FAIL: Infant Hep B Vaccines Perform Shamefully; Time To End Them?

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.

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.

Why is the hepatitis B virus so difficult to detect?

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]

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