Hepatitis B Strains

Hepatitis B Strains

  

HBV is a mostly double-stranded DNA virus in the Hepadnaviridae family. HBV causes hepatitis in human and related virus 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 function of protein X is not clear but it may be involved in the activation of host cell genes and the development of cancer.

 

Organization of the HBV Genome

The genomes of more than a dozen isolates of hepatitis B virus have been cloned and the complete nucleotide sequences determined. Analysis of the coding potential of the genome reveals four open reading frames (ORFs) which are conserved between all of these isolates.

The first ORF encodes the various forms of the surface protein and contains three in-frame methionine codons which are used for initiation of translation. A second promoter is located upstream of the pre-S1 initiation codon. This directs the synthesis of a 2.4 kb mRNA which is co-terminal with the other surface messages and is translated to yield the large (pre-S1) surface proteins.

The core open reading frame also has two in-phase initiation codons. The “precore” region is highly conserved, has the properties of a signal sequence and is responsible for the secretion of HBeAg.

The third ORF, which is the largest and overlaps the other three, encodes the viral polymerase. This protein appears to be another translation product of the 3.5 kb RNA, and is synthesized apparently following internal initiation of the ribosome.

The amino terminal domain is believed to be the protein primer for minus strand synthesis. There is then a spacer region followed by the (RNA and DNA-dependent) DNA polymerase.

The fourth ORF was designated “x” because the function of its small gene product was not known. However, “x” has now been demonstrated to be a transcriptional transactivator.

…The discovery of variation in the epitopes presented on the surface of the virions and subviral particles identified several subtypes of HBV which differ in their geographical distribution. All isolates of the virus share a common epitope, a, which is a domain of the major surface protein which is believed to protrude as a double loop from the surface of the particle. Two other pairs of mutually exclusive antigenic determinants, d or y and w or r, are also present on the major surface protein. These variations have been correlated with single nucleotide changes in the surface ORF which lead to variation in single amino acids in the protein. Four principal subtypes of HBV are recognized: adw, adr, ayw and ayr. Subtype adw predominates in northern Europe, the Americas and Australasia and also is found in Africa and Asia. Subtype ayw is found in the Mediterranean region, eastern Europe, northern and western Africa, the near East and the Indian subcontinent. In the Far East, adr predominates. But the rarer ayr occasionally may be found in Japan and Papua New Guinea.

The major response of recipients of hepatitis B vaccine is to the common a epitope with consequent protection against all subtypes of the virus. First generation vaccines were prepared from 22 nm HBsAg particles purified from plasma donations from chronic carriers. These preparations are safe and immunogenic but have been superseded in some countries by recombinant vaccines produced by the expression of HBsAg in yeast cells. The expression plasmid contains only the 3′ portion of the HBV surface ORF and only the major surface protein, without pre-S epitopes, is produced. Vaccines containing pre-S2 and pre-S1, as well as the major surface proteins expressed by recombinant DNA technology, are undergoing clinical trials.

Types of HBV Genomes


The following is a list of the major types of HBV genomes found in the human population:

  • 1993: Genetic relatedness of hepatitis B viral strains of diverse geographical origin and natural variations in the primary structure of the surface antigen.
  • 1995: Subtypes, genotypes and molecular epidemiology of the hepatitis B virus as reflected by sequence variability of the S-gene.
  • 1998: Antigenic diversity of hepatitis B virus strains of genotype F in Amerindians and other population groups from Venezuela.

6 Genotypes (A,B,C,D,E,F) [PMID: 8336122]

  • Group A – Orig – N. Europe – Sub-Saharan Africa
  • Group B – Confined to – Eastern Asia (China)
  • Group C – Far East (Japan)
  • Group D – Mediterranean – Near, Mid East, South Asia
  • Group E – W. Sub-Saharan Africa, south to Angola
  • Group F – New World – Brazil, N. + S. America

121 Strains Exist as Quasispecies

There are four serotypes which are based on subtypes of the hepatitis B surface antigen (HBsAg). These are defined by two mutually exclusive determinant pairs d/y and w/r with a common determinant ‘a’. These subtypes are adw, ayw, adr, and ayr.

Four genomic groups of HBV were later referred as genotypes designated with A-D. Sequencing of the S-gene of HBV is the molecular basis for the assessment of the serological variations of HBsAg within the major four subtypes. Two new genotypes of HBV are designated with E and F. The F genotype diverges from other HBV genomes sequenced by 14%. So far, it is the most divergent HBV genome. Worldwide molecular epidemiology of HBV is based on the variability of the S-gene. The E and F strains appear to originate from aboriginal populations of Africa in the New World.

Characterization of genotype H hepatitis B virus strain identified for the first time from a Japanese blood donor by nucleic acid amplification test

Hepatitis B virus (HBV) has been classified into seven genotypes A–G. However, recently genotype H, which is phylogenetically closely related to genotype F, has been reported (Arauz-Ruiz et al., 2002 ). These genotypes of HBV show a distinctive geographical distribution and a relevance to clinical severity (Mayert et al., 1999 ; Kobayashi et al., 2002 ; Locarnini, 2002)

Possible New Hepatitis B Virus Genotype, Southeast Asia

(Emerging Infectious Diseases Volume 14, Number 11–November 2008)

Abstract
We conducted a phylogenetic analysis of 19 hepatitis B virus strains from Laos that belonged to 2 subgenotypes of a new genotype I. This emerging new genotype likely developed outside Southeast Asia and is now found in mixed infections and in recombinations with local strains in a geographically confined region.

 

Hepatitis B Vaccines:

 

 

COMVAX® [HAEMOPHILUS b CONJUGATE (MENINGOCOCCAL PROTEIN CONJUGATE) and HEPATITIS B (RECOMBINANT) VACCINE]

 

HBsAg is produced in recombinant yeast cells. A portion of the hepatitis B virus gene, coding for HBsAg, is cloned into yeast, and the vaccine for hepatitis B is produced from cultures of this recombinant yeast strain according to methods developed in the Merck Research Laboratories. The antigen is harvested and purified from fermentation cultures of a recombinant strain of the yeast Saccharomyces cerevisiae containing the gene for the adw subtype of HBsAg. The fermentation process involves growth of Saccharomyces cerevisiae on a complex fermentation medium which consists of an extract of yeast, soy peptone, dextrose, amino acids and mineral salts.

The HBsAg protein is released from the yeast cells by mechanical cell disruption and detergent

extraction, and purified by a series of physical and chemical methods, which includes ion and hydrophobic chromatography, and diafiltration. The purified protein is treated in phosphate buffer with formaldehyde and then coprecipitated with alum (potassium aluminum sulfate) to form bulk vaccine adjuvanted with amorphous aluminum hydroxyphosphate sulfate. The vaccine contains no detectable yeast DNA, and 1% or less of the protein is of yeast origin.

The individual PRP-OMPC and HBsAg adjuvanted bulks are combined to produce COMVAX. Each 0.5 mL dose of COMVAX is formulated to contain 7.5 mcg PRP conjugated to approximately 125 mcg OMPC, 5 mcg HBsAg, approximately 225 mcg aluminum as amorphous aluminum hydroxyphosphate sulfate, and 35 mcg sodium borate (decahydrate) as a pH stabilizer, in 0.9% sodium chloride. The vaccine contains not more than 0.0004% (w/v) residual formaldehyde.

The potency of the PRP-OMPC component is measured by quantitating the polysaccharide

concentration by an HPLC method. The potency of the HBsAg component is measured relative to a standard by an in vitro immunoassay.

ENGERIX-B® [Hepatitis B Vaccine (Recombinant)]

ENGERIX-B [Hepatitis B Vaccine (Recombinant)] is a noninfectious recombinant DNA hepatitis B vaccine developed and manufactured by GlaxoSmithKline Biologicals. It contains purified surface antigen of the virus obtained by culturing genetically engineered Saccharomyces cerevisiae cells, which carry the surface antigen gene of the hepatitis B virus. The surface antigen expressed in Saccharomyces cerevisiae cells is purified by several physicochemical steps and formulated as a suspension of the antigen adsorbed on aluminum hydroxide. The procedures used to manufacture ENGERIX-B result in a product that contains no more than 5% yeast protein. No substances of human origin are used in its manufacture.

Pediatric/Adolescent: Each 0.5-mL dose contains 10 mcg of hepatitis B surface antigen adsorbed on 0.25 mg aluminum as aluminum hydroxide. The pediatric formulation contains sodium chloride (9 mg/mL) and phosphate buffers (disodium phosphate dihydrate, 0.98 mg/mL; sodium dihydrogen phosphate dihydrate, 0.71 mg/mL).

Adult: Each 1-mL adult dose contains 20 mcg of hepatitis B surface antigen adsorbed on 0.5 mg aluminum as aluminum hydroxide. The adult formulation contains sodium chloride (9 mg/mL) and phosphate buffers (disodium phosphate dihydrate, 0.98 mg/mL; sodium dihydrogen phosphate dihydrate, 0.71 mg/mL).

PEDIARIX®[Diphtheria and Tetanus Toxoids and Acellular Pertussis Adsorbed, Hepatitis B (Recombinant) and Inactivated Poliovirus Vaccine Combined]

 

It contains diphtheria and tetanus toxoids, 3 pertussis antigens (inactivated pertussis toxin [PT] and formaldehyde-treated filamentous hemagglutinin [FHA] and pertactin [69 kiloDalton outer membrane protein]), hepatitis B surface antigen, plus poliovirus Type 1 (Mahoney), Type 2 (MEF-1), and Type 3 (Saukett). The diphtheria toxoid, tetanus toxoid, and pertussis antigens are the same as those in

INFANRIX® (Diphtheria and Tetanus Toxoids and Acellular Pertussis Vaccine Adsorbed). The hepatitis B surface antigen is the same as that in ENGERIX-B® [Hepatitis B Vaccine (Recombinant)].

…The hepatitis B surface antigen (HBsAg) is obtained by culturing genetically engineered Saccharomyces cerevisiae cells, which carry the surface antigen gene of the hepatitis B virus, in synthetic medium. The surface antigen expressed in the S. cerevisiae cells is purified by several physiochemical steps, which include precipitation, ion exchange chromatography, and ultrafiltration.

…The diphtheria, tetanus, and pertussis antigens are individually adsorbed onto aluminum hydroxide; hepatitis B component is adsorbed onto aluminum phosphate. All antigens are then diluted and combined to produce the final formulated vaccine. Each 0.5-mL dose is formulated to contain 25 Lf of diphtheria toxoid, 10 Lf of tetanus toxoid, 25 mcg of inactivated PT, 25 mcg of FHA, 8 mcg of pertactin, 10 mcg of HBsAg, 40 D-antigen Units (DU) of Type 1 poliovirus, 8 DU of Type 2 poliovirus, and 32 DU of Type 3 poliovirus.

TWINRIX® [Hepatitis A Inactivated & Hepatitis B (Recombinant) Vaccine]

 

TWINRIX® [Hepatitis A Inactivated & Hepatitis B (Recombinant) Vaccine] is a sterile bivalent vaccine containing the antigenic components used in producing HAVRIX® (Hepatitis A Vaccine, Inactivated) and ENGERIX-B® [Hepatitis B Vaccine (Recombinant)].

The purified hepatitis B surface antigen (HBsAg) is obtained by culturing genetically engineered Saccharomyces cerevisiae cells, which carry the surface antigen gene of the hepatitis B virus, in synthetic media containing inorganic salts, amino acids, dextrose, and vitamins. Bulk preparations of each antigen are adsorbed separately onto aluminum salts and then pooled during formulation.

A 1.0-mL dose of vaccine contains 720 ELISA Units of inactivated hepatitis A virus and 20 mcg of recombinant HBsAg protein. One dose of vaccine also contains 0.45 mg of aluminum in the form of aluminum phosphate and aluminum hydroxide as adjuvants, amino acids, sodium chloride, phosphate buffer, polysorbate 20, Water for Injection, traces of formalin (not more than 0.1 mg), and residual MRC-5 cellular proteins (not more than 2.5 mcg). Neomycin sulfate, an aminoglycoside antibiotic, is included in the cell growth media; only trace amounts (not more than 20 ng) remain following purification. The manufacturing procedures used to manufacture TWINRIX result in a product that contains no more than 5% yeast protein.

RECOMBIVAX HB® HEPATITIS B VACCINE (RECOMBINANT)

 

RECOMBIVAX HB* Hepatitis B Vaccine (Recombinant) is a non-infectious subunit viral vaccine

derived from hepatitis B surface antigen (HBsAg) produced in yeast cells. A portion of the hepatitis B virus gene, coding for HBsAg, is cloned into yeast, and the vaccine for hepatitis B is produced from cultures of this recombinant yeast strain according to methods developed in the Merck Research Laboratories.

The antigen is harvested and purified from fermentation cultures of a recombinant strain of the yeast Saccharomyces cerevisiae containing the gene for the adw subtype of HBsAg. The fermentation process involves growth of Saccharomyces cerevisiae on a complex fermentation medium which consists of an extract of yeast, soy peptone, dextrose, amino acids and mineral salts. The HBsAg protein is released from the yeast cells by cell disruption and purified by a series of physical and chemical methods. The purified protein is treated in phosphate buffer with formaldehyde and then coprecipitated with alum (potassium aluminum sulfate) to form bulk vaccine adjuvanted with amorphous aluminum

hydroxyphosphate sulfate. The vaccine contains no detectable yeast DNA but may contain not more than 1% yeast protein. The vaccine produced by the Merck method has been shown to be comparable to the plasma-derived vaccine in terms of animal potency (mouse, monkey, and chimpanzee) and protective efficacy (chimpanzee and human).

Pediatric/Adolescent Formulation (Without Preservative), 10 mcg/mL: each 0.5 mL dose contains 5 mcg of hepatitis B surface antigen.

Adult Formulation (Without Preservative), 10 mcg/mL: each 1 mL dose contains 10 mcg of

hepatitis B surface antigen.

Dialysis Formulation (Without Preservative), 40 mcg/mL: each 1 mL dose contains 40 mcg of hepatitis B surface antigen.

All formulations contain approximately 0.5 mg of aluminum (provided as amorphous aluminum

hydroxyphosphate sulfate, previously referred to as aluminum hydroxide) per mL of vaccine. In each formulation, hepatitis B surface antigen is adsorbed onto approximately 0.5 mg of aluminum (provided as amorphous aluminum hydroxyphosphate sulfate) per mL of vaccine. The vaccine is of the adw subtype.

RECOMBIVAX HB is indicated for vaccination of persons at risk of infection from hepatitis B virus

including all known subtypes. RECOMBIVAX HB Dialysis Formulation is indicated for vaccination of adult predialysis and dialysis patients against infection caused by all known subtypes of hepatitis B virus.

 Nabi-HB® Hepatitis B Immune Globulin (Human)

 

DESCRIPTION

 

Hepatitis B Immune Globulin (Human), Nabi-HB, is a sterile solution of immunoglobulin (5 ± 1%

protein) containing antibodies to hepatitis B surface antigen (anti-HBs). It is prepared from plasma

donated by individuals with high titers of anti-HBs. The plasma is processed using a modified

Cohn 6 / Oncley 9 cold-alcohol fractionation process1,2 with two added viral reduction steps

described below. Nabi-HB is formulated in 0.075 M sodium chloride, 0.15 M glycine, and 0.01%

polysorbate 80, at pH 6.2. The product is supplied as a nonturbid sterile liquid in single dose

vials and appears as clear to opalescent. It contains no preservative and is intended for single

use by the intramuscular route only.

The manufacturing steps for Nabi-HB are designed to reduce the risk of transmission of viral disease.

The solvent/detergent treatment step, using tri-n-butyl phosphate and Triton® X-100, is

effective in inactivating known enveloped viruses such as hepatitis B virus (HBV), hepatitis C

virus (HCV), and human immunodeficiency virus (HIV) 3. Virus filtration, using a Planova® 35

nm Virus Filter, is effective in reducing some known enveloped and non-enveloped viruses4. The

inactivation and reduction of known enveloped and non-enveloped model viruses were validated

in laboratory studies as summarized in the following table…

BayHepB Immune Globulin (Human)

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HepB vaccine injury case

JANE DOE/23, Petitioner, v. SECRETARY OF THE DEPARTMENT OF HEALTH AND HUMAN SERVICES, Respondent

 Office of Special Masters – U.S. Court of Federal Claims – “Each expert in the instant case agrees that optic neuritis is frequently a hallmark for MS. There is a logical sequence of cause and effect connecting petitioner’s exposure to hepatitis B vaccine and her onset of demyelinating disease. Petitioner has proved causation in fact.”

Hepatitis B triple series vaccine and developmental disability in US children aged 1–9 years

Hepatitis B triple series vaccine and developmental disability in US children aged 1–9 years

 

Abstract

This study investigated the association between vaccination with the Hepatitis B triple series vaccine prior to 2000 and developmental disability in children aged 1-9 years (n = 1824), proxied by parental report that their child receives early intervention or special education services (EIS). National Health and Nutrition Examination Survey 1999-2000 data were analyzed and adjusted for survey design by Taylor Linearization using SAS version 9.1 software, with SAS callable SUDAAN version 9.0.1. The odds of receiving EIS were approximately nine times as great for vaccinated boys (n = 46) as for unvaccinated boys (n = 7), after adjustment for confounders. This study found statistically significant evidence to suggest that boys in United States who were vaccinated with the triple series Hepatitis B vaccine, during the time period in which vaccines were manufactured with thimerosal, were more susceptible to developmental disability than were unvaccinated boys.

Hepatitis B Vaccines

Hepatitis B Vaccines:

·         Engerix B

·         Recombivax HB

·         Twinrix (Hep A and B)

·         Pediarix (DTaP, IPV and Hep B)

·         Comvax (Hep B and HIB)

·         Nabi-HB = Immune Globulin

 ·         Bay Hep B = Immune Globulin (human)

 ·         HB-vax II

·         PTY LTD

 ·          Hexa (DTaP, Hep B, HIB, IPV)

Contains Thimerosal (mercury): Engerix B and Twinrix

Contains Aluminum: Pediarix, Recombivax, Comvax

Contains Fetal Cell lines: Twinrix (MRC-5)Hexa (MRC-5)

Energix B (Hep B) Glaxo:  

The CONTROL GROUP received plasma-derived vaccines. The vaccines administered to the CONTROL GROUP are not revealed.

Ten double-blind studies involving 2,252 subjects showed no significant difference in the frequency or severity of adverse experiences between ENGERIX-B and plasma-derived vaccines.
In 36 clinical studies, a total of 13,495 doses of ENGERIX-B were administered to 5,071 healthy adults and children who were initially seronegative for hepatitis B markers, and healthy neonates. All subjects were monitored for 4 days post-administration.

 

 
Recombivax HB (Hep B) Merck:

 

This vaccine was not evaluated for safety using a control group.

In three clinical studies, 434 doses of RECOMBIVAX HB, 5 mcg, were administered to 147 healthy infants and children (up to 10 years of age) who were monitored for 5 days after each dose.
In a study that compared the three-dose regimen (5 mcg) with the two-dose regimen (10 mcg) of RECOMBIVAX HB in adolescents, the overall frequency of adverse reactions was generally similar.
In a group of studies, 3258 doses of RECOMBIVAX HB, 10 mcg, were administered to 1252 healthy adults who were monitored for 5 days after each dose.

 

     

    • At no point was Hepatitis B evaluated at birth, to see what effect it would have on either liver enzymes, or immune system parameters.

    In 1982, the C.D.C., the F.D.A., and the manufacturer created a surveillance system to monitor spontaneous reports of adverse events occurring after inoculation with the new-plasma derived hepatitis B vaccine (Heptavax-B, Merck Sharp and Dohme, West Point, PA). In the three years between June 1, 1982 and May 31, 1985, an estimated 850,000 persons received the vaccine. During that period, a total of 41 reports were received for one of the following neurologic adverse events: convulsions (5 cases), Bell’s palsy (10 cases), Guillain-Barre syndrome (9 cases), lumbar radiculopathy (5 cases), brachial plexus neuropathy (3 cases), optic neuritis (5 cases), and transverse myelitis (4 cases).  Half of these occurred after the first of three required vaccine doses. In some analyses, Gullain-Barre syndrome was reported significantly more often that expected (p=<0.05). Shaw FE, Jr., Graham DJ, Guess HA, Milstien JB et. al.   Postmarketing surveillance for neurologic adverse events reported after hepatitis B vaccination. Experience of the first three years   Am J Epidemiol 1988 (Feb);   127 (2):   337-352

     When Evidence Based Medicine (EBM) Fuels Confusion: Multiple Sclerosis after Hepatitis B Vaccine as a Case in Point.M. Girard/Medical Veritas 4 (2007) 1436-1451.

    •  

         

        One of the major side effects of the Hepatitis B vaccine in the kids ‘catch-up campaign’ is “bronchospasm” and kids who have asthma are nearly always guaranteed to have a serious asthma attack on the day of their shot.  

      RHEUMATIC DISORDERS DEVELOPED AFTER HEPATITIS B VACCINATION
      Aim
      : to obtain an overview of rheumatic disorders occurring after hepatitis B vaccination.

      Conclusion: hepatitis B vaccination might be followed by various rheumatic conditions, and might trigger the onset of underlying inflammatory and/or auto-immune rheumatic diseases. However, a causal relation between hepatitis B vaccination and the observed rheumatic manifestations cannot be easily established. Further epidemiological works are needed to establish whether hepatitis B vaccination is associated or not with an incidence of rheumatic disorders higher than normal.

      Other Studies:

      Several papers have been published linking immunization to lupus and other rheumatoid diseases. A study of lupus patients receiving polio vaccines showed 5% had a flare following immunization (Schattner et al., 1992). Several papers have reported patients with lupus developing deterioration in kidney function following immunization (Ristow et al., 1978); (Louie et al., 1978). Lupus has been reported to occur following immunization with the Hepatitis B (Tudela et al., 1992), and pneumococcal (Ries & Shemonsky, 1981) vaccines. Immunization with the influenza vaccine has been associated with a rise in anti-double stranded DNA antibodies, an marker for lupus (Huang et al., 1992). Rheumatoid arthritis has been observed to occur following immunization with Hepatitis B vaccine (Vautier & Carty, 1994). Rheumatoid factor, auto antibodies that bind other antibodies, have been reported to develop following vaccination (Aho et al., 1962); (Aho et al., 1967); (Palit et al., 1977); (Welch et al., 1982).

       The Genetic Centers of America, MedCon, Inc., Silver Spring, Maryland 20905, USA.

       OBJECTIVES: Adverse events and positive re-challenge of symptoms reported in the scientific literature and to the Vaccine Adverse Event Reporting System (VAERS) following hepatitis B vaccination (HBV) were examined.

       

       

       

      METHODS: The VAERS and PubMed (1966-2003) were searched for autoimmune conditions including arthritis, rheumatoid arthritis, myelitis, optic neuritis, multiple sclerosis (MS), Guillain Barre Syndrome (GBS), glomerulonephritis, pancytopenia/thrombocytopenia, fatigue, and chronic fatigue, and Systemic Lupus Erythematous (SLE) following HBV.  

       

      RESULTS: HBV was associated with a number of serious conditions and positive re-challenge or significant exacerbation of symptoms following immunization. There were 415 arthritis, 166 rheumatoid arthritis, 130 myelitis, 4 SLE, 100 optic neuritis, 101 GBS,
      29 glomerulonephritis, 283 pancytopenia/thrombocytopenia, and 183 MS events reported following HBV A total of 465 positive re-challenge adverse events were observed following adult
      HBV that occurred sooner and with more severity than initial adverse event reports. A case-report of arthritis occurring in identical twins was also identified.

      CONCLUSIONS: Evidence from biological plausibility, case-reports, case-series, epidemiological, and now for positive re-challenge and exacerbation of symptoms, and events in identical twins was presented. One would have to consider that there is causal relationship between HBV and serious autoimmune disorders among certain susceptible vaccine recipients in a defined temporal period following immunization. In immunizing adults, the patient, with the help of their physician, should make an informed consent decision as to whether to be immunized or not, weighing the small risks of the adverse effects of HBV with the risk of exposure to deadly hepatitis B virus. (NEUROLOGY 2004; 63:838-842 American Academy of Neurology,   Miguel A. Hernán, MD et al)

      • Recombinant hepatitis B vaccine and the risk of multiple sclerosis-A prospective study.
        Miguel A. Hernán, MD et al.

         

        • Conclusions: These findings are consistent with the hypothesis that immunization with the recombinant hepatitis B vaccine is associated with an increased risk of MS, and challenge the idea that the relation between hepatitis B vaccination and risk of MS is well understood.
         

         

         

      Celiacs less likely to gain immunity from Hep B:  

      A total of 23 subjects were reviewed. All had a clinical and pathological diagnosis of celiac disease. All subjects reported receiving the full series of hepatitis B vaccinations. Of the subjects, 19 had testing for hepatitis B vaccine response. Of these 19 subjects, 13 did not achieve long-term immunity as seen by the negative qualitative or quantitative anti-HBs antibody titer.

      Hepatitis B Study:

      Conclusions: Anti-HBs disappeared by 5 years of age in most children who were vaccinated with hepatitis B vaccine from birth. Although most children showed immunologic memory, one-third failed to demonstrate an anamnestic response to a booster dose. Additional long term studies of low risk infants are needed to determine duration of protection and the necessity for or timing of booster doses.

      HEPATITIS B VACCINE: The first hepatitis B virus vaccines developed in the 1970s were made using virus isolated from the blood of human chronic hepatitis B carriers. A plasma-derived hepatitis B vaccine was licensed by the U.S. in 1981 and used in high-risk populations in the 1980s until a genetically engineered, recombinant hepatitis B vaccine was developed. Today, hepatitis B recombinant vaccine used in the U.S. is derived from hepatitis B surface antigens produced in yeast cells. A portion of the hepatitis B virus gene is cloned into the yeast (a common baker’s yeast) and the vaccine is produced from cultures of this recombinant yeast strain. The vaccine is treated with formaldehyde and contains 95 percent hepatitis B virus surface antigen, 4 percent yeast protein, aluminum hydroxide and thimerosal added as a preservative.” (source: The Consumer’s Guide to Childhood Vaccines by Barbara Loe Fisher).

       

       

       

       

       

       

    Hepatitis and Helpful Nutrients

    Hepatitis occurs when infection or toxins cause the liver to inflame. Symptoms first resemble the flu: fever, swollen lymph glands, weakness, drowsiness, stomach discomfort and headache, often followed by extreme fatigue and loss of appetite. Soon the liver is unable to eliminate poisons, allowing them to build up and no longer store and process certain nutrients vital to the body.  

    To recover from hepatitis, one must rest, abstain from alcohol, and follow a diet rich in essential nutrients: high in vegetable protein and complex carbohydrates, unsaturated fatty acids, including coldwater fish, liberal amounts of fluids, and vitamins B complex, C and E. This regimen should be continued long after recovery, since sensitivity to toxins may persist. Along with whole foods and nutritional supplementation, consume plenty of filtered water. Drinking fresh lemon juice in water every morning and evening followed by a vegetable juice is believed to be beneficial. Do this consistently for two to four weeks and then several mornings a week for several months and whenever liver symptoms occur.

    Because hepatitis results from toxic substances in the body, vitamin C therapy is particularly important. Large intravenous doses of vitamin C (sodium ascorbate) along with B complex and calcium supplements can help reduce the severity of the infectious hepatitis symptoms and speed up the healing process.

    This treatment originated with Dr. Frederick Klenner, M.D., of North Carolina in the 1940s and has been used successfully elsewhere, most recently by Dr. Akira Murata of Saga University in Japan.

    Source: (http://home3.inet.tele.dk/omni/nutrition.htm)

     

    Other Resources:

    ·         Hepatitis Information Center- http://www.hepatitis-central.com/hbv/hepbfaq/comp.html

    ·         Hepatitis Information Center- http://www.hepatitis-central.com/hbv/hepbfaq/other.html

    ·         iherb-http://healthlibrary.epnet.com/GetContent.aspx?token=e0498803-7f62-4563-8d47-5fe33da65dd4&chunkiid=21384

    Hepatitis B

    Hepatitis means inflammation of the liver. Toxins, certain drugs, some diseases, heavy alcohol use, and bacterial and viral infections can all cause hepatitis. Hepatitis is also the name of a family of viral infections that affect the liver; the most common types in the United States are hepatitis A, hepatitis B, and hepatitis C.
     

    Hepatitis B is a contagious liver disease that results from infection with the hepatitis B virus. It can range in severity from a mild illness lasting a few weeks to a serious, lifelong illness. Hepatitis B is usually spread when blood, semen, or another body fluid from a person infected with the hepatitis B virus enters the body of someone who is not infected. This can happen through sexual contact with an infected person or sharing needles, syringes, or other drug-injection equipment. Hepatitis B can also be passed from an infected mother to her baby at birth.

    Hepatitis B can be either acute or chronic. Acute hepatitis B virus infection is a short-term illness that occurs within the first 6 months after someone is exposed to the hepatitis B virus. Acute infection can — but does not always — lead to chronic infection. Chronic hepatitis B virus infection is a long-term illness that occurs when the hepatitis B virus remains in a person’s body. Chronic hepatitis B is a serious disease that can result in long-term health problems, and even death.

    Hepatitis B Universal Vaccination: Learning from the French Experience

    The First Cancer Vaccine: Facts and Failings by F. Edward Yazbak, MD, FAAP

    Hepatitis B: Discrimination and Vaccine Damage:  

     

    For more than 20 years, the National Vaccine Information Center (NVIC) has been receiving reports that adults, children and infants are suffering serious reactions to hepatitis B vaccine. Hepatitis B vaccine reaction reports began to come in to NVIC’s Vaccine Reaction Registry in the late 1980’s from adult health care workers, who reported extreme fatigue, muscle weakness, joint pain, loss of vision, memory loss, heart problems, and development of multiple sclerosis after hepatitis B vaccination.
    Infants who contract hepatitis B, either from their infected mother or infected blood transfusions, are at highest risk for chronic infection. But for the majority of healthy teenagers and adults, who come down with hepatitis B infection, symptoms include nausea, vomiting, low grade fever, pain and swelling in the joints, headache, and cough for two weeks before the onset of jaundice and enlargement/tenderness of the liver that lasts for three to four weeks. Fatigue can last up to a year but “most patients do not require hospital care” and “95 percent of patients have a favorable course and recover completely” with the case fatality ratio being “very low (approximately 0.1 percent)” according to Harrison’s Principles of Medicine (11th Edition).
    Those who recover completely from hepatitis B infection acquire life-long immunity. One medical textbook (Robbins Pathologic Textbook of Disease) points out that among those who do not recover completely from hepatitis B infection, fewer than 5 percent become chronic carriers of the virus, with just one quarter of these in danger of developing life threatening disease later in life.

     

     

     

     There is no reason a pregnant mother can’t be tested for Hepatitis B before she delivers, or after delivery, and have her baby tested as well in lieu of a vaccine given at birth. Some states mandate testing pregnant mothers before birth as well, so you would know ahead of time if you were positive or negative. If a mother is positive, the baby would be given hepatitis B immue globulin (HBIG).

     
    Hepatitis B and Titers

     One feature of the Hepatitis B is that if you never show antibodies, there is no point in having more shots. Some people may even test false positive with titers.

    There are two groups of people:

    • 1. Those who have an immune response to hepatitis B that is weak, and have difficulty clearing the virus from their system. These are the people who may become carriers, and whose responses to the vaccine are naturally stunted as well. Booster shots in this group would be short lived.
      2. For others, the immune system gets rid of the virus without a problem. They produce higher titers, and even if their detectable antibodies become next to nothing, they will still respond well to re-infection or a vaccine booster. They are also the group of people who would never become carriers or get cancer in the first place.
      Basically, the people who need the vaccine the most because they would be most likely carriers or get cancer, is the group least likely to respond well to the vaccine, and to have the poorest response to boosters.
      In a nut shell- those who don’t need the vaccine, respond best. Those who do need it, respond the worst.

    Vaccination tries to mimic a natural process of on real exposure but doesn’t do it well and adds some risks that were not there in the first place. Therefore, the group that would suffer the most from the disease is still at risk by vaccine failure and side effects. 

     

     

    If 30-50% of persons who develop adequate antibody after 3 doses of the vaccine, loose detectable antibody within 7 years, by the time a child is 7 years old, they won’t show any benefits of the vaccine! (Parent Information. Understanding infant hepatitis B immunisation. Immunise Australia program, NHMRC) Further more, carriers can be carriers for over 40 years and not know until they have a blood test that tells them. People, who are carriers that live clean lives, don’t drink alcohol, and maintain a good diet, carriage will mean nothing as it will not  be a problem in their lives. It will only be a problem if there was a second, third and beyond tiers done of co-carcinogens to trigger the virus into creating potential cirrhosis and subsequent cancer. If the parents have no antibodies to the disease, how do they know the vaccine will give their children antibodies? When you read medical literature on carriers, you will see it runs in families because there is an immune defect that prevents the body from either clearing it, or creating antibodies.  

     

     

     A study in Science Direct:

    Short-term response to a booster dose of hepatitis B vaccine in anti-HBs negative adolescents who had received primary vaccination 16 years ago:

    Abstract

    We conducted a revaccination study to investigate the short-term response to booster hepatitis B (HB) vaccination in seronegative adolescents who had received primary infantile HB vaccination. A booster dose of recombinant HB vaccine was administered to 395 adolescents 15–18 years of age whose serum titers of antibody against hepatitis B surface antigen (HBsAg) (anti-HBs) were <10 mIU/mL. Seventy-seven percent of the booster recipients converted to anti-HBs seropositivity (postbooster titers ≥ 10 mIU/mL). As compared with adolescents who had undetectable prebooster anti-HBs titers (<0.1 mIU/mL), the seropositive rates and geometric mean titers (GMTs) of 2-month and 1-year postbooster were significantly higher for those of prebooster titers of 0.1–0.9 and 1.0–9.9 mIU/mL (all p < 0.0001). Postbooster titers declined significantly more rapidly for those with undetectable prebooster anti-HBs titers than for those with prebooster titers of 0.1–0.9 and 1.0–9.9 mIU/mL. Our observations indicate that a booster dose of HB vaccine maybe unable to induce sufficient immunological response in adolescents who had undetectable residual anti-HBs titers.

    So, that means all the babies being vaccinated now will have to do the whole series again when they are older and might have a small risk of developing Hepatitis B. Tell me again what was the point in vaccinating all babies from birth again???

         

    Hepatitis B Vaccines…safeStay tuned…