FAIL: Infant Hep B Vaccines Perform Shamefully; Time To End Them?
By Sayer Ji
An eye-opening new study published in the Journal of Viral Hepatitis reveals that conventional hepatitis B vaccine- and hepatitis B immunoglobulin-based treatment for infants of mothers who tested positive for hepatitis B infection is nothing near “95% effective in preventing infection and its chronic consequences” that the World Health Organization (WHO) and a myriad of health organizations around the world claim it to be. [i] To the contrary, researchers were able to detect through highly sensitive polymerase chain reaction (PCR) DNA testing that 42% of the infants still had ‘occult’ hepatitis B infection, 24 months after initiating treatment at birth, despite the fact that the vaccine reduced the incidence of overt infection.
In the researchers’ own words: “The results of this large prospective longitudinal study show that 42% of babies born of HBsAg-positive mothers develop occult HBV infection, which is not prevented by administration of recombinant HBV vaccine to the newborn.“ [italics added]
This study not only clearly calls into question the standard of care for preventing hepatitis B infection in infants born to infected mothers, but it also challenges core tenets of vaccinology, including hepatitis B vaccine safety and effectiveness.
A closer look at the study
The new study titled, ‘Hepatitis B vaccination with or without hepatitis B immunoglobulin at birth to babies born of HBsAg-positive mothers prevents overt HBV transmission but may not prevent occult HBV infection in babies: a randomized controlled trial‘, tracked pregnant women found to be HBsAg positive (i.e. Hepatitis B surface antigen was found in their blood work) until delivery, and then tracked their babies for 2 years.
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The study design and results were as follows:
Immediately after delivery, babies were randomized to receive either HBIG [Hepatitis B immunoglobulin] or placebo in addition to recombinant HBV vaccine (at 0, 6, 10 and 14 weeks). The primary end-point of the study, assessed at 18 weeks of age, was remaining free of any HBV infection (either overt or occult) plus the development of adequate immune response to vaccine. The babies were further followed up for a median of 2 years of age to determine their eventual outcome. Risk factors for HBV transmission and for poor immune response in babies were studied. Of the 283 eligible babies, 259 were included in the trial and randomized to receive either HBIG (n = 128) or placebo (n = 131) in addition to recombinant HBV vaccine. Of the 222 of 259 (86%) babies who completed 18 weeks of follow-up, only 62/222 (28%) reached primary end-point. Of the remaining, 6/222 (3%) developed overt HBV infection, 142/222 (64%) developed occult HBV infection, and 12/222 (5%) had no HBV infection but had poor immune response. All 6 overt infections occurred in the placebo group (P = 0.030), while occult HBV infections were more common in the HBIG group (76/106 [72%] vs. 66/116 [57%]; P = 0.025). This may be due to the immune pressure of HBIG. There was no significant difference between the two groups in frequency of babies developing poor immune response or those achieving primary end-point. The final outcome of these babies at 24 months of age was as follows: overt HBV infection 4%, occult HBV infection 42%, no HBV infection but poor immune response 8% and no HBV infection with good immune response 28%.
The authors concluded, in a startling reversal of conventional wisdom regarding the treatment’s efficacy:
The current practice of administration of vaccine with HBIG at birth to babies born of HBsAg-positive mothers is not effective in preventing occult HBV infection in babies, which may be up to 40%.
Known as hepatitis B post-exposure prophylaxis, infants of mothers infected with hepatitis B are administered 4 doses of recombinant hepatitis B vaccine (birth, 6 weeks, 10 weeks and 14 weeks), in combination with hepatitis B immunoglobulin (HBIG). All pregnant women are encouraged today to be screened for hepatitis B, and all are made to undergo this treatment because it is believed to be ‘highly effective.’ This despite evidence that the hepatitis B vaccine may actually cause liver damage,[ii] and has been linked to over four dozen adverse health effects.[iii]
The recombinant hepatitis B vaccine is produced by isolating hepatitis B surface antigen (HBsAg) from genetically modifying yeast engineered to express this viral antigen-protein. It was, in fact, the first vaccine produced by DNA recombinant technology, i.e. genetic modification.[iv] The HBIG is isolated from the blood plasma of infected donors with high concentrations of anti-Hepatitis B viral antigen antibodies. [v]
Hepatitis B virus infection is a major health problem worldwide, with the WHO estimating that about one third of the world population has been infected at some point in their lives and that it kills 600,000 people each year. The virus contributes to a variety of liver diseases, including acute, fulminant and chronic hepatitis, liver cirrhosis and liver cancer (hepatocelullar carcinoma). It is believed that mother-to-infant transmission accounts for 50% of the chronic infection cases.[vi]
So, what is occult hepatitis B infection, and what causes it?
The definition of “occult” hepatitis B infection has different meanings to different researchers, but in general it indicates that even when blood tests show a disappearance of HBeAg and HBsAG viral antigens, or antibodies to these antigens, hepatitis B virus remains active (replication capable) within the body. The ‘occult’ form is often referred to as an ‘escaped mutant’ and is a version of hepatitis B other than the one(s) being tested for, whose presence is ascertained DNA testing (PCR), which is far more sensitive than antibody- or antigen- based testing.
The new study offered the following definition: “Occult HBV infection is defined as the existence of HBV DNA in the serum, or cells of the lymphatic (immune) system, and/or hepatic tissue in the absence of serum HBsAg [13,14].”
Strangely, even when there is no hepatitis B virus (HPV) DNA detectable through PCR DNA testing, it may still be there lying dormant. For instance:
[T]he elimination of HBV genomes is usually not complete after acute hepatitis B (even after mild infections) because some HBV genomes remain as cccDNA [covalently closed circular DNA] in an occult form in the liver; but their expression is largely controlled by the immune system. The levels of HBV production are in most cases so low that even with the most sensitive techniques no HBV DNA is detectable in serum.[vii]
In other words, hepatitis B virus can integrate into the DNA of cells in a form (cccDNA) which remains dormant and reactivates only rarely when the immune system is severely compromised. This dormant form does not produce hepatitis B DNA (unless reactivated) and therefore is virtually (if not actually) impossible to detect.
Because conventional criteria for assessing the effectiveness of hepatitis B vaccine and/or hepatitis B immunoglobulin treatment are based solely on the presence or absence of viral antigen or antibodies against viral antigens, their actual effectiveness at clearing all pathogenic variants of the hepatitis B virus from the body is largely unknown. This also means that vaccine policy today is based on outdated criteria. This is now poignantly evident by the fact that 42% of these vaccinated infants had signs of occult infection 2 years later.
The hepatitis B virus is a DNA virus with such a high replication and mutation rate, [viii] that it has been described as a ‘quasispecies’ due to its highly varied (heterogeneous) viral population:
The HBV population is highly heterogeneous and is comprised of genomes that are closely related, but not identical; hence, it is considered a viral quasispecies, a term commonly associated with RNA viruses. The complex viral replication cycle of HBV may be the cause of this quasispecies nature.
It has been estimated that an infected individual produces mutations of every viral genome base at least two times per day. The so-called mutated version of the hepatitis B virus is known as an ‘escape mutant’:
Hepatitis B virus (HBV) reverse transcriptase is an error-prone enzyme, and this results in a large number of nucleotide substitutions during replication. As a result, HBV has a “quasispecies” distribution in infected individuals, meaning that HBV circulates as a complex mixture of genetically distinct but closely related variants that are in equilibrium at a given time point of infection in a given replicative environment. The quasispecies distribution of HBV implies that any newly generated mutation conferring a selective advantage to the virus in a given replicative environment will allow the corresponding viral population to overtake the other variants. Such selection processes occur at any step of infection to allow the emergence of variant viruses, such as precore and core promoter mutants during the natural course of infection, HBs antigen mutants under the pressure of active or passive anti-HBs immunization, or HBV mutants that are resistant to the antiviral action of specific HBV inhibitors.[ix]
Due to its complex nature it is extremely difficult to detect all its variants through conventional serological testing. This is one reason why DNA testing is valuable and more sensitive.
Furthermore:
The occult HBV infection may be due to infection by HBV variants with mutations in the S gene (escape mutants) producing a modified HBsAg that is not recognized by some or all commercially available detection assays [14].
Even the CDC acknowledges in their hepatitis B immunization guidelines that “escape mutants” can replicate even in the presence of treatment-induced anti-HB antibodies:
Mutations in the S gene of HBV can lead to conformational changes in the a determinant of the HBsAg protein, which is the major target for neutralizing anti-HBs. These variants have been detected in humans infected with HBV, and concern has been expressed that these variants might replicate in the presence of vaccine-induced anti-HBs or anti-HBs contained in HBIG (194,195). Although no evidence suggests that S gene immunization escape mutants pose a threat to existing programs using hepatitis B vaccines (196), further studies and enhanced surveillance to detect the emergence of these variants are high priorities for monitoring the effectiveness of current vaccination strategies.[x]
Is the treatment driving the creation of mutant, ‘occult’ forms of hepatitis B?
Despite the CDC’s dismissal of concerns that escape mutants could threaten the effectiveness of existing hepatitis B immunization programs, research published in the Asian Journal of Transfusion Science has raised exactly this concern:
[Vaccinations] apply selective pressures on HBV in infected individuals leading to the generation and accumulation of mutations in the S gene. Most of these mutations occur in the major hydrophilic region (MHR) of the S gene. These mutations create public health concerns as they can be responsible for reactivation of hepatitis B and occult hepatitis B infection. The inability to detect occult infections means that these individuals may become blood donors.[xi]
The AJTS study furthermore reveals:
Mutations within the S gene are known to be responsible for occult hepatitis B infections, reactivation of hepatitis B,[58,59] diagnostic assay failure[58,60–63] and reinfection in HBV-infected recipients of orthotopic liver transplantations.[17,64] Occult infections create public health concerns because asymptomatic carriers can be blood donors.[65–67] These mutations are stable and can be transmitted horizontally and vertically.[56,68–71]
Vaccination and the administration of HBIG and anti-viral drugs like lumavidine exert evolutionary pressures to select mutants.[70,80].
Research with childhood vaccinations shows that mutations accumulate with higher frequency in vaccinated than unvaccinated children, with more mutations emerging in children vaccinated with plasma-derived vaccine than recombinant vaccine.[80] Vaccinated children generated a preferential accumulation of mutations in the second loop of the MHR, while unvaccinated children generated random mutations.[81]
This iatrogenic problem is not a new discovery. The first case of a vaccine-induced escape mutant of hepatitis B virus was reported in Lancet a quarter of a century ago in an Italian child:
In southern Italy, 44 contacts of hepatitis B virus carriers, including infants of carrier mothers, became HBsAg positive despite passive and active immunisation according to standard protocols. In 32 of these vaccinees infection was confirmed by the presence of additional markers of viral replication. In 1 infant, serious disease occurred. The virus from this patient is an escape mutant with a different sequence from that of the isolate from the mother.[xii]
Indeed, the actual treatment itself may exert evolutionary/selective pressure on the Hepatitis B virus to mutate:
The viral sequences in the S gene can be changed after active or passive immunization. HBV surface gene variants emerge or are selected under the immune pressure generated by the host or by HBIG and hepatitis B vaccination. The most frequent mutation causing vaccine escape is the G145R substitution located in the ‘a’ determinant region of HBsAg [15,16]. This was first identified in successfully immunized infants who became HBV carriers, despite the presence of protective levels of antibodies to HBsAg [16]. In HBV DNA–positive children from four sequential surveys in Taiwan, the prevalence of hepatitis B surface gene ‘a’ determinant mutants increased from 7.8% before the launch of the vaccination programme, to 19.6% at 5 years after, 28.1% at 10 years after, and 23.1% at 15 years after the programme [17]. In few other recent studies from countries endemic for HBV, occult HBV infection was frequently found in children and young adults who were vaccinated for HBV at birth [16,18,19].
The new study also found indication that occult infection with hepatitis B can be, and often is, cleared from the body with adequate time:
Our study also addresses a major issue of the natural history of occult HBV infection in children. We found that the frequency of occult HBV infection was 64% at 18 weeks, which decreased significantly to 42% by 2 years. Similarly, in a study from Taiwan [18], 11% of children were found to have occult HBV infection, while in a study on young adults aged 19–21 years from China [19], 4% were found to be having occult HBV infection. In our study, we also found that one of the major determinants for persistence of occult HBV infection is the poor immune response to the HBV vaccine. Thus, it seems that as children grow old, some of them may lose their infection depending on the improvement of their immune status.
In ca. 23 – 28% of the perinatal vaccine failures HBsAg escape mutations have been observed whereas in the pre-vaccination era the proportion of these mutants was only 8%.[xiii]
The occult or reactivated HBV strains in most cases contain several HBsAg escape mutants against which the vaccine-induced immune response may not protect as shown in Figure 8. [xv]
Does the new study not open up a larger question regarding the universal immunization of all infants for hepatitis B on the CDC vaccine schedule? Couldn’t vaccination be simply reducing acute infectious episodes with a vaccine-specific strain (as measured by HBsAg), while increasing occult infections with wild type or escape mutants?
In 1992, the WHO recommended the implementation of universal childhood vaccination for hepatitis B worldwide, with 180 countries presently adopting this measure.[xiv] This was spurned by the advent of inexpensive, recombinant DNA hepatitis B vaccine, which contained HBV subgenotype A2. And yet amazingly, more than 99% of the HBV carriers worldwide have other genotypes. [See a global diagram of the different types]
The first, most obvious implication is that the recombinant hepatitis B vaccine may be exerting selective pressure on hepatitis B virus to produce ‘escaped mutants’ capable of evading detection but nonetheless contributing to ‘occult’ morbidity and mortality in these vaccinated populations.
As Dr. Kelly Brogan, having thoroughly reviewed this study, recently opined:
What does this mean?
The implications of this is that immune response to the vaccine, which is heralded as “proof of efficacy”, in fact had no statistical bearing on infectious outcomes. Exposure to maternal infection at birth did not correlate with future outcomes either. The only thing that did was maternal viral DNA and HBeAg indicative of acute/active infection, and giving the babies Hepatitis IG (not the vaccine) may have suppressed overt infection in some cases, but it just sent it underground.
Contrary to claims of cited studies which assert 85-95% efficacy of the vaccine alone and in combination with HBIG (the majority of which, I have confirmed were industry funded as opposed to this paper which declares no conflicts) in preventing acute and chronic infection in babies born to infected mothers, this study found that, not only were babies going on to develop chronic infection, but the type of infection they developed was “covert”, which means that it did not prompt the expected antibody response and would likely smolder there chronically without routine detection including when these individuals may go on to donate blood, have sex, and use IV drugs. This covert infection is theorized to develop as a result of “immune pressure” from these treatments, which result in viral mutations eluding the host. These mutations accumulate in vaccinated children.
What this means is that, current practice, as applied to the group of people most appropriate for the intervention, is not effective and may contribute to mutations in the virus that allow for covert infection.
Finally, Dr. Brogan asks the question: “So, if it works even 8% more than a coin toss in preventing infection, than why not just do it?” To that she answers (we think correctly):
Because it is a toxic exposure that has unknown and unpredictable effects. It has never been studied in humans, and what we are observing from population-based reports is that 443,093 adverse events (headache, irritability, extreme fatigue, brain inflammation, convulsions, rheumatoid arthritis, optic neuritis, multiple sclerosis, lupus, Guillain Barre Syndrome (GBS) and neuropathy ) have been registered including >1500 deaths, often labeled as Sudden Infant Death Syndrome. NVIC discusses:
An historic report in 1994 published by the Institute of Medicine, National Academy of Sciences, reviewed the medical literature for evidence that vaccines, including hepatitis B vaccine, can cause a variety of immune and neurological health problems. An independent committee of physician experts concluded that there were no case controlled observational studies or controlled clinical trials conducted on hepatitis B vaccine either before or after licensure to scientifically evaluate persistent reports that hepatitis B vaccine can cause sudden infant death syndrome; Guillain-Barre syndrome (GBS) and other central demyelinating diseases including transverse myelitis, optic neuritis, and multiple sclerosis; and immune system dysfunction including chronic arthritis.
Ultimately what this new study reveals is that hepatitis B is not really a vaccine-preventable disease; at least not in the sense of a ‘highly effective’ intervention that popular consciousness, and an increasingly faith- and not evidence-based conventional medical establishment believes it to be. While hepatitis B vaccine may reduce the occurrence of overt forms of a particular vaccine-specific form of hepatitis B, this quasi-species has a wide range of genotypes and variants to draw from to produce so-called ‘occult’ or covert infections that are largely under the radar of vaccine post-marketing surveillance and viral epidemiology, despite causing chronic liver disease in those infected with it.
Vaccine-induced antibody elevations against a target pathogen are no real-world measure of effectiveness; this is a proxy indication, and highly misleading. Either a vaccine works in reality or it does not; 42% of these infants were infected at year 2 after no less than 4 of the same vaccine. This is a tragic example of vaccine failure. Driving an overt infection into a covert one does not count. Claiming so is disingenuous, and considering how harmful hepatitis B vaccines are on a less than one day old newborn’s body, immune system and nervous system, probably much worse. A central dogma of vaccinology is that elevating antibody titers against a pathogen through synthetic means results in improved health. And yet, not to long ago, a study published in the journal Immunity challenged this core tenet, essentially calling into question the primary justification for vaccination by showing that antibody elevations are not always necessary for the immune system to launch an effective response against a pathogen.
For a vaccine declared to be “95% effective” by the World Health Organization, we should all be seriously considering the implications of this study, especially as concerns an ever-expanding immunization schedule increasingly foisted upon the public as “necessary.”
[i] World Health Organization, Hepatitis B
[ii] 1Hepatitis B vaccine induces apoptotic death in Hepa1-6 cells. Apoptosis. 2012 Jan 17. Epub 2012 Jan 17. PMID: 22249285
[iii] GreenMedInfo.com, Hepatitis B Vaccine Side Effects
[iv] Wolfram H Gerlich. Medical virology of hepatitis B: how it began and where we are now.
[v] CDC.gov, A Comprehensive Immunization Strategy to Eliminate Transmission of Hepatitis B Virus Infection in the United States. View PDF
[vi] http://www.ncbi.nlm.nih.gov/pubmed/17336170
[vii] IBID, iv
[viii] Francisco Rodriguez-Frias, Maria Buti, David Tabernero, Maria Homs. Quasispecies structure, cornerstone of hepatitis B virus infection: Mass sequencing approach.
[ix] http://www.ncbi.nlm.nih.gov/m/pubmed/16461211/?i=21&from=hepatitis b vaccine selective
[x]http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168123/
[xi] Ibid
[xii] http://www.ncbi.nlm.nih.gov/pubmed/1697396
[xiii] Hsu HY, Chang MH, Ni YH, Chiang CL, Chen HL, Wu JF, Chen PJ. No increase in prevalence of hepatitis B surface antigen mutant in a population of children and adolescents who were fully covered by universal infant immunization. J Infect Dis. 2010;10:1192–1200. doi: 10.1086/651378. [PubMed] [Cross Ref]
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