Measles looks to be 1000 years old. It jumped from cattle. And you can read more about it here.

Can the bacteria in our bodies control our behavior in the same way a puppetmaster pulls the strings of a marionette? I tremble to report that this wonderfully creepy possibility may be true.

The human body is, to some extent, just a luxury cruise liner for microbes. They board the SS Homo sapiens when we’re born and settle into their assigned quarters–the skin, the tongue, the nostrils, the throat, the stomach, the genitals, the gut–and then we carry them wherever we go. Some of microbes deboard when we shed our skin or use the restroom; others board at new ports when we shake someone’s hand or down a spoonful of yogurt. Just as on a luxury cruise liner, our passengers eat well. They feed on the food we eat, or on the compounds we produce. While the biggest luxury lines may be able to carry a few thousand people, we can handle many more passengers. Although the total mass of our microbes is just a few pounds, the tiny size of their cells means that we each carry about 100 trillion microbes–outnumbering our own cells by more than ten to one.

It’s important to bear in mind that you can carry this galaxy of microbes around and enjoy perfect health. These microbes, for reasons that are not entirely clear, behave like well-mannered passengers. They do not barge into the kitchen, take a cleaver to the cooks, and then eat all the food. Aboard the SS Homo sapiens, the crew includes a huge staff of security guards armed with lethal chemical sprays and other deadly weapons, ready to kill any dangerous stowaway (also known as the immune system). For some reason, the immune system does not unleash its deadly fury on the microbes–even when the microbes are fairly close relatives to truly dangerous pathogens.

In fact, our microbial passengers may actually help out the cruise liner’s crew. They can close up the ecological space in our bodies, so that invading pathogens can’t get a solid foothold. Some species in our guts can break down our food in ways that we can’t, and synthesize certain vitamins and other compounds beyond our biochemistry. The genes that the microbes carry–millions of them–expand our biochemical powers enormously.

To understand the human microbiome better, scientists have been cataloging the microbes in and on people’s bodies, and they’ve been sequencing their DNA. (Listen to my recent podcast with biologist Rob Knight for more.) Yesterday, Nature published a head-spinningly huge study on the microbiome from a team of European and Chinese researchers. Lurking in the stool of 124 volunteers, the scientists found, were 3.3 million microbial genes. The scientists identified a core of bacteria species carried in most people’s guts, as well as other species that varied from person to person.

As Ed Yong rightly points out, this study is most impressive as a titanic database. It is not the Theory of Everything for the human microbiome. That will take a lot longer to build, because the microbial ecosystem inside of us is so complex. Individual species don’t just sit in isolation, surviving in their own special way. Microbes cooperate with one another to get the food they need and produce the conditions in which they can thrive. In Microcosm, for example, I write about research suggesting that E. coli–a minor member of the gut ecosystem–may keep oxygen levels low enough for other species to invade and dominate. And it’s not as if there is some Platonic ideal of a microbiome that we all carry around with us from birth to death. The diversity of microbes I carry is different from the one you carry, and they both change over our lifetimes. Every time we take a dose of antibiotics, for example, the balance can change dramatically. And as the diversity of microbes changes, so do its ecological functions.

Which brings me, at last, to the possibility that the human microbiome can become our puppetmaster.

First some background. A lot of parasites have evolved the ability to manipulate their hosts for their own benefit. (I get into more detail about this in my book Parasite Rex and in this segment of the show Radio Lab.)

Very often, the parasites cause hosts to do things that help the parasites, instead of themselves. For example, a protozoan called Toxoplasma needs to get from rats to cats, and to help the process along, it makes rats lose their fear of cats. Parasites can also change the diet of their host as well as the way in which their hosts digest their food. Parasitic wasps living inside caterpillars, for example, cause catepillars to convert the plants they eat into compounds that supply quick energy (good for wasp larvae growing quickly) instead of storing them as fat for their own metamorphosis.

I was reminded of this sinister manipulation by a paper that was published in Science today by Rob Knight and his colleagues. They built on previous research that revealed that mice genetically engineered to be obese have different kinds of microbial diversity in their guts than normal mice. Scientists have found that if they transfer microbes from an obese mouse to a regular mouse that has had all its own germs stripped out, the recipient mouse will develop extra fat. In the case of these obese mice, it appears that the microbes become less efficient at helping the animals digest food, triggering a series of changes that leads the mice to be fat.

Knight and his colleagues discovered a different–and more disturbing–way that microbes can make mice fat. They started out by engineering mice so that they didn’t produce a protein normally found on the surface of gut cells, called TLR5. TLR5 can recognize bacteria, and some studies suggest that the cells can then pass along signals to the immune system, possibly sending a stand-down command so that the immune system doesn’t start trying to kill the microbes (and end up killing gut cells too).

Born without TLR5, mice got 20% fatter than normal. Not only that, but the mice had lots of other familiar symptoms that go along with being overweight, such as high levels of triglyceride, cholesterol, and blood pressure. Without TLR5 exerting its soothing influence, the mice suffered from chronic inflammation, probably thanks to the low-level war they were waging on their microbes. And things got worse for the mutant mice when they had to eat a high-fat diet. They gained more weight on a high-fat diet than regular mice, suffered even more inflammation, and even ended up diabetic.

The obesity of these TLR5-deficient mice was not the result of inefficiency, as in previous studies. Instead, the mice wanted to eat more–about 10 percent more than regular mice. Knight and his colleagues restricted the diet of the mutant to what the regular mice ate. A lot of their symptoms went away. So the change in their behavior was critical to their weight change.

The scientists also discovered that the make-up of the microbial diversity changed significantly in the mutant mice. Were the microbes giving the mice their symptoms? To find out, Knight and his colleagues knocked out the microbes with antibiotics. The mice ate less, put on less fat, and showed less diabetes-like symptoms.

To isolate the effects of the microbes even more, the scientists transferred them from mutant mice into the bodies of ordinary mice that had first had all their own germs stripped out. Remember–these mice have a normal set of TLR5 receptors. The scientists found that the microbes made the recipient mice hungry–and also made them obese, insulin resistant, and so on.

So here we are. Mice with a genetic make-up that alters the diversity of their gut microbes get hungry, and that hunger makes them eat more. They get obese and suffer lots of other symptoms. Get rid of that particular set of microbes, and the mice lose their hunger and start to recover. And that distinctive diversity of microbes can, on its own, make genetically normal mice hungry–and thus obese, diabetic, and so on.

When I first learned of this work, I asked Knight–with a mix of dread and delight–whether the microbes were manipulating their hosts, driving them to change their diet for the benefit of the microbes. He said he thinks the answer is yes.

This discovery doesn’t just have the potential to change the way we think about why we eat what we eat. (Am I really hungry? Or are my microbes making me hungry?) It also provides a new target in the fight against obesity, diabetes, and related disorders. What may be called for is some ecological engineering.

[Update: Links to papers fixed.]

In my newest podcast, I talk to a kind of viral Indiana Jones. Michael Worobey of the University of Arizona chases down the evolutionary origins of viruses such as HIV and the flu no matter what it takes–including getting dangerously ill in the middle of a civil war. Check it out.

Plush Alien Facehugger out of stock and not back until mid-2010?? This is an outrage–let’s get to work, people!

Last March a new kind of flu came on the scene–the 2009 H1N1 flu, a k a swine flu. Hatched from an eldritch mingling of viruses infecting humans, birds, and pigs, it swept across the world. Here in the United States, the CDC estimates that between 41 and 84 million people came down with swine flu between April and January. Of those infected, between 8,330 and 17,160 are estimated to have died. For more details on the evolution of this new flu strain, here’s a video of a lecture I gave in November.

This flu strain has been nothing if not surprising. It was lurking around in humans for several months, undetected, before becoming a planetary infection. And before that, the ancestor of the virus was circulating among pigs for a decade, again unknown. And while the new swine flu has killed some 10,000 people in the United States alone and many more abroad, it has proven to be relatively low key–as flu goes. Some 30,000 people die in the United States every year from seasonal flu, the cocktail of flu strains that show up year in and year out.

Now the swine flu is surprising us once more. It has dwindled away to very low levels and stayed there. Meanwhile, the seasonal flu, which was expected to kick in at some point as well this flu season, is a virtual no-show. The San Francisco Chronicle has the story. In this CDC chart of total reports of flu-like symptoms, you can see that we’re in a deep trough. At this point in previous years, we were fast approaching the peak of the flu. This season, the peak came months ago, at the height of the fall swine flu outbreak.

When swine flu started to crash, some observers expected it to bounce back soon, as other flu strains have in the past. Ian York, at his blog Mystery Rays from Outer Space, offers some interesting ideas about why this hasn’t happened. He suggests that the virus has been stymied by pre-existing immunity in a lot of old people, new immunity from vaccinated children, and the protection that infected survivors now have. In other words, the virus just doesn’t have enough hosts now to sustain a new outbreak.

It’s possible that the swine flu’s raging success in the fall may have also led to the weird situation we’re in right now, with no seasonal flu at exactly the time you’d expect it. One possibility is that getting sick with swine flu provides some cross-immunity to seasonal flu. Another is ecological: the swine flu outcompeted seasonal flu so effectively at the start of flu season that the seasonal flu hasn’t been able to get a toehold since.

That, of course, could change. Seasonal flu has been known to peak as late as March. And while flu may be in a lull in the United States, it’s doing just fine in other parts of the world. For example, a nasty kind of flu called influenza B is raging around China right now according to the Chronicle. In normal years B makes up a pretty small fraction of US flu. But this is no normal year.

Scientists did a better job tracking the 2009 H1N1 outbreak than they have with previous emergent strains. They’ve got new machines to sequence virus genes, online databases to pool information from around the globe, and powerful computers to help figure out where the viruses came from. And yet, with just ten genes, the flu still continues to move enigmatically ahead of our understanding.

Here’s a talk I just gave on Big Think–about viruses, synthetic biology, and tapeworms that carry my name. The sound quality isn’t as good as I’d like, but I hope the words make up for it.

One year. 365 parasites. Be a part of it.

In tomorrow’s New York Times, I dig up some of the fossil viruses that have been buried in our genome for tens of millions of years.

This is a subject I’ve explored here on the Loom before (1, 2), but now is a great time to stop and take stock of just how much progress scientists have made in exhuming the ancient invaders that helped make us what we are.

There was one dimension of this research that I didn’t have space to describe, but it’s too cool to let go unmentioned. In the article, I describe a virus protein called syncitin that is essential for placentas to develop. Cells push the protein to their surface, where it lets them latch onto other cells, fusing together to create a special layer through which nutrients can pass from mother to child. The protein got its start on viruses, which use it to latch onto host cells and fuse to them, allowing their genes to slip in.

But recent research has revealed an intriguing new twist to our viral legacy. It turns out that the viral surface protein in question has a second job. It also tamps down the immune system of its host. If the protein is altered to make it unable to suppress the immune response, viruses cannot successfully infect their hosts.

Thierry Heidmann, a leading paleovirologist whom I spoke to for the article, suspects that this second function may have been critical in the evolution of the placenta. That’s because there are two major challenges to being a placental mammal. First off, mothers need to be able supply their embryos with lots of nutrition for a long time through their circulatory system. Second, they have to cool down their immune systems. A baby’s tissues would otherwise look to the mother’s immune system like foreign tissue and be quickly rejected. So it’s possible that viruses not only let mothers feed their babies, but not kill them either.

This is a story that’s just going to get cooler, so expect updates as necessary.

Parasite Rex has made a very special list of books to read after you get dumped. To quote from Lemondrop over at the AOL collective:

Do you need something to so totally fill you with paranoia and fear that you can’t even think about the worm that just dumped you? How about a terrifying book about worms! AGH! You’ll never walk barefoot in the street again, plus you’ll be so full of disgusting factoids that you won’t even have time to mention what’s-his-name at a party — you’ll be too busy grossing people out. FTW!

I would suggest waiting to find a new special someone until the book has cleared your system.  I was still single while I was writing Parasite Rex, and the book made going out on dates very awkward.

So, what’s your next book about?

Parasites, and why they’re totally awesome. See, like, there’s this worm that crawls across your eye…

Check, please!

On the plus side, it’s a very quick test to see if your date shares your taste for the grotesque.

This fall, I gave a number of lectures about the evolution of swine flu. By the time I got to the end of the talk, I could tell that a lot of people in the audience were feeling a bit resigned, given the way evolution allows viruses like the flu to evade our best attacks. (Here’s the full video of my lecture at the University of British Columbia.)

To try to cheer up the crowd, I’d offer a note of hope–the notion that we could turn the evolution of viruses against them, by pushing them into mutation overdrive. (This slide gets across the basic idea–the flu virus is like a sports car. Going fast is cool. Going too fast–not so cool.)

In tomorrow’s New York Times, I lay out this intriguing idea, that goes by the profoundly cool name of lethal mutagenesis. Check it out.

Tasmanian devils have given rise to a weird new quasi-form of life: a cancer that spreads from animal to animal like a parasite. In tomorrow’s New York Times, I report on the latest analysis of devil’s facial tumour disease, published in this week’s Science. Scientists have now tracked down the cancer to its progenitor: nerve cells known as Schwann cells.

Now scientists can use this evolutionary history to design diagnostic tests for the cancer and perhaps even vaccines. Let’s hope they succeed–the cancer has wiped out 60 percent of all Tasmanian devils since 1996 and has the potential to drive the whole species extinct in a matter of decades.

For more on cancer as a new form of life, check out my earlier blog post on the only other documented case in the wild: a tumor that jumps from dog to dog. (The one major update to that post is that it now looks as if the tumor escaped its original dog host thousands of years ago, instead of hundreds as previously thought.) While dogs and Tasmanian devils are so far the only known hosts to these sorts of cancer, free-ranging tumors may actually be more common than we know right now. They may be particularly likely to arise in small, inbred populations. The similar immune systems of these animals may be easy for the cancer to evade, allowing it to spread quickly. Another hint that infectious cancer isn’t all that rare is the violence with which we reject transplanted organs. Why should our bodies be so well-primed to attack the cells of other humans? One possibility is that invasive cancers have been a long-term threat to the health of our ancestors.

(And for more on cancer as an evolutionary disease, see my article in Scientific American, reprinted in The Best American Science Writing 2008 )

Reference: EP Murchinson et al, “The Tasmanian Devil Transcriptome Reveals Schwann Cell Origins of a Clonally Transmissible Cancer.” Science http://dx.doi.org/10.1126/science.1180616

Image: Wikipedia

[Update 12/31 3 pm: Headline de-apostrophed.]

What’s with all the tongue-eating parasites popping up these days?

At least this one is pretty. (As it should be, given that it’s the winner of the symbiosis-and-parasitism photo contest over at WetPixel.)