'Germs' Beat Vaccines At Their Own Game: Anti-Malarial Probiotics Show Promise

'Germs' Beat Vaccines At Their Own Game: Anti-Malarial Probiotics Show Promise

A groundbreaking new study finds probiotic 'germs' may provide an alternative to vaccination for malaria – a finding that challenges fundamental tenets of both vaccinology and germ theory. 

The development of a malaria vaccine has been a persistent and heavily funded goal now for over half a century,[1] but to date not a single effective solution has been produced.

This is all the more surprising when you consider the roster of powerful organizations presently invested in finding one:

  • Bill and Melinda Gates Foundation (particularly through PATH Malaria Vaccine Initiative)
  • The US National Institute for Allergy and Infectious Disease
  • The European Union DG 
  • The United States Agency for International Development
  • The Wellcome Trust
  • The Medical Research Council UK 
  • The European Vaccine Initiative (formerly EMVI)
  • The European and Developing Countries Clinical Trials Partnership
  • The World Health Organization [2]

Today, anti-malarial chemotherapy and so-called "vector control methods," e.g. pesticides, are the primary prevention techniques, all of which carry serious unintended adverse health effects – some at least as serious a health threat as malaria itself. Ostensibly, a malaria vaccine would reduce the need for these 'external' measures by educating the body's own immune system to fight a disease which accounts for over 207 million cases and 627,000 deaths annually, according to the World Health Organization's "World Malaria Report" (2009). [3]

The scientific justification for the development of vaccines in general and the malaria vaccine in particular is based on the observation that surviving natural exposures to pathogens often results in lasting immunity. In the case of malaria, survival from initial infection and frequent re-exposures can result in the absence of clinical symptoms of infection. Also, when gamma-globulin fractions are transferred from semi-immune to naïve humans malaria disease severity is mitigated.[4] [5]

So why, given the feasibility of a vaccine and the virtually limitless financial, scientific and technological resources available to developing an effective solution, has none yet been produced?

This question could be raised for any number of vaccines either in development or already in present day 'immunization' schedules. HIV vaccines, for instance, have been a notorious failure, even increasing death rates in a recent clinical trial. And then there are the vaccines for mostly benign childhood infections, e.g. chickenpox, measles, mumps, etc., which now require multiple 'boosters' because the synthetic immunity they produce have a dismally short if not non-existence effectiveness.  Given the growing tide of vaccine failures in highly vaccine compliant populations, including: chickenpoxshingles, measlesmumpswhooping cough (pertussis)influenzaHPV (Gardasil)hepatitis B, the problem may not lie in the virulence or resistance of a particular pathogen -- be it Ebola or malaria -- rather, the problem may lie with the fundamental tenets of vaccinology itself, including germ theory, which our discovery of the microbiome and even the viral nature of key elements of our own genome has effectively obliterated.  In other words, vaccines cannot and do not replace the type of immunity produced through natural processes and natural exposures, and surprisingly, some 'germs' are actually required to fend off infection.

The Dawn of 'Probiotic Vaccines'

Illustrating exactly this point, a recent study published in the journal Cell titled "Gut Microbiota Elicits a Protective Immune Response against Malaria Transmission," [6]  reveals that the human gut bacteria Escherichia coli 086:B7, normally considered a microbe of pathogenic potential within the host, may help us fend off malaria infection. This was the first study of its kind to demonstrate a beneficial effect of what is normally considered a pathogenic 'germ' on malaria infection.

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In the new study, Yilmaz and colleagues found that both the E. coli and malaria parasite (Plasmodium sporozites) exhibit the sugar-containing molecule glycan  Gala1-3Galb1-4GlcNAc-R (a-gal) on their surface, which is not present in humans due to the inactivation of the gene (a1,3GT ) which has been estimated to have occurred in our pre-human ancestors about 28 million years ago.[7]  This genetic deletion prevents the body from unintentionally forming autoantibodies against itself, as human are no longer capable of expressing this glycan on cell surfaces. In fact, because of this mutation the human immune system is capable of producing up to 5% of all of its circulating immunoglobulin IgM and IgG against this particular glycan.[8]

Why is this important?

Yilmaz et al observed several important phenomena that together indicate this E. coli strain (and by implication perhaps other commensal bacteria) in our gut may prime the immune system to produce anti-glycan antibodies that protect against malaria. They came to this conclusion through the following observations, summarized by a recent review of their work titled, "Coming soon: probiotics-based malaria vaccines":

  • Higher anti-a-gal antibodies are correlated to lower incidence of malaria infection: "As Yilmaz et al. [7] demonstrated in their study, individuals in malaria-endemic Mali exhibit twice the levels of anti-a-gal IgM antibodies compared to adults with no previous malaria exposure. Levels were in general higher in non-infected individuals, indicating that the high titers of a-gal antibodies protect these individuals from being infected by the malaria parasite."
  • Mice engineered to be deficient in the glycan-producing 1,3 GT gene (like humans) produce protective anti-a-gal antibodies following exposure to E. coli 086:B7 or vaccination with a-gal antigen: "The most interesting discovery of the authors was the demonstration that 'human-like' a1,3GT-deficient mice produce anti-a-gal antibodies following enteric exposures to E. coli O86:B7 or immunization with a-gal antigen and that these antibodies protected the mice against Plasmodium berghei infection by Anopheles stephensi mosquitoes."
  • Anti-a-gal antibodies bind to the parasite surface and activate classical complement pathway of the immune system within the skin: "Yilmaz and colleagues then dissected the mode of action of the anti-a-gal antibodies during malaria transmission from the mosquito to the human. The antibodies were shown to bind to the sporozoite surface and here induced the classical pathway of complement, resulting in lysis of the sporozoites. Due to the fact that following the mosquito bite sporozoite RNA was detectable in the mouse skin, but not the liver, the initial deposition of the parasites in the skin appears to be the target for complement-mediated destruction."
  • A-gal antibodies produced as a result of gut microbe exposure are able to protect against malarial infection of the skin: "[E]xisting a-gal antibodies, originally generated by the host in response to a-gal-presenting gut microbes, are able to target Plasmodium sporozoites once the mosquito injects them into the skin, resulting in complement-mediated destruction of the parasite (Figure 1)."

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