The other day, I wrote about a couple of fascinating new papers that provide yet more evidence that measles is not a “benign childhood disease.” Basically, the papers presented yet more confirmation that the measles virus can attack the immune system, resulting in “immune amnesia,” in which the immune system “forgets” how to make antibodies against antigens it’s previously encountered before. If you want the details, feel free to go back to my previous post on immune amnesia, which discusses links back to the original studies, but a good way of looking at it is this: The measles virus kills off memory cells that lurk in the background after an infection, waiting for an encounter with the same antigen to reactivate and stimulating antibody production against the antigen again. Another way to look at it is that the immune system is reset back to infancy and has to relearn immunity through re-exposure to many of the antigens and diseases that it had already encountered. Together, the two studies for the first time suggested the mechanism behind longlasting immunosuppression observed after measles infection previously described. Naturally, antivaxers, seeing yet more evidence demolishing one of their core beliefs, in this case that the measles is a “harmless childhood illness,” didn’t take long to counterattack. Enter Tetyana Obukhanych.
Who is Tetyana Obkhanych?
Interestingly, I’ve hardly mentioned Obukhanych before, which in retrospect strikes me as odd, because she has a PhD in immunology from the Rockefeller University and completed postdoctoral fellowships at Harvard and Stanford, having published in high profile journals such as Nature, Cell, and the Journal of Experimental Medicine. Even with an apparently respectable background in immunology, Obukhanych has somehow managed to become an antivaccine activist. (It is very odd.) One place I’ve encountered her is in writing about the antivaccine group, Physicians for Informed Consent, where she is listed as a founding director/board member since 2015, her name listed alongside many antivaxers that I’ve encountered before, such as Christopher Shaw, Paul Thomas, Gary Goldman, Jane Orient, Dr. Bob Sears, and several others. On the group’s website, Obukhanych is quoted thusly:
All throughout my PhD training I was a faithful believer in vaccination. I believed for almost two decades that the reason I had contracted measles and whooping cough during my teenage years was because I wasn’t vaccinated against these diseases. Then, when I had to check my childhood vaccination records, I discovered that I was in fact fully vaccinated for both measles and whooping cough, and the resulting contradiction necessitated me to reexamine all my previous beliefs about the immunologic theory behind vaccination.
There’s only one reaction to this sort of statement:
Vaccines have a failure rate? Who knew? Damn those Illuminati lizard people pharma puppet masters for not telling us that the measles vaccine has a 5% failure rate! (That’s assuming she even ever got the full series of each vaccine, which we have no idea if she did.) If the 5% failure rate of the MMR vaccine and the fact that there is waning immunity due to the pertussis vaccine that has prompted recommendations for a booster dose during the teen years were enough to make Obukhanych “reexamine all her previous beliefs about the immunologic theory behind vaccination,” it’s a wonder she got through graduate school! Her acceptance of the well-established science in immunology had clearly been paper-thin before that.
Looking at Obukhanych’s publication record on PubMed, I’m both impressed and underwhelmed. Yes, she is listed as an author on papers published in Cell and Nature, two of the highest impact journals there are, but she is only first author on one out of the eight publications, a paper from 2006 in the Journal of Experimental Medicine with Michael C. Nussenzweig, her PhD thesis advisor at Rockefeller University. As for her ever having done a postdoc at Harvard, I can’t find evidence of it. Certainly it resulted in no publications, as there’s a six year gap (2006-2012) between her last publication at Rockefeller and her first publication at Stanford in the Department of Psychiatry and Behavioral Sciences. (Ironically it was a paper reporting a distinct plasma profile of polar neutral amino acids, leucine, and glutamate in children with Autism Spectrum Disorders.) This six year gap suggests to me that, if she was indeed ever a postdoc at Harvard, her time there was incredibly unproductive and it took her a couple of more years after arriving at Stanford to start to publish again. Worse, though, in each of the four papers from Stanford, Obukhanych’s name is buried in the middle of the list of authors, which means that she contributed, but that she was not a primary contributor to the work.
Both Skeptical Raptor and Vaxopedia have published examinations of Obukhanych’s background. Let’s just say that she never got past her second postdoc, never became faculty anywhere, and appears mostly to have been surviving on antivaccine grift since 2012 or 2013. Harriet Hall has dissected her antivaccine book, as well. Finally, the VaccinesWorkBlog analyzed an interview that she gave to Polly Tommey on the VAXXED bus (yes, she traveled with antivaxers in the VAXXED crew for a while), examining the reasons why she became antivaccine.
Unfortunately, it is Obukhanych’s superficial background as a seemingly once-legitimate PhD research scientist in immunology that makes her a powerful weapon in the antivaccine arsenal. She knows immunology enough to be able to distort it in ways that sound convincing, which is why a post she’s written has been making the rounds since the publication of the two immune amnesia papers last Friday. The post appears on her blog and is entitled Should you be afraid that measles can give you immune amnesia? Because of Obukhanych’s PhD in immunology, it’s a particularly painful bit of cherry picking, denialism, and Gish galloping to behold, and I’m sure that if any antivaxer reads my post here they’ll likely reject my deconstruction because I am not a PhD immunologist. Appeal to authority is just that strong. But I have to try anyway, mainly because there’s so much bullshit to unpack in Obukhanych’s post, and unpacking bullshit is one of the things I do best.
Cherry picking galore
If there’s one thing that I noticed about Obukhanych’s post, it’s cherry picking. Actually, it’s cherry picking and Gish galloping. You remember the Gish gallop? Duane Gish is a creationist whose name was attached to the dishonest rhetorical technique of citing so many obscure studies and references that an opponent either couldn’t be familiar with them all or would waste time trying to swat down all the bad and pseudoscientific studies and assertions.
You’ll soon see why I say this:
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.”
Naturally, I had to go straight to the source and look up the paper. Interestingly, she left out that this study was primarily looking at less severe cases of measles, and the authors themselves pointed out that their results didn’t refute the hypothesis that measles infection results in excess mortality due to infectious causes other than the measles:
These observations on the beneficial long-term conse- quences of mild measles infection do not exclude that measles infection may have an important negative effect on long-term survival under certain conditions. Children intensively exposed to measles receive a high dose of in- fection and have severe infection  and children exposed very early in life  may be particularly likely to suf- fer long-term excess mortality. We have previously found that secondary cases had significantly higher long-term mortality than index cases (, authors unpublished obser- vations). Though they had only an insignificant increase in post-measles mortality compared with uninfected commu- nity controls in the Senegalese outbreak between 1983 and 1986 , long-term consequences could be more severe in outbreaks with a higher case fatality. We have also found that very young children exposed to measles when less than 6 months old have long-term excess mortality . Both high-dose  and young age  may favour Th2 immune responses.
Also, the paper is 17 years old. There are a number of studies since then. Let’s move on, though. Obukhanych cites three more papers, a study looking at Senegal, a study from Guinea-Bisseau, and a study in rural Bangledesh. Notice anything about them? I did! they’re all by the same author, Peter Aaby, who was first author on all of them. One interesting thing about Aaby is that he agrees with the results showing that vaccination against measles in a population produces a reduction in mortality far greater than can be explained by its effect preventing measles infections. He says so in the papers cited by Obukhanych and has said so in interviews.
What happened was that once we started vaccinating against measles, the general child mortality dropped by 60 pct. It made us understand that not only did the new vaccination scheme prevent measles infection, but it also had other preventive effects.
Here’s the thing. He also believes that the measles produces an “activation” of the immune system that could result in decreased mortality after a measles infection. He even said as much in the conclusions of first paper cited, in which he asks whether the improved survival he saw in the population after measles is due to selection bias or immune activation and argues that immune activation is a better explanation than bias. (Selection bias occurs when there is an unacknowledged or unknown bias in the selection of subjects in clinical trial or epidemiological study that could contribute to the result seen.) There’s also the issue that these studies are all from developing countries with (at the time) relatively poor vaccination coverage. To boil it down to its essence, Obukhanych cherry picked papers from a single author with a pet hypothesis about nonspecific effects of vaccination. Indeed, it is very telling to me that the newest paper Obukhanych cites here is 16 years old.
Let Obukhanych’s Gish gallop begin!
Amusingly, Obukhanych next pivots to a review article published in 2012 that looked at macaque monkey models showing immunosuppression by a mechanism similar to that found in the two studies published last week, namely preferentially infecting memory lymphocytes and thereby degrading immune memory:
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.”
First off, “critical reviews” are not the same thing as systematic reviews. A critical review is basically an opinion piece. True, in scientific journals critical reviews are usually peer-reviewed, but their authors are also given wider latitude to speculate. If you don’t believe me, just look at the abstract, where Zinkernagel states:
So-called ‘immunological memory’ is, in my view, a typical example where a field of enquiry, i.e. to understand long-term protection to survive reexposure to infection, has been overtaken by ‘l’art pour l’art’ of ‘basic immunology’. The aim of this critical review is to point out some key differences between academic text book-defined immunological memory and protective immunity as viewed from a co-evolutionary point of view, both from the host and the infectious agents.
That first sentence strikes me as, well, trolling. One notes that, were Zinkernagel actually correct that immunological memory has little or nothing to do with long term immunity, he could very well have won his second Nobel Prize. Remember the Nobel Disease? It’s a term I coined (at least I think I was the first to coin it—I can never be 100% sure—but I certainly adopted it and popularized it). Basically, it’s a term that describes the propensity of Nobel Prize winners to adopt contrarian views later in their careers or to become outright quacks or cranks, as, for example, Luc Montagnier and Louis Ignarro did. Is this an incipient case of Nobel disease? Who knows? Maybe he’s just being a contrarian. Oh, wait. He’s fine, if a bit contrarian! Zinkernagel also argues that antibodies are very important for long term immunological protection! He even says so in the abstract:
These often do correlate with, but are not the key mechanisms of, protection. Protection depends on pre-existing neutralizing antibodies or pre-activated T cells at the time of infection—as documented by the importance of maternal antibodies around birth for survival of the offspring. Importantly, both high levels of antibodies and of activated T cells are antigen driven.
Successful vaccines protect humans by neutralizing antibodies via reexposure and immune complexes [6–9, 11, 60]. In contrast, we still lack efficient vaccines that maintain activated T cell responses (and/or neutralizing antibody responses) against highly variable agents for a long time as is necessary against HIV, HCV, malaria, TB, and many other infections [17, 18, 27, 57, 60].
Of course, immune memory response is complex and depends on a lot of factors, more than just antibodies. For instance, this review article notes:
One of the hallmarks of our immune system is the ability to “remember” past exposure to pathogens. Such exposure can be from infection or vaccination, and by remembering we are, ideally, fully protected from infection upon future encounter with the same pathogen (1). Although humoral immunological memory is mediated in part by serum antibodies secreted by long-lived plasma cells (LLPCs), these cells are usually not described as memory B cells. Instead, memory B cells are defined as long-lived and quiescent cells that are poised to quickly respond to antigen upon recall (2–5).
During an initial infection, naive B cells are activated by antigen in the presence of a specific type of T cell in the follicles of lymphoid organs, like the spleen and lymph nodes, undergoing a clonal expansion (proliferation from a single genetically identical cell) to produce B cells specific for the antigen. These cells differentiate into plasma cells (also known as effector B cells) to produce a first wave of antibodies to clear the infection. A fraction persist as dormant memory cells. I won’t go into the details. There are rounds of selection for B cells whose antibodies have the greatest affinity for the antigen, resulting in the production of B cells with the highest number of mutation events in their immunoglobulin chain producing superior affinity for the antigen. The point is, memory B cells do a lot of things. For instance, when they encounter the same antigen again, they can reactivate rapidly, proliferate, create new plasma cells, and reenter germinal centers to undergo further selection improving the affinity of their antibodies. This reactivation depends on a specific kind of T cell, however. The Wikipedia entry is actually pretty good if you want the gory details.
The point is that the immune system is complicated, and memory B cells work in concert with specific T cell subtypes to reactivate an immune response.
The “antibodies don’t protect” gambit
After that bit of dancing around the evidence, Obukhanych’s Gish gallop continues:
‘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)
Wow! That sounds devastating! But is it? Not at all. First, it’s been known for a very long time that seroconversion after measles vaccination, with induction of measles neutralizing antibody titers greater than 120, correlates with protection against wild-type measles infection. It’s also known that, yes, children with congenital agammaglobulinemia can fight off measles. Why? The immune system is redundant! It’s also known that children with cellular immunodeficiencies are susceptible to severe progressive or even fatal measles. To put it simply (but hopefully not simplistically), it’s currently thought that cell-based immune responses are most important for clearing an acute measles infection, while antibody response is most important for preventing re-infection.
But did you see the bait-and-switch there? I almost missed it. Notice how Obukhanych is only talking about antibodies clearing measles infections, and then only the first acute infection. That’s not what the two papers were about! They were about how measles decimated memory B cells, thus decreasing antibody production against antigens other than measles, antigens from other infectious agents the individual had encountered during life. Just because a cell-based response is more important in clearing a measles infection than the humoral (antibody) response isn’t generalizable to other infections, which vary in terms of which response is most important to fight them off. Tricky, that Tetiana Obukhanych.
She gets trickier. After noting that adults with preexisting antibodies to measles can sometimes still get the measles, once again showing amazement that vaccines aren’t 100% effective, even for measles, Obukhanych writes:
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.
Sure, but remember what the papers published last week showed. They showed the loss of antibodies to specific antigens after measles infection. If there are no antibodies to a particular antigen on a particular infectious agent, there won’t be any protection. Remember, Zinkernagel himself, whom Obukhanych cited, stated that preexisting antibodies are the most important indicator of protection against a pathogen. In other words, she’s just throwing out a shiny little fact that demonstrates precisely diddly squat about the papers she’s attacking.
Transfer factor, or: Enter the…red herring!
After going on about how opinions in immunology have shifted over the years over what part of the immune response is most important to immunity, cellular or antibody, Obukhanych then throws out a red herring:
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.
Notice the multiple slights of hand here, the multiple “if this then that” speculations? First off, leukocytes, the source of transfer factor, are not the same thing as lymphocytes. They’re different kinds of white blood cells types, and transfer factor was originally described as being isolated from leukocytes! Of course, surely she knows this. She just hopes that you won’t notice. It’s also why she blatantly speculates that in reality they must have been dialyzing memory B cells, which are a type of lymphocyte. Transfer factor can be isolated from lymphocytes, too, and it is true that lymphocytes are s subset of leukocytes (although they come from different precursor cells), but that doesn’t absolve her of her sleight of hand.
Moreover, there’s a reason almost no one is investigating transfer factor any more. First, the use of blood-derived products, except when necessary, took a major hit in the 1980s during the AIDS epidemic. Also, transfer factor has a rather strange history, with its proponents from the 1950s to the 1980s making miraculous claims for it, ending in a major scandal, as described in this 1973 New Scientist article, describing how a researcher was accused of falsifying his data in guinea pigs:
It’s a compound that’s never really been characterized, other than being a peptide below a certain size, and just perusing the scientific literature on it gives me the distinct feeling that it’s probably pseudoscience, given that transfer factors are touted for cancer, multiple sclerosis, asthma, hepatitis, AIDS, and many other diseases. (It doesn’t help that transfer factor has been turned into a supplement isolated from cows, mainly.) In any case, all Obukhanych is doing by invoking transfer factors is wildly speculating without evidence in order to try to cast doubt on the findings that measles kills memory B cells and thus leads to long lasting immune system compromise.
Finally, Obukhanych throws up another red herring:
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.
Of course, most children don’t have asthma or severe allergies. Even if this “benefit” of measles infection were real, they wouldn’t benefit, and for children with asthma the risk of respiratory complications from measles (like pneumonia), plus its other risks of long term immune suppression, death, and the deadly subacute sclerosing panencephalitis (SSPE) are too high a price to pay for a possible benefit of reducing asthma symptoms.
Tetyana Obukhanych: Antivax immunologist
I don’t know why Obukhanych became antivax and probably will never know. I just know from reading her attempt at deconstructing and refuting the two studies published last week that reinforced what we already knew about the effect of the measles virus on immune memory that she’s now using her PhD training and background in immunology to spread antivaccine misinformation that sounds more convincing that the usual antivaccine propaganda because she knows enough immunology to make that propaganda sound more “science-y.” Using a combination of cherry picked science, red herrings, and a fairly decent Gish gallop, she weaves a pseudoscientific tale of misinformation that is likely to be very effective at keeping wavering antivaxers from entertaining too many doubts based on these new findings about the measles virus.
Given how undistinguished her career has been since she finished graduate school, with no papers from her Harvard postdoc (if she was ever there at all) and no first author papers from her Stanford postdoc, I have to wonder if after her PhD she functioned more as a glorified laboratory technician than a true postdoc. It’s not a knock on her at all that she only had one first author paper during her PhD thesis work; many PhD programs require only one or at most two good first author paper, and a fair number of graduate students finish with only one. However, her productivity after her PhD work was abysmal, and it was probably clear that she wasn’t going to get a faculty position at a university and might even have trouble getting a job in industry. A more sympathetic explanation for her lack of productivity might be that she was being used as cheap lab labor. (This is just speculation on my part and could be wrong, but it happens with foreign postdocs more often than we in medical academia would like to admit.) So why not reinvent herself as an antivax immunologist? She’d gain instant respect at least.
My speculation could be entirely off-base, but what isn’t off-base is my conclusion that Obukhanych is now spreading dangerous antivaccine misinformation and using her PhD to project an air of scientific authority while doing it. Unfortunately, in her case, it’s false authority.