Dr. Tetyana's Perspective
on Vaccination and Natural Immunity
By Tetyana Obukhanych, Ph.D.
Does measles suppress your immune system via immune amnesia? Let’s do some ‘fact-checking.’
In 2002, Dr. Peter Aaby and co-authors published a study conducted in rural Senegal, in the area that had an outbreak of measles. According to the study: "No index or secondary case of measles died in the acute phase of infection nor did any of the children exposed to measles die in the first 2 months after exposure." (And given what we know from the 2015 Lancet Global Health publication, identifying vitamin A deficiency as a risk factor for mortality from measles, we can safely assume that perhaps children in this area were not as deficient in vitamin A, as children in other parts of Africa and Asia, where measles infection is known to result in high mortality.)
Dr. Aaby and co-authors were testing a commonly held assumption that after surviving measles, children would have a higher mortality rate from other infections due to long-term immune-suppression, which is thought to follow measles. But they got the opposite results. In fact, they found that "exposed children developing clinical measles had lower age-adjusted mortality over the next 4 years than exposed children who did not develop clinical measles.”
The outcome of their 2002 study was consistent with prior studies: "No long-term excess mortality after measles infection: a community study from Senegal" and "No persistent T lymphocyte immunosuppression or increased mortality after measles infection: a community study from Guinea-Bissau."
Then in 2003, they did a similar study, this time in rural Bangladesh, to assess the long-term effects of measles by comparing the survival of unvaccinated children after measles with those who have not yet contracted measles. Again, they found that "post-measles cases had significantly lower mortality than uninfected, non-immunized children in the following 9 months."
Why then all this recent hysteria about measles resulting in immune amnesia, as if that’s going to kill you?
There are a few research publications that have been picked up by the media or referenced by other research publications to unnecessarily feed these fears.
Let’s first look at the PLoS Pathogens 2012 publication titled “Measles immune suppression: lessons from the macaque model.”
Researchers state: “Here we show that MV preferentially infects CD45RA(-) memory T-lymphocytes and follicular B-lymphocytes, resulting in high infection levels in these populations. After the peak of viremia MV-infected lymphocytes were cleared within days... Our findings indicate an immune-mediated clearance of MV-infected CD45RA(-) memory T-lymphocytes and follicular B-lymphocytes, which causes temporary immunological amnesia.”
OK, here we have a preferential infection of memory lymphocytes by the measles virus resulting in a temporary loss of immunologic memory. So what? When was it ever proven that immunologic memory has anything to do with protection from re-infection? In fact, the opposite has been demonstrated by the research conducted in the lab of Swiss scientist (and a Nobel Prize winner in 1996) Dr. Rolf Zinkernagel. In the title of his 2012 critical review, he clearly states: “Immunologic memory does not equal protective immunity.”
Furthermore, the varicella (chickenpox) virus does exactly the same thing as the measles virus – infects memory lymphocytes – as reported by another research paper published in PLoS Pathogens in 2013: “During viremia the virus preferentially infected memory T-cells, initially central memory T-cells and subsequently effector memory T-cells.”
Yet, no one is screaming from rooftops that chickenpox will make you die from the next common cold you contract, because that would be too obvious a lie to the current generation of chickenpox survivors who do not remember suffering from any type of immune-suppression, despite the fact that the varicella virus infected their memory T cells. But because it is only the older generation that has had natural measles, the media can get away with spreading such fears without common sense to stop them.
Another paper published recently in Science is titled “Measles virus infection diminishes preexisting antibodies that offer protection from other pathogens.”
'Antibodies that offer protection'? Let’s pause right here. When was it ever proven that antibodies offer protection? In fact, the opposite has been observed. Don’t we remember another prominent scientist (and a Nobel Prize winner in 1960) Sir Frank Macfarlane Burnet telling us the following regarding the role of antibodies (or rather lack thereof) for immunity in children who lacked antibody production due to a genetic condition called agammaglobulinemia:
“To everyone’s surprise [children with agammaglobulinemia] showed a normal measles course with a typical rash which faded at the normal time and was followed by just as substantial immunity against reinfection as would be shown by any other convalescent. Antibody production is therefore not necessary either for recovery from or for the development of immunity to measles.” (Burnet and White. Natural History of Infectious Disease. Cambridge University Press, 1940)
And don’t we know of a modern-day paper showing that medical professionals with positive antibody titers for measles can still develop measles:
“Hospital employees working in patient care areas from July through November 1990 were screened for measles antibody levels using a commercially available enzyme immunoassay (EIA). Four healthcare workers vaccinated in the past developed measles. All had positive pre-illness measles antibody levels.”
Then who cares what is temporarily happening with antibodies that bind to other pathogens after the measles infection?
A true correlate of protection is not the level of antibodies that bind to pathogens but virus- neutralizing serum titers. Those are measured by a technique called plaque-reduction neutralization, which is quite distinct from how antibodies are detected. When measured side- by-side using the same serum samples from research animals, virus-neutralizing measurements and antibody-binding titers do not follow the same pattern over time and therefore do not measure the same entity.
Before we start panicking over the demonstrated effects of the measles infection on the temporary loss of immunologic memory or diminished levels of virus-binding antibodies, let’s ask ourselves: do we even fully understand the biological basis of immunity from viral re-infection? Is the science really settled here? Because it doesn’t appear so to me.
Over the past century, the immunologic theory has been vacillating back and forth between holding a cell-based vs. humoral-based view of immunity. That debate was futile, because the majority of immunologic research has been done with non-infectious immunogenic substances that couldn’t really test the theory in action.
In 1942, Merrill Chase postulated that immunity could be transferred with immune cells from immunized animals to naïve animals.
In 1995, Zinkernagel’s research disproved that, showing that immunologic transfer of memory cells didn’t confer protection, when animals were then challenged with a virus. But the transfer of serum from immune animals did confer protection, which to Dr. Zinkernagel implied that protective immunity is mediated by antibodies that can neutralize the virus.
Yet, back in the 1940s, Burnet already knew that it could not be antibodies, based on his clinical observations in agammaglobulinemic patients who lacked them, yet could generate robust immunity to a viral disease, like measles.
So, which is it: cell-based, antibody-based, or neither? And what is missing from the picture?
And what is missing from the picture is immune cell-derived factor called Transfer Factor. TF was discovered in the 1950s by Henry Sherwood Lawrence.
In 1980, a seminal clinical research paper was published in The New England Journal of Medicine, showing that TF administered to children with leukemia in a double-blind saline placebo-controlled trial protected them from chickenpox during 12-30 months of the follow-up.
In this clinical trial, TF was prepared by extracting (dialyzing) it from leukocytes of donors who had a history of chickenpox. Researchers had to kill those leukocytes in order to extract TF out of them. And most likely, those were memory lymphocytes that contained TF, since it had to be obtained from people who already had chickenpox.
Let’s get back to the known propensity of the measles virus to infect and kill memory lymphocytes. Could it be that rather than making you less immune by killing your memory lymphocytes, the measles infection would make you more immune by killing your memory lymphocytes—due to releasing TF from all of those killed memory lymphocytes into your bloodstream? Did scientists measure the levels of serum TF to previously encountered infections before and after measles, the way they did for antibodies? I bet, no. Because that would put an end to the spread of the panic. And that wouldn’t be good for vaccine industry business and for vaccine mandates.
Now, let’s address yet another facet of memory lymphocytes. A subset of them (memory Th2) is known to be an immunologic reservoir for allergic diseases, including asthma. In fact, it was even proposed in a 2006 publication in Pharmacology & Therapeutics that drugs are needed to target and eliminate these pesky memory Th2 cells, in order to reduce their contribution to allergic asthma.
And if the measles and chickenpox viruses already do just that – kill memory T cells – shouldn’t that lead to a reduced risk of asthma and other allergic diseases following these childhood diseases? Indeed, it should. And there are publications documenting such effects for measles in Africa and Europe, and for chickenpox in the USA.
Let’s re-read the summary of Dr. Aaby’s 2002 study findings and let it sink in: ‘Exposed children developing clinical measles had lower age-adjusted mortality over the next 4 years than exposed children who did not develop clinical measles.”
Are you still afraid?
Tetyana Obukhanych, PhD is a Founding Member and Immune Science Educator at BBCH (Building Bridges in Children's Health), an online community of parents, health advocates, and doctors dedicated to learning the science that impacts healthy immunity and children's health.
PubMed links used in this article:
Copyright © 2019 by Tetyana Obukhanych, Ph.D. All rights reserved.
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