U.K.-based artist Luke Jerram has spent the last decade making painstakingly accurate portrayals of microbes with blown glass. The above microbe is E. coli, but he has also made bacteriophages, HIV, Swine Flu and many more (you can even see some genetic material floating around in a few). Most of his work is on permanent display at the Metropolitan Museum of Art in New York City, but you can find high-quality photos over at his website.
Also, in the name of making microbes more visible to the public, the website Giant Microbes offers plush renditions of microbes, replete with googly-eyes, despite the terrible diseases they cause. Despite the very obvious opportunity the website provides for easy gag gifts (“Look, I gave you herpes”), they have a surprising number of obscure diseases available, including flesh-eating bacteria and Bifido (that’d be your yogurt-y pro-biotics). For my roommate, who has three cats, I bought toxoplasmosis (which is also probably my favorite parasite – if I have one – and will most likely be the topic of a subsequent post).
Last week there was a bunch of alarmist blogs and various websites that ran pieces examining what was purported to be a Harvard Medical School Professor’s desire to impregnate a woman with a cloned Neanderthal child. Here are some choice headlines from last week:
Wanted: Surrogate for Neanderthal Baby – MIT Technology Review
Geneticist seeks woman to help make a cloned cave baby – MSNnow (their given source was the above MIT Tech Rev article)
Scientist seeks ‘adventurous woman’ to have Neanderthal baby – FoxNews.com
There is a problem, however. A bit of a snag, you might say. The scientist, Harvard geneticist George Church, who helped initiate the Human Genome Project, doesn’t actually want to do this. At all. But he’s caught quite a bit of ethical flak in the past week for apparently calling for an ‘adventurous female’ to act as a surrogate for a Neanderthal baby.
Here’s what happened.
Church wrote a book in 2012 called Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves. He was even on the Colbert Report in October to promote its release. In the book, Church asserts that it would be possible to clone a Neanderthal, but if we were to do it, it would necessitate an “adventurous female” as surrogate. That’s quite a bit different than soliciting volunteers for an experiment. Personally, I read the term “adventurous female” as more of a slight joke on Church’s end than a description of the ideal candidate. Point being, he isn’t actually going to do this. Never was.
More recently, the German magazine Der Spiegel interviewed Church on his book and his views on cloning Neanderthals. An excerpt (emphases mine):
SPIEGEL: Setting aside all ethical doubts, do you believe it is technically possible to reproduce the Neanderthal?
Church: The first thing you have to do is to sequence the Neanderthal genome, and that has actually been done. The next step would be to chop this genome up into, say, 10,000 chunks and then synthesize these. Finally, you would introduce these chunks into a human stem cell. If we do that often enough, then we would generate a stem cell line that would get closer and closer to the corresponding sequence of the Neanderthal. We developed the semi-automated procedure required to do that in my lab. Finally, we assemble all the chunks in a human stem cell, which would enable you to finally create a Neanderthal clone.
SPIEGEL: And the surrogates would be human, right? In your book you write that an “extremely adventurous female human” could serve as the surrogate mother.
Church: Yes. However, the prerequisite would, of course, be that human cloning is acceptable to society.
That’s as close as he got.
Faye Flam tracked down the evolution of this mistranslation a bit on her blog. Apparently the Daily Mail was one of the first to pick up on this interview, writing the following (again, emphasis mine):
“So what woman would want to give birth to a Neanderthal baby? Yet this incredible scenario is the plan of one of the world’s leading geneticists, who is seeking a volunteer to help bring man’s long-extinct close relative back to life.”
Which in turn birthed the Fox News article I cited earlier. In fact, Fox News took the liberty to completely fabricate a quote from Church, attributing the phrase “I can create a Neanderthal baby, if I can find a willing woman,” to him, which doesn’t appear in Der Spiegel’s published interview. And since Fox News is so fantastic at spin, if you run a quick Google search (at least on 01.26.13) for “George Church,” and go to Google News, that very non-quote is the only one displayed across the top of the search results (apparently this is something Google News has started doing). All of this, of course, spun out of control and went a bit viral, with many, many sources reporting on this ‘mad scientist.’
And then, Church took control. He was interviewed about his ‘comments’ this past Wednesday and, surprisingly, he didn’t blame the media…he blamed public scientific literacy. “The public should be able to detect cases where things seem implausible…Everybody’s fib detector should have been going off. They should have said, ‘What? Who would believe this?’ … This really indicates that we should have scientific literacy.” This interview led to another burst of coverage, except this time there was substantially more truth involved, and quite a bit more shoe-eating.
In many ways, Church’s diagnosis is right on the nose, especially when he says things that geneticists normally don’t get to publically complain about, such as “We really should get the public of the entire world to be able to detect the difference between a fact and a complete fantasy that has been created by the Internet.” I, for one, am a huge proponent of scientific literacy. The U.S.’s somewhat embarrassing history of scientific literacy is the main reason I became re-enamored with the Sciences after my long affair with creative writing (For a great example of this, search “dihydrogen monoxide ban”). On the other hand, it doesn’t seem to me that public scientific literacy is the real culprit here. Sure, I also think that the public’s collective “fib detector” could use a thorough calibration. But, can we expect everyone to be on top of the latest developments of Neanderthalic DNA sequencing, cloning ethics and whether or not such a widely-respected institution such as Harvard might offer tenure to a ‘mad scientist?’ I would venture to say no.
The real issue, at least within this scope, is the hair-trigger nature of the blogosphere. Clicks are a commodity, and Fox News’s headline would garner much more ad revenue than, say, “Geneticist George Church Thinks We May Be Able To Clone Neanderthals Someday, Maybe, But He’s Not Making Any Promises And He’s Certainly Not Looking For A Surrogate Womb.” Compound this fact with the fact that there is no sort of accountability w/r/t accuracy when you’re not the first to break a story on the internet (and there is certainly nothing that resembles peer-review), and you start to see how this can happen, and how little it has to do with scientific literacy. If there was an article titled “Alien Life Found On Moon,” I would certainly click on that. Once I realized it was complete bunk, it really wouldn’t matter: my click was registered and that article was deemed ‘successful,’ regardless of my level of scientific literacy.
This has become somewhat of an epidemic in the past few years. When Hurricane Sandy happened, people were literally posting press photos from the movie The Day After Tomorrow, which depicted a monstrous wave crashing around the Statue of Liberty, and citing them as real. And then there was the time when an Iranian girl unknowingly became the face of a revolution because her Facebook profile picture was mixed up with a girl who had been shot and killed (their photos looked similar). Protestors were marching around with her face on pickets, and she eventually had to flee the country. Or how about when Brian Ross from ABC news incorrectly identified James Holmes (of Aurora tragedy infamy) as a member of the Tea Party because there was another James Holmes from the area registered as such. Or when CNN jumped the gun and said that the Supreme Court had shut down the Affordable Care Act? And then there was the other Ryan Lanza who didn’t commit a heinous crime, who had his Facebook photo touted around the internet and broadcast on Fox News as the gunman of Sandy Hook.
I suppose I don’t quite have a point, other than to say that scientific literacy, as important as it is, is not the issue here. I’m feeling a bit Aaron Sorkin-y, so I suppose I’ll end it here and promise that subsequent posts will mostly follow the format of my previous ones – i.e. they’ll be significantly less soap-box-y. If any of this stuff interests you, however, I would suggest listening to On the Media, which is a radio program a la WNYC which has more-or-less taken this on as their crusade. Fine stuff.
 Just so we’re all on the same page here, Neanderthals were another species of the Homo genus, which went extinct somewhere around 30,000 years ago, allowing Homo sapiens to take the reins. They were a pretty advanced species – being bipedal and using tools and even having somewhat of a language (allegedly). In all likelihood, their extinction was brought about thanks to competition for resources with Homo sapiens (although some scientists support the interbreeding theory, which suggests that we kind of just adsorbed the remaining Neanderthals once they reached a low enough population level).
 Even though she was further perpetuating misinformation, Ms. Young showed much journalistic prowess, making sure to state that she couldn’t “personally attest to the original story as it [was] behind a paywall.” However, that dubious sentiment didn’t quite translate to the heading of the article.
 Especially when, you know, Kim Kardashian is preggers and Justin Beiber is toking up.
Earlier this week, Carl Zimmer (one of my favorite science writers) published a great article in the New York Times examining the conservation efforts of Australian scientists to combat Devil Facial Tumor Disease, which I wrote about back in December.
I highly recommend Carl Zimmer’s books, especially Parasite Rex, which explores some of the more interesting parasites inside us, and how they have driven the evolution of their hosts. Unless you are particularly squeamish. Then I recommend you avoid it.
Before I get into the following things that I hope aren’t boring, I need you to know: there is now a dinosaur named after Obama: Obamadon. Which is infinitely cooler than Obamasaurus or Obamapoda.
[Edit: the accompanying rendition of Mesozoian jungle in the link includes a couple dinosaurs. Upon further inspection, I am realizing that Obamadon is not the armor-clad uber-Gila lizard I thought it to be, but instead the smallish wintergreen-blue guy in the corner, clinging to either a gnarled tree root or a stone. Which is a smidgen disappointing. Also, there is a devastating comet approaching Earth in the background. Is this par for the course for dino-depictions?] [[Also, Obamadon gracilis literally translates into “Obama’s teeth slender,” which, hmm.]]
Medical research is taxing and exhaustive. Once a week, I sit through a Molecular Medicine Seminar that my institution puts together on Tuesdays. Different scientists from around the country are invited to give ~50 minute talks about their medical research. Many times it is interesting, other times it is dry and soporific, and every once in a while, it is funny (I.e. there was a hematologist with a thick Romanian accent and I had to stifle laughs every time he said “blood” like Dracula, which was no less than 100 times). But there is always free lunch (thus, my impeccable attendance record). Sometimes there is ice cream, for the drier of topics.
Anyway, something you are bound to see if you attend these, besides full-grown adults nodding off like teenagers, are diagrams of proteins. You might recognize these if you’ve taken any Bio classes, and certainly if you’ve taken any Biochemistry classes (in fact, if you’ve taken any BioChem, or are feeling a bit sleepy yourself, you might be OK skipping the next few paragraphs).
For example, the protein above is representative of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator). This protein gets really screwed up in people who have, you guessed it, cystic fibrosis. The protein essentially helps with proper mucus production, particularly in the lungs, so when it isn’t acting correctly, the patient suffers. As you can tell, there is very little in the way of pattern with the above protein. It looks like a bit of a mess. But researchers have spent countless hours making sure that this is indeed how the protein actually is (more or less – I mean it’s actually quite a deal messier than that and not color coded).
When your cells initially make a protein, it is essentially a long, long string. The string ends up folding up into a pattern that gives the protein its function. The order of the protein’s components is what dictates its folding. Think of a protein as a bracelet made entirely of charms. Each charm represents an amino acid (which is what proteins are made of – its “building blocks” I believe is how it’s often put). There are (for the most part) 22 different amino acids, thus 22 different charms, allowing for pretty much an infinite combination (since most proteins are thousands of amino acids). These amino acids can be either positively or negatively charged, or neutral. So, the positive charms will be attracted to the negative charms and repelled from other positive charms. The neutral charms will not interact with other charms. So, when an unfolded protein is initially made, it crumples up into a semi-organized lump, which usually makes a functional protein.
If all you have is a chain of amino acids that goes, for example, [nnn+nnnn-] (“n” being neutral), you can safely assume that the positive amino acid will be attracted to the negative amino acid, and the protein will be a little ring with a little neutral tail hanging off of it (can you picture it?). Unfortunately, proteins can be hundreds of thousands of amino acids long and so there are waaaay too many combinations for a scientist to sit down and figure out. Factor in the fact that there are plenty of ways that a protein could fold that would render it useless (see the picture below). More recently, programs have been developed which can accurately predict the specific glob that any protein would fold into. But these take so much computing power to run through the permutations, scientists have had to turn to other methods.
This astounds me. Knowing the shape of a protein of interest is very, very important to studying and curing countless diseases. Often researchers only know the sequence of the unfolded protein string, and can’t even make a swipe at its final form. And even with all of their seemingly endless grant money, running the calculations takes a staggering amount of computational power.
The solution? Playstation 3s.
Well, and also other types of computers. That’s called a hook.
There is a program called Fold@Home that is available to download (for free, of course) here. It is somewhat of a passive program: whenever your computer is inactive for a certain period of time, the program begins (as somewhat of a screensaver). The program uses your computer’s idling processing power to download raw protein folding data from the internet, and process it, sending the results back to the institution when it is finished. The idea is that large crowds of people have downloaded the software, allowing researchers who upload their data to have access to much more computing power than they could ever imagine.
So, theoretically, you can contribute to medical research without ever having to pick up a pipet or step foot inside of Academia. And your computer might also be the one that unlocks the secret to curing cancer.
The program’s model is also being used to find extraterrestrial life. The SETI program monitors radio signals from space (and covers about 20% of the celestial sphere), which generates an equally unfathomable amount of data. SETI@home is a similar program that you can download that will analyze raw space radio data and search for signals. If you want to increase your chances of being famous from virtually doing nothing, I would suggest installing Folding@home on your laptop and SETI@home on your desktop.
Even though these two people are the closest that have ever come to discovering aliens. I can dream, can’t I?
If you’ve ever read David Foster Wallace’s Infinite Jest, you may recall a short, wonderfully written passage about a woman who received a “Jarvik IX Exterior Artificial Heart” im(/ex?)plant, which she carried around in her purse, only to be stolen by a transvestite on the streets of Boston. It’s written a bit too well to just paraphrase:
“The 46-year old recipient of the Jarvik IX Exterior Artificial Heart was actively window shopping in Cambridge, Massachusetts’ fashionable Harvard Square when a transvestite purse snatcher, a drug addict with a criminal record all well known to public officials, bizarrely outfitted in a strapless cocktail dress, spike heels, tattered feather boa, and auburn wig, brutally tore the life sustaining purse from the woman’s unwitting grasp.
The active, alert woman gave chase to the purse snatching ‘woman’ for as long as she could, plaintively shouting to passers by the words ‘Stop her! She stole my heart!’ on the fashionable sidewalk crowded with shoppers, reportedly shouting repeatedly, ‘She stole my heart, stop her!’ In response to her plaintive calls, tragically, misunderstanding shoppers and passers by merely shook their heads at one another, smiling knowingly at what they ignorantly presumed to be yet another alternative lifestyle’s relationship gone sour.”
(Wallace, David Foster. Infinite Jest. 1st. ed. Boston, MA: Little, Brown and Company. 1996)
Well, in the manner with which he was often prescient, (he arguably predicted the rise of on-demand media consumption as early as 1996), another piece of Wallace’s fiction has come true.
Doctors at UCLA have performed the first successful exterior temporary heart transplant. Here is the deal: artificial hearts take a ton of power to ensure that they don’t malfunction (because that would be very bad). Artificial hearts are often used to keep patients alive while a donor heart is tracked down. Typically, however, these patients can’t leave the hospital – the artificial heart is connected to a (literal) ton of expensive and stationary machinery.
But now they have mobilized it. Chad Washington, a patient from UCLA has a fully artificial heart and can walk around and live his life outside of the hospital. The catch is that the heart still requires a significant power source – thus, Washington has to carry around a backpack from which a pair of wires extend, entering his chest. This essentially allows him to perform everyday talks – such as continuing to work – while waiting for a donor match.
You can read more, and check out a photo here:
In other, unrelated stuff, bees from a farm in France began producing blue and green honey this past fall, much to the chagrin of their owner (it’s rather difficult to sell blue honey). After much hand-wringing and temple-rubbing, the source of the colored honey was elucidated. And it was an M&M’s factory. Apparently, the Mars factory had been shuttling some of its red, blue, green, yellow, and brown waste to a biogas factory. The bees were attracted to the sugar in the waste and flew over 2.5 miles to get it. The honey they produced from the M&M’s tended to be a dull blue or green color.
There is a pretty awesome photo here:
 I think it would be extremely safe to presume Wallace’s referencing of Dr. Robert Jarvik here, who invented the first permanent artificial heart transplant.
 If you initially read this with Spanish pronunciation as “BEE-OH-GHAS,” you’re not alone. It really should be written as BioGas. I don’t know why they don’t write it that way.
So there are still a few bugs to work out, but this is a brilliant idea.
Repairing cracks in concrete is a constant pain and a huge cost for cities, as well as a popular problem to tackle for engineers.
Scientists at TU Delft have recently developed a self-healing concrete using bacterial spores. In short, they mix dormant bacterial spores with the concrete. These spores remain dormant until they are hit with water. Once the concrete cracks, the spores revitalize within the concrete. The spores are also packed with calcium lactate, which the bacteria munch on when they wake up. The byproduct of this digestion? Calcite, one of the two main forms of limestone. So when there is a microscopic crack in the concrete, the bacteria arise and fill it quickly with limestone. And there is no human interaction required.
On a completely unrelated note, I just came across DIYBio, which is a site geared towards having free-sourced plans for building home versions of centrifuges, PCR machines, etc. to allow ‘citizen scientists’ to perform research outside of industries and universities. Pretty cool. Unfortunately, as far as I can tell, the project has fallen a bit wayward at this point, but I hope to see it continue.
I’d like to take a minute to talk to you about cancer. And Tasmanian devils. Specifically, cancers of the Tasmanian devils. Stick with me.
The Looney Tunes depiction of the Tasmanian devil is inaccurate in a couple huge ways, not surprising for a cartoon (but at least you can sort of tell that Porky is an anthropomorphized pig). For starters, real Tasmanian devils have necks and torsos and are not 40% mouth. Nor do real Tasmanian devils harbor the ability to walk on two legs or turn into cyclones of fur. The aspirations of the cartoon (if you can call them that) are more closely informed by the real animal: Tasmanian devils tend to be incredibly ferocious and gluttonous, and spend much of their time fighting one another for food sources; many Tasmanian devils are extensively scarred much like manatees (albeit for different reasons). They tend to be about the size of a raccoon, with black fur and (sometimes) white markings. Adding to their ferocity, their bite is abnormally strong, and their teeth and mouth tend to be quite frightening (a point for Looney Tunes’ depiction), allowing them to bite through metal wires and even bones.
But they look pretty cute:
Anyway, there is much cause for concern for Tasmanian devil lovers. As it turns out, their population, which is confined to the island of Tasmania (off the coast of Australia), is being completely decimated by what is known as Devil Facial Tumor Disease (DFTD). As a result, the number of Tasmanian devils alive today is 30% what it was in 1994. Most people blame DFTD for this sharp decline.
Now I’m not decrying the demise of the TD, albeit sad in ways; species do go extinct and have done so since the beginning of time (there is probably a bacterial species that went extinct when you microwaved your holiday leftovers). It is kind of a major driving force behind evolution. Spending large amounts of sometimes public funds on preserving an endangered species makes a bit of sense when humans are destroying its habitat or poaching it, but it’s a different story when the cause is natural: i.e. not human. I’ve had a bit of a rocky and complex history with conservationalist ideologies, so I’m going to steer clear from here on out. Just know that I’m not expecting you to donate to anything (although, I’ll provide links if you’re so inclined).
I want to talk about DFTD because it’s absolutely fascinating (in the way that terrible, sad things can be a bit fascinating). As you may have gathered from the name, Devil Facial Tumor Disease is a cancer of the facial area of Tasmanian devils. The tumors often get so large that they occlude the devil’s mouth, leading to starvation. The cancer has been spreading throughout the population and there are estimates that 80% of the population is infected. Did you catch that? Not the 80% part. Although, damn. But spreading. DFTD is killing so many devils because it is a contagious cancer.
If there is anything at all good about human cancers (read: good = not entirely horrible), it would be that they aren’t contagious. Sure, there are certain viral infections that can lead to cancer, but vaccines have been developed for many of these, so they remain somewhat preventable. Oncoviruses (onco – (greek): tumor, mass, swelling) aside, you cannot ‘catch’ cancer just from hanging out or being intimate with someone who has cancer. Even if you were to, say, excise a tumor from a patient and transplant it into another (unrelated) individual, the receiving body would (thankfully) reject it (but you’d still lose your medical license). Some mammals, however, are not so lucky.
The reason our cancers aren’t transmissible arises largely from our immune system’s ability to recognize a particular molecule (or subset of molecules) displayed on the outside of all of our cells. These are called major histocompatibility complex (MHC) molecules. There are two types (MHC I and MHC II) and nearly all vertebrate cells exhibit them on their membranes. A large function of these molecules is to give immune cells an idea of the internal condition of the cell, as sort of a ‘window.’ Cells constantly break down proteins inside themselves and put the shreds on the MHC platforms, often referred to as ‘presenting’ to immune cells. Thus, passing immune cells can sample the insides of cells without invasive procedures, in order to see if the cells are sick or doing OK. For example, an immune cell might bump into a regular body cell and take a look at his one of his many MHC molecules. He might say “Oh, that’s just part of your cytoskeleton or your mitochondria you have on the platform there. Terribly sorry to bother you, sir” and be on his way. However, the immune cell may instead see part of a virus being presented, at which point he would be more likely to say “You, sir, are very, very sick. I hope you have your will in order, because we’re going to have to make sure whatever is inside of you doesn’t get inside other cells. I promise this won’t hurt.” This is a pretty broad way that the immune system controls infections that happen to be primarily inside of cells. The infected cells put little pieces of whatever may be ailing them on these MHC molecules, and patrolling immune cells will check on them. The process is the same for humans and Tasmanian Devils.
MHC molecules have even more functions though. The actual platform portion of the molecule is one of the most highly variable proteins within human beings. The subset of genes that code for these MHC molecules vary between individuals much, much more than any other human trait. This is extremely helpful, as the immune cells are then able to recognize “self” from “other.” These platforms are highly personalized for each individual. Mine, for example, might be the protein equivalent of an cypress-wood, five legged, hexagonal platform, each side being a very particular length, all shellacked with a particular shellac (maybe Kusmi Seed Lac) and painted with a very recognizable and tessellating pattern of a hunter green background with deep maroon squares. All of my cells would have the same type of platform, but very few humans would share a similar platform – so if my immune cells would see a cell with, say, the MHC equivalent of a pink, heart-shaped, three-legged oak platform, they wouldn’t care what was on the platform. They would say “Great Ocean’s Depth! This isn’t the hexagonal green table we’re used to…Intruder!!!” and act accordingly. By act accordingly, I mean they would kill the cell. This is why skin grafts are typically rejected between individuals. Same for organ transplants. Before performing any transplant, many tests on both the recipient and donor must be performed in order to make sure that the MHC molecules between the two (and the blood types) are similar (this is why relatives are good candidates for transplants). Even then, immunosuppressive therapy is often administered to the recipient (for a really, really long time) to make sure that rejection will not occur.
Phew. OK. The thing about all of this that spells trouble for Tasmanian devils is that their MHC molecules have a very low diversity. Meaning that all of the cellular platforms across the TD’s population are of a similar wood, color, shape and shellac. So, if you were to transplant part of a Tasmanian devil on/into any other Tasmanian devil, you wouldn’t have to worry about immunosuppressive therapy: the TD’s immune system can’t tell ‘self’ from ‘other,’ as long as it’s a Tasmanian devil cell. Which leads to a transmissible cancer.
The problem is that Tasmanian devils are ferocious little guys. They often fight, viciously, over food. This fighting involves a bunch of face-scratching between both parties – and this is how the cancer is transmitted. Two devils meet near a nice steak (or road kill, however you’d like to imagine it) and they go at it. One is infected with DFTD and has bulbous tumors on his face. The other is, for the time being, healthy. The healthy one ferociously paws at the tumored face of the other, cutting into the swelling growths (sorry). Here is the important part: the diseased devil retaliates and pins the healthy devil down, biting his face. Inevitably, there is a mixture of blood, as both have open wounds. A few tumor cells slip into the open wounds of the healthy devil. A couple weeks later, he begins growing tumors on his own face, and the cycle starts anew.
Why this is mind-blowing:
· This is not how cancer works. There are only three types of transmissible cancer (that we know of) in the world: one is in canines and the other is in hamsters and is spread by mosquitos. Neither has been nearly as devastating to their host’s populations as DFTD has been to Tasmanian devils.
· All of the tumors, taken from any in/affected Tasmanian devil are not only genetically distinct from their host, but (nearly) genetically identical (the cancer cells have evolved a bit since their extrusion from patient zero). This means that one initial Tasmainian devil developed cancer, in the canonical way we are used to: a mutation in the cells. But because their MHC proteins are so similar, and the devils fight so often, his cancer cells spread to almost all of the Tasmanian devil population. If you take any devil with DFTD and take a sample of his tumors, those are technically cells from the first devil that are now thriving in a new host.
· By many definitions, this cancer line is sort of its own species. Its own organism. It thrives in its own definitive habitat. And it may have evolved enough by this point to be genetically dissimilar enough from Tasmanian devil cells themselves.
All fascination aside, however, it really is a complete bummer for Tasmanian devils and those that care about them. If you’d like more information, or would like to donate to the conservation efforts, check out http://www.tassiedevil.com.au/tasdevil.nsf and click on “how you can help.”
 Human papillomavirus (HPV) is one, for example; a transmissible virus that can lead to cervical cancer. Hepatitis C can lead to liver cancer. Epstein-Barr virus can lead to Hodgkin’s lymphoma. These are just a small sample. The World Health Organization thinks that over 17% of human cancers are due to viral infections, many due to the fact that viruses tend to stick genes into our cells that make them multiply like crazy (or at least turn off the cellular protocols that would normally prevent such overgrowth).
 Most of these functions that I am describing are functions of MHC I molecules, which are on the majority of your non-immune-system cells. MHC II molecules tend to be on a couple different types of immune cells and serve slightly different physiological functions, although their structure is pretty similar to MHC I molecules and they still serve as communication tools for cells – MHC II’s are mostly for communication between two immune cells though, whereas MHC I cells are most for communication between a regular cell and an immune cell.
 This sort of skims over the complexity of it all, as there are subsets of MHC I molecules with slightly different functions in any individual. But the individuality of each still applies.
(photos from http://www.tasmaniandevilpark.com/ and http://www.redorbit.com/education/reference_library/science_1/mammalia/2577518/tasmanian_devil/, respectively)