by Sayer Ji
According to the Centers for Disease Control and Prevention (CDC), “Immunity to a disease is achieved through the presence of antibodies to that disease in a person’s system.” This, in fact, is the main justification for using vaccines to “boost” immunity, and a primary focus of vaccine research and development.
And yet, newly publish research has revealed that in some cases no antibodies are required for immunity against some viruses.
Published in the journal Immunity in March, 2011, and titled, “B cell maintenance of subcapsular sinus macrophages protects against a fatal viral infection independent of adaptive immunity,” researchers found that mice infected with vesicular stomatitis virus (VSV) can suffer fatal invasion of their central nervous system even in the presence of high concentrations of “neutralizing” antibodies against VSV.
The researchers found that while B-cells were essential for surviving a systemic VSV infection through the modulation of innate immunity, specifically macrophage behavior, the antibodies they produce as part of the adaptive immune response were “neither needed nor sufficient for protection.” These findings, according to the study authors, “…contradict the current view that B cell-derived neutralizing antibodies are absolutely required to survive a primary cytopathic viral infection, such as that caused by VSV.”
The discovery that antibodies are not required for protection against infection, while counterintuitive, is not novel. In fact, not only are antibodies not required for immunity, in some cases high levels are found in the presence of active, even lethal infections. For example, high serum levels of antibodies against tetanus have been observed failing to confer protection against the disease. A report from 1992 published in the journal Neurology found severe tetanus in immunized patients with high anti-tetanus titers, one of whom died as a result of the infection.
These research findings run diametrically opposed to currently held beliefs regarding the process by which we develop immunity against infectious challenges. Presently, it is a commonly held view that during viral infections, innate immunity must activate adaptive responses in order to achieve effective immunity. It is believed that this is why the immune system has developed a series of innate defenses, including complement, type I interferon, and other “stopgap measures,” which work immediately to lower pathogen burden and “buy time” for the much slower adaptive immune response to develop.
This view, however, has been called into question by the new study: “Although this concept may apply to other viral infections, our findings with VSV turn this view upside down, indicating that during a primary infection with this cytopathic virus, innate immunity can be sterilizing without adaptive immune contributions.”
Does this strike a mortal blow to the antibody theory which underlies vaccinology, and constitutes the primary justification for the CDC’s focus on using vaccines to “boost” immunity?
Indeed, in vaccinology, which is the science or method of vaccine development, vaccine effectiveness is often determined by the ability of a vaccine to increase antibody titers, even if this does not translate into real-world effectiveness, i.e. antibody-antigen matching. In fact, regulatory agencies, such as the FDA, often approve vaccines based on their ability to raise antibody titers, also known as “vaccine efficacy,” without requiring proof of vaccine effectiveness, as would seem logical.
The obvious problem with these criteria is that the use of vaccine adjuvants like mercury, aluminum hydroxide, mineral oil, etc. – all of which are intrinsically toxic substances — will increase antibody titers, without guaranteeing they will neutralize the targeted antigen, i.e. antibody-antigen affinity. To the contrary, many of these antibodies lack selectivity, and target self-structures, resulting in the loss of self-tolerance, i.e. autoimmunity.
Here is another way of understanding vaccine-induced antibody elevations….
Introducing foreign pathogenic DNA, chemicals, metals, preservatives, etc., into the body through a syringe will generate a response not unlike kicking a beehive. The harder you kick that beehive, the greater will be the “efficacy” (i.e. elevated antibodies), but the actual affinity that these antibodies will have for the antigen (i.e. pathogen) of concern is in no way ensured; to the contrary, the immune response is likely to become misdirected, or disproportionate to the threat.
Also, valuable immune resources are wasted by generating “false flag” responses to threats which may not readily exist in the environment, e.g. there are over 200 forms of influenza A, B & C which can cause the symptoms associated with annual influenza A,* so the seasonal trivalent flu vaccine only takes care of little more than 1% of the possible vectors of infection – and often at the price of distracting resources away from real threats, as well as exhausting and/or damaging the entire immune apparatus.
It is clear that one can create a synthetic immune response through vaccination, but it is not likely to result in enhanced immunity, insofar as real-world effectiveness is concerned, which is the only true judge of whether a vaccine is valuable or not. One might view the basic criteria used by vaccine researchers, namely, that generating elevated antibody titers proves the value of the vaccine, oppositely: proving the vaccine is causing harm to the body, especially that of the developing infant and child, by generating unnecessarily elevated antibodies by any means necessary, i.e. throwing the chemical and biological kitchen sink at the immune system, e.g. aluminum, phenol, diploid (aborted fetal) cells, peanut oil, pertactin, etc.
We leave the reader with a series of quotes addressing the inherent weaknesses of the antibody theory of immunity:
Just because you give somebody a vaccine, and perhaps get an antibody reaction, doesn’t mean a thing. The only true antibodies, of course, are those you get naturally. What we’re doing [when we inject vaccines] is interfering with a very delicate mechanism that does its own thing. If nutrition is correct, it does it in the right way. Now if you insult a person in this way and try to trigger off something that nature looks after, you’re asking for all sorts of trouble, and we don’t believe it works.”- Glen Dettman Ph.D, interviewed by Jay Patrick, and quoted in “The Great American Deception,” Let’s Live, December 1976, p. 57.
The fallacy of this (antibody theory) was exposed nearly 50 years ago, which is hardly recent. A report published by the Medical Research Council entitled ‘A study of diphtheria in two areas of Gt. Britain, Special report series 272, HMSO 1950 demonstrated that many of the diphtheria patients had high levels of circulating antibodies, whereas many of the contacts who remained perfectly well had low antibody. – Magda Taylor, Informed Parent
Human trials generally correlate ‘antibody’ responses with protection – that is if the body produces antibodies (proteins) which bind to vaccine components, then it must be working and safe. Yet Dr March says antibody response is generally a poor measure of protection and no indicator at all of safety. ‘Particularly for viral diseases, the ‘cellular’ immune response is all important, and antibody levels and protection are totally unconnected.’ – Private Eye 24/1/2002
Whenever we read vaccine papers the MD researchers always assume that if there are high antibody levels after vaccination, then there is immunity (immunogencity). But are antibody levels and immunity the same? No! Antibody levels are not the same as IMMUNITY. The recent MUMPS vaccine fiasco in Switzerland has re-emphasized this point. Three mumps vaccines-Rubini, Jeryl-Lynn and Urabe (the one withdrawn because it caused encephalitis) all produced excellent antibody levels but those vaccinated with the Rubini strain had the same attack rate as those not vaccinated at all, there were some who said that it actually caused outbreaks. Ref: Schegal M et al Comparative efficacy of three mumps vaccines during disease outbreak in Switzerland: cohort study. BMJ, 1999; 319:352-3.- Ted Koren DC