudine (Epivir) also known as 3TC is a nucleoside analog introduced in 1999. It inhibits the (reverse transcriptase) DNA polymerase of the HBV virus. The activity of this enzyme is essential for the replication of the virus. It is also used for the treatment of HIV infection. The HIV has a DNA polymerase also called reverse transcriptase that is inhibited by Almandine. It is administered orally while interferon is administered by injection. Among all the FDA approved anti-viral drugs Epivir is the best tolerated. Known side effects include, loss of appetite, neuropathy, depression, skin rash, itching, bone aches, coughing, nervousness, diarrhea, fatigue, headache. It can cause abnormally too much acid in the blood causing lactic acidosis, severe hepatomegally and hepatitis. Abnormal laboratory tests due to Epivir include low red blood cells count, neutropenia (low white blood cell count), low platelet count, increased liver enzymes (ALT) and swollen lymph glands. Like all antiviral therapies, the HBV virus does mutate and become resistant to Epivir. Hence there are at least 20 new antiviral released annually in the United States because the HBV virus always mutate to new species to elude currently available anti-viral. It worth knowing that viruses do not mutate against all available botanical antiviral and antibiotic herbs and they have been in existence since creation. They do not have generics and god never modified them. They are not marketed by pharmaceutical companies because they were given freely by the creator for his creations.
Adefovir Dipivoxil (Hepsera) can suppress HBV strains that developed resistance to Epivir. The FDA approved it in 2002. Hepsera can cause worse or very serious hepatitis in some people when they stop taking Hepsera. It can cause liver enlargement and damage. The warning signs include yellowing of the skin or eyes, dark urine, light colored stools, nausea, lower stomach pain and loss of interest in eating for several days. Kidney damage and lactic acidosis. Lactic acidosis is a medical emergency. It’s warning signs includes weakness, tiredness, unusual muscle pain, difficulty breathing, stomach pain, nausea, vomiting, cold feelings in the arms and legs, dizziness or irregular heartbeat. In individuals with untreated HIV, Hepsera may increase the chances that HIV infection cannot be helped with usual HIV medicines. When Hepsera is discontinued, it comes back with more vigorous symptoms. Cummings and Ullman (2004) believes that if drugs are used to suppress conditions, when the drug effects wears off, the suppression often force the system to create deeper symptoms to handle the underlying imbalance.
The HBV is never completely eradicated from the body. It goes to low explicative phase, which is undetectable by blood test. It could stay undetectable with strong immunity and the absence of stressors.
WHAT ARE THE FACTS ABOUT THE HEPATITIS B VACCINE?
The rationale behind vaccination is the assumption that when a genetically engineered, weakened life or killed virus is injected into the body, it will trick the body into producing antibodies to the disease. This is what happens when the body contracts the illness naturally. The duration of the immunity in the development of mutant strains and the adverse reactions from taking multiple shorts are a few of the unknown variables.
In the development of HBV vaccine, it is important to note that the availability of successful immunoprophylaxis will not be useful to individuals who have developed chronic infections.
After discovering the HBV, Dr Blumberg and his colleague Irvin Milkman, invented the first HBV vaccine (Green, 2002). The first vaccine was the inactivated or denatured HBV using heat to denature HBV antigen. This vaccine elicited unwanted immunological responses. In 1973, plasma derived vaccines were developed by collecting antibodies from individuals who overcame the HBV viral infection. Initially, the HBV vaccine was derived from the blood products of homosexual men who had hepatitis. These serum based vaccines were later replaced with genetically engineered or recombinant DNA version that is grown on yeast cells in the 1990. The vaccines are given in three shots between 6 to 12 months period and they are thought to confer immunity between 6 to 12 years. Majority of individuals who get the first shots are protected against the HBV virus but full protection is attained after the final shots.
WHO NEEDS TO BE VACCINATED AGAINST HBV?
People undergoing hemodyalysis, IV drug users, family members and co- workers of infected persons, sexual partners of infected persons, nurses, doctors, laboratory workers, people who engage in risky sexual behaviors, people with multiple sex partners, people who plan to travel to high risk arrears. It is important for people who work regularly with infected persons to check their antibody levels and make sure it is above 10 units per ml. it antibody levels fall below this level, the need to go for booster shots to refill. Individuals who are unvaccinated and exposed to the HBV virus through blood or body fluids should get the intramuscular injection of Hepatitis B immunoglobulin (HBIG) within 14 days of exposure followed by the Hepatitis B vaccine immediately.
WHAT ARE LIKELY ADVERSE REACTIONS OF HBV VACCINES?
The body sees genetically engineered products as foreign. In the process the body elicits auto immune responses that can lead to wide varieties of auto-immune diseases. This is what accounts for majority of the adverse reactions associated with vaccination. Side effects suffered by children vaccinated with the HBV vaccine include lethargy, malaise, asthma, diarrhea, arthritis, faintness, pallor, loss of consciousness, and drop in blood pressure. Between 1990 and 1994 about 12,000 adverse events linked to the HBV vaccine was reported in the United States .30-50 percent of those vaccinated with the HBV vaccine will need booster shots every five years for the rest of their lives. The major problem with vaccination is eradication of one strain of a virus encourage other forms to proliferate-new diseases from vaccines. (Mctaggart, 1996).Improved sanitation’s education, stress reduction, hygiene, better nutrition, housing, and quarantine procedures also played noble roles in the eradication of communicable diseases.
Back
Liver Shield. Email: Info@livershield.net
Copyright © 2010 Liver Shield. All Rights Reserved.