Edmonston B, Measles, Vaccination?
February 21, 2013 11:43 AM Subscribe
I just finished reading an article from the New York Times Magazine about controversial anthropologist Napoleon Chagnon. One thing in particular about the article struck me- there is a claim (at least that's how I read it) that measles vaccine caused a breakout of measles in a group of isolated indigenous people that did not have measles exposure or immunity. I'm confused because I'm pretty sure you can't get measles from vaccine. Is there something different about the Edmonston B vaccine?
*please do not comment if you are just going to deny the efficacy of vaccines generally. I am interested in scientifically corroborated evidence related to this specific case.
Here's the quote from the article from the New York Times Magazine:
"In his galleys, Tierney speculated that Neel, who died in 2000, hoped to simulate a measles epidemic among the Yanomami as part of a genetics experiment. In the published book, this theory was no longer explicit — Tierney had made last-minute changes — but it was insinuated. “Measles,” Tierney wrote, “was tailor-made for experiments.” Moreover, Neel’s choice of vaccine, Edmonston B, “was a bold decision from a research perspective” because it “provided a model much closer to real measles than other, safer vaccines, in the attempt to resolve the great genetic question of selective adaptation.” Although he quoted a leading measles researcher emphatically denying that measles vaccine can transmit the virus, he nevertheless maintained that it was “unclear whether the Edmonston B became transmissible or not.” (This line was excised from the paperback edition.)"
*please do not comment if you are just going to deny the efficacy of vaccines generally. I am interested in scientifically corroborated evidence related to this specific case.
Here's the quote from the article from the New York Times Magazine:
"In his galleys, Tierney speculated that Neel, who died in 2000, hoped to simulate a measles epidemic among the Yanomami as part of a genetics experiment. In the published book, this theory was no longer explicit — Tierney had made last-minute changes — but it was insinuated. “Measles,” Tierney wrote, “was tailor-made for experiments.” Moreover, Neel’s choice of vaccine, Edmonston B, “was a bold decision from a research perspective” because it “provided a model much closer to real measles than other, safer vaccines, in the attempt to resolve the great genetic question of selective adaptation.” Although he quoted a leading measles researcher emphatically denying that measles vaccine can transmit the virus, he nevertheless maintained that it was “unclear whether the Edmonston B became transmissible or not.” (This line was excised from the paperback edition.)"
The Edmonston B vaccine is a "live, attenuated" version of the measles virus. The idea is an application of "that which does not kill you makes you stronger".
And as per this,
"Measles vaccine produces an inapparent or mild, noncommunicable infection. Measles antibodies develop in approximately 95% of children vaccinated at 12 months of age and 98% of children vaccinated at 15 months of age."
posted by Gyan at 12:01 PM on February 21, 2013
And as per this,
"Measles vaccine produces an inapparent or mild, noncommunicable infection. Measles antibodies develop in approximately 95% of children vaccinated at 12 months of age and 98% of children vaccinated at 15 months of age."
posted by Gyan at 12:01 PM on February 21, 2013
Yes, Edmonston B is/was a live attenuated virus vaccine, as is the modern MMR vaccine. (I assume the modern one is a different viral strain.) Apparently there isn't a (sufficiently effective) measles vaccine using killed or otherwise nonviable viruses.
posted by hattifattener at 12:11 PM on February 21, 2013
posted by hattifattener at 12:11 PM on February 21, 2013
Best answer: From the CDC:
The Edmonston B vaccine was a "live attenuated" vaccine. This means that it was a mix containing live virus* which had been altered in such a way that it no longer causes disease but still looks enough like the original to teach the immune system how to fight it. This is generally achieved by growing the virus in non-human cells, until the virus evolves to be suited to e.g. hamsters instead of humans.
With any such virus, there is always the possibility that the "harmless" virus is not actually harmless -- especially to immunocompromised people, or people who are co-infected with something else -- or that the virus will evolve back to a form that's suited to making humans ill. The art and science of making these things is finding the sweet spot between "similar enough to the original to confer immunity" and "different enough from the original that it's completely safe".
In modern live vaccines, the risk of such events is extraordinarily small and, crucially, extremely well-understood thanks to close monitoring of vaccine programmes; in a sample of ten million patients, an epidemiologist will tell you with high accuracy how many will have various side-effects, and how many will be protected from the disease. The acceptable thresholds for these numbers are set differently for each vaccine, largely depending on the how nasty the disease is.
As an extremely messy rule of thumb, inactivated or recombinant vaccines (containing chemically inactivated or synthesised-from-scratch fragments of virus) tend to have better safety profiles, while live attenuated vaccines tend to give better and/or longer-lasting protection from disease. Of course there are many exceptions to this in both directions, and if you have questions about a specific vaccine, you should talk to a medical doctor (I am not a medical doctor), instead of believing strangers on the internet.
*Most biologists will tell you that you can't describe viruses as "alive" because outside a suitable host cell they're completely inert, and even inside a cell it's hard to argue that they're actually doing much of the work that we normally say counts as "life", like regulating an internal environment, breaking down nutrients for energy, etc. "Viable" is a better word, but "alive" is a useful shorthand for conversations like this.
posted by metaBugs at 12:13 PM on February 21, 2013 [2 favorites]
Measles virus was first isolated by John Enders in 1954. The first measles vaccines were licensed in 1963. In that year, both an inactivated (“killed”) and a live attenuated vaccine (Edmonston B strain) were licensed for use in the United States. The inactivated vaccine was withdrawn in 1967 because it did not protect against measles virus infection. Furthermore, recipients of inactivated measles vaccine frequently developed a unique syndrome, atypical measles, if they were infected with wild-type measles virus (see Atypical Measles, above). The original Edmonston B vaccine was withdrawn in 1975 because of a relatively high frequency of fever and rash in recipients. A live, further attenuated vaccine (Schwarz strain) was first introduced in 1965 but also is no longer used in the United States. Another live, further attenuated strain vaccine (Edmonston-Enders strain) was licensed in 1968. These further attenuated vaccines caused fewer reactions than the original Edmonston B vaccine.(My emphasis)
The Edmonston B vaccine was a "live attenuated" vaccine. This means that it was a mix containing live virus* which had been altered in such a way that it no longer causes disease but still looks enough like the original to teach the immune system how to fight it. This is generally achieved by growing the virus in non-human cells, until the virus evolves to be suited to e.g. hamsters instead of humans.
With any such virus, there is always the possibility that the "harmless" virus is not actually harmless -- especially to immunocompromised people, or people who are co-infected with something else -- or that the virus will evolve back to a form that's suited to making humans ill. The art and science of making these things is finding the sweet spot between "similar enough to the original to confer immunity" and "different enough from the original that it's completely safe".
In modern live vaccines, the risk of such events is extraordinarily small and, crucially, extremely well-understood thanks to close monitoring of vaccine programmes; in a sample of ten million patients, an epidemiologist will tell you with high accuracy how many will have various side-effects, and how many will be protected from the disease. The acceptable thresholds for these numbers are set differently for each vaccine, largely depending on the how nasty the disease is.
As an extremely messy rule of thumb, inactivated or recombinant vaccines (containing chemically inactivated or synthesised-from-scratch fragments of virus) tend to have better safety profiles, while live attenuated vaccines tend to give better and/or longer-lasting protection from disease. Of course there are many exceptions to this in both directions, and if you have questions about a specific vaccine, you should talk to a medical doctor (I am not a medical doctor), instead of believing strangers on the internet.
*Most biologists will tell you that you can't describe viruses as "alive" because outside a suitable host cell they're completely inert, and even inside a cell it's hard to argue that they're actually doing much of the work that we normally say counts as "life", like regulating an internal environment, breaking down nutrients for energy, etc. "Viable" is a better word, but "alive" is a useful shorthand for conversations like this.
posted by metaBugs at 12:13 PM on February 21, 2013 [2 favorites]
Which reminds me of the difference between the Salk and Sabin vaccines for Polio.
posted by Ruthless Bunny at 12:15 PM on February 21, 2013
posted by Ruthless Bunny at 12:15 PM on February 21, 2013
Best answer: Regarding Patrick Tierney's allegations about Chagnon and Neel specifically, here's a very thorough article on the whole affair by Alice Dreger, a medical historian and bioethicist, published in Human Nature, that concludes that Tierney's claims were "baseless and sensationalistic".
posted by strangely stunted trees at 12:36 PM on February 21, 2013 [1 favorite]
posted by strangely stunted trees at 12:36 PM on February 21, 2013 [1 favorite]
Response by poster: metaBugs I think this is the article from CDC that you quoted from:
http://www.cdc.gov/vaccines/pubs/pinkbook/meas.html
I'm still confused because even though the Edmonston B strain seems to be have more side effects, I still don't quite understand that it can cause full-blown measles.
The quote in the article, “unclear whether the Edmonston B became transmissible or not,” is implying that the vaccine gave people full-blown measles that spread.
posted by forkisbetter at 2:02 PM on February 21, 2013
http://www.cdc.gov/vaccines/pubs/pinkbook/meas.html
I'm still confused because even though the Edmonston B strain seems to be have more side effects, I still don't quite understand that it can cause full-blown measles.
The quote in the article, “unclear whether the Edmonston B became transmissible or not,” is implying that the vaccine gave people full-blown measles that spread.
posted by forkisbetter at 2:02 PM on February 21, 2013
MetaBugs addresses your concern in the second paragraph. If the live attenuated vaccine (Edmonston B in this case) should evolve back to a form that could cause illness (in scientific terminology this is called "reverting to wild type" or reverting to virulence) then yes, it could cause full blown transmissible measles.
posted by treehorn+bunny at 2:27 PM on February 21, 2013
posted by treehorn+bunny at 2:27 PM on February 21, 2013
Best answer: Yeah, I did sort of miss the point of your question, sorry. treehorn+bunny has said what I didn't express well: all live attenuated viruses have the potential to evolve (back) into a form that's symptomatic in and transmissible between humans.
I can imagine a virulent form that's weakly transmissible and causes slightly different and/or reduced symptoms but, broadly, the closer it gets to being properly transmissible, the closer you'd expect it to get to its original symptoms. This is because the virus' only goal* is to get the body to make copies of it and spread them to new hosts; the symptoms are just the tissue damage caused by this, combined with side-effects of the immune system's efforts to wipe it out. As such, as the virus evolves to fit the evolutionary pressures within human bodies again, it'll likely end up attacking the same (or very similar) pattern of tissues in the same ways, thereby causing broadly the same symptoms.
It has happened a handful of times with the live Polio vaccine, including an outbreak in Nigeria a few years back. It's tragic, but you can mop up these outbreaks just like any other (good hygiene, and vaccinate anyone who might have been exposed), and when you weigh the lives saved and improved by protecting from the disease (in the case of Polio, literally billions) against those ruined by reversions to wild type, the risk:reward analysis is a no-brainer. Epidemiology is a numbers game, no matter how cold it can sound.
I can't find a source which definitively states whether this has ever actually happened with the Edmonston B vaccine, but this paper from 2011 ends with:
That paper actually has a pretty great introduction to measles virus biology and a potted history of measles vaccine development, if you're in the mood to plough through the technical language.
*obviously, not being alive, a virus can't have a goal. Even if a virus could have a goal, an evolutionary process couldn't. Another linguistic shortcut.
posted by metaBugs at 3:08 PM on February 21, 2013
I can imagine a virulent form that's weakly transmissible and causes slightly different and/or reduced symptoms but, broadly, the closer it gets to being properly transmissible, the closer you'd expect it to get to its original symptoms. This is because the virus' only goal* is to get the body to make copies of it and spread them to new hosts; the symptoms are just the tissue damage caused by this, combined with side-effects of the immune system's efforts to wipe it out. As such, as the virus evolves to fit the evolutionary pressures within human bodies again, it'll likely end up attacking the same (or very similar) pattern of tissues in the same ways, thereby causing broadly the same symptoms.
It has happened a handful of times with the live Polio vaccine, including an outbreak in Nigeria a few years back. It's tragic, but you can mop up these outbreaks just like any other (good hygiene, and vaccinate anyone who might have been exposed), and when you weigh the lives saved and improved by protecting from the disease (in the case of Polio, literally billions) against those ruined by reversions to wild type, the risk:reward analysis is a no-brainer. Epidemiology is a numbers game, no matter how cold it can sound.
I can't find a source which definitively states whether this has ever actually happened with the Edmonston B vaccine, but this paper from 2011 ends with:
The complex pathway to cell culture adaptation and, ultimately, attenuation together with the absence of recombination suggest that it would be extremely unlikely for measles vaccine strains to revert to a virulent phenotype....which would be a weird thing to say if it was known to have happened at any point. And while I don't know, the authors of a paper on measles vaccines probably would.
That paper actually has a pretty great introduction to measles virus biology and a potted history of measles vaccine development, if you're in the mood to plough through the technical language.
*obviously, not being alive, a virus can't have a goal. Even if a virus could have a goal, an evolutionary process couldn't. Another linguistic shortcut.
posted by metaBugs at 3:08 PM on February 21, 2013
Best answer: While Edmonston B was clearly more reactogenic than Moraten (the line still used to make the measles portion of the MMR-II vaccine that everybody gets) or Schwarz, this article makes an outright assertion that it has never reverted to wild type.
posted by lakeroon at 8:03 PM on February 21, 2013
posted by lakeroon at 8:03 PM on February 21, 2013
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