Monday, April 25, 2011

Zombie science!

In addition to my day job as a scientist, I am also an aspiring writer of Young Adult fiction.  I like the concept of the teenage biohacker, because there is so much fertile ground to work with.  Science fair projects that go horribly wrong or the biology teacher who has an odd obsession with road kill.  In my first novel, a group of teens create primitive life in their basement lab.  The protagonist’s mom is a scientist studying extremophilic bacteria, and he learns from her that it is pretty easy to make long chains of amino acids (ie, proteins) using a temperature cycler.  When he tries to do this himself, disaster strikes and they force the system to evolve into an organized, self-replicating structure with life-like characteristics.  A prominent scientist learns about their discovery and steals it for his secret research on zombies. 
Sound crazy?  Check out the new book by Dr. Steven Schlozman called The Zombie Autopsies.  CNN interviewed the Harvard/Mass Gen psychiatrist about the book (see link) and I think it should be essential reading for any high school AP Biology class.  He uses a very scientific framework to discuss the pathogenesis of the disease, the mathematical models that predict how fast it could spread, and, of course, offensive and defensive strategies for our survival.  (Spoiler alert: The odds are pretty good for the zombies.) 

So, what is his take for the root cause?  Interestingly, he uses infectious proteins called prions as a source.   A paper published in 1982 by Stanley Prusiner first described these infectious proteins, and at the time it violated many dogmas of molecular biology (he won the Nobel Prize in 1997 for this work).  Prions are the culprit behind Creutzfeldt-Jakob disease, fatal insomnia (how awful!), Gerstmann-Straussler-Scheinker (GSS) disease, bovine spongiform encephalopathy (the technical term for Mad Cow disease), and probably other diseases and conditions that have not been linked yet.  Infectious prions are simply misfolded proteins that get into the brain and result in amyloids (aka ginormous blobs) that destroy brain tissue.  But they aren’t just any ginormous blob, they actually have a pretty well-defined structure and are quite stable.  The current thinking is that the infectious prion serves as a template that allows normal prion proteins in the brain to structurally convert to the infectious form.  However, even today the exact mechanism remains controversial.   What is known, however, is that as the infection spreads the brain disintegrates.  In CJD, this results in the slow death of the patient but in Schlozman’s book, it results in a zombie.  He makes a compelling case that if a different prion variant were to evolve such that the brain gets chewed down to the core, the patient would remain alive but would no longer be capable of cognitive thought.  All that would be left is basic brain function, an unquenchable hunger, and a dysfunctional fight-or-flight response (a “drunk crocodile” was Schlozman’s description). 
So does this mean that future college biology majors will be using Schlozman’s book for courses in Zombie Biology?  Maybe.  Although prions make for a compelling zombie disease, there are also other pathogens that have been suggested to turn your awkward, hormone-crazed, teenage neighbor into a clumsy, teenage zombie.  (Trust me, there’s a difference.)  In many zombie apocalypse movies, a virus causes people to wig-out and, just like rabies, is transmitted to hapless store clerks (and other minor characters) through a bite or a scratch.  This is also a very real possibility, since there are many brain-damaging viruses in circulation.  A few mutations in one of these guys and the brain buffet is open for business.  There are some scientists who also speculate that prion diseases are initially triggered by viruses. 

Then there is Toxoplasma gondii.  T. gondii is a parasitic protozoa whose primary host is the cat but requires a rat host as part of the full lifecycle.  Rats have a natural aversion to cats and are hard-wired to avoid areas with evidence of feline activity.  So how in the world does T. gondii manage to thrive?  Yup. Zombies.  When rats are infected with T. gondii, the infection affects brain function.  Instead of aversion, there is strong scientific evidence that rats become attracted to cats and lose their sense of risk aversion (for example, see Berdoy et al, “Fatal attraction in rats infected with Toxoplasma gondii.” Proc. Biol. Sci, Vol 267 pp1591-4, 2000).  If they could write, these zombie rats would carry little signs that say “Eat me… nom, nom, nom”.  Human infection by T. gondii usually has mild, flu-like symptoms but in some cases, it can produce symptoms very similar to schizophrenia (for a recent review, see Henriquez, et al., 2009 “Neuropsychiatric disease and Toxoplasma gondii infection.” Neuroimmunomodulation, Vol 16, pp122-133).  Crazy, unihibited humans?  Only a small step from zombies... or college freshmen.
Anyhow, this is a great example of some really cool, but offbeat, science. Yeah, this is on the fringe and is half-entertainment and half-science, but in reality, zombies are not only plausible, but something we may actually have to contend with someday.  A  prion-like protein that my protagonist discovered may be one of the catalysts.  Will he and his friends find a way to stop the zombie apocalypse?  Will his girlfriend become the first victim… or the first zombie!?  Let’s just hope she doesn’t own a cat.


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