Carl Zimmer's Blog, page 21

The Great Puppet-Master Debate

Life is rough for parasites. Say you’re a tapeworm that only lives in the gut of one species of shark. You start out as an egg inside an adult tapeworm. Your parent releases you and a bunch of other eggs from its body, and its shark host shoots you out of its own body. Now you float in the vast ocean, stretching out on all sides. You are not made for the free-living world. If you don’t get into another host, you will never reach adulthood. Not just any host, but a fish. And not just any fish, but one species of shark. Chances are good, in other words, that you’ll die.

The miserable odds for individual parasites can potentially drive the evolution of something remarkable: the ability of parasites to manipulate their hosts. By controlling their hosts, the parasites can raise their odds of surviving and reproducing.

Scientists have gathered a number of examples of host manipulation over the years. I dedicated a chapter of my book Parasite Rex to some of them, and a group of scientists published a whole book on the topic last year. A lot of these parasites are cool just in and of themselves, whether they infect caterpillars or spiders, but inevitably people want to know whether parasites control us. I put it down to a combination of our species’s narcissism and love of zombie movies. There are a few potential cases of parasites influencing–if not outright manipulating–human behavior. And the most intriguing one of them all involves a single-celled parasite called Toxoplasma gondii.

Toxoplasma gondii forms cysts in people’s brains. Unless their host has a weak immune system, their cysts cause no apparent harm. But they make up in numbers what they may lack in deadliness. Perhaps a billion or more people carry Toxoplasma cysts in their brain. They pick up the parasites in the soil, undercooked meat, or cat litter.

It’s in cats that the Toxoplasma life cycle gets its start. The parasites mate in the intestines of cats and then produce egg-like offspring, which are passed out with cat droppings. The durable eggs can stay viable for months as they wait for their next host–which can be any species of mammal or bird. Those hosts swallow the parasites, which migrate out of their gut and wander their body; the ones that make it to the brain form protective cysts and play the waiting game again. Only if they can get back into a cat’s gut will they be able to take the next step in the Toxoplasma life cycle.

As other cases of parasite manipulation came to light, some scientists wondered whether Toxoplasma might have some tricks of its own. After all, there’s one obvious opportunity for increasing its odds of getting into cats: make its host easier for cats to catch.

Starting in the late 1990s, a number of researchers published evidence indicating that the parasite does, in fact, do this. Most of the work has been carried out on rats and mice. In a number of experiments, infection with Toxoplasma appears to make the rodents less frightened by the smell of cat urine. Some studies even hint at an attraction to the scent of their killer. (I’ve written about some of the research in recent years here and here.)

Now, in the journal Trends in Parasitology, a team of Australian parasitologists have challenged the Toxoplasma puppet-master hypothesis, in a commentary entitled “Adaptive host manipulation by Toxoplasma gondii: fact or fiction?”

“In our opinion,” the authors declare, “the accepted dogma that T. gondii manipulates host behavior to increase transmission to cats, tells an appealing story but does not stand up to scrutiny.”

They make their way systematically through the published record of experiments on Toxoplasma. They observe that the parasites produce a range of effects on the behavior of their hosts. In some studies, animals become more active, while in others they become less active, and in others they experience no change at all. In one study, scientists found that Toxoplasma impaired a host’s ability to learn, and in another, it didn’t. The same split in results turns up in tests on memory, a preference for exploring new things, time spent near cat urine, and anxiety.

The scientists also attack the elements that make up the manipulation hypothesis. Just because a parasite does something that appears to make it easier prey does not mean that natural selection produced that change to improve its odds of completing its life cycle. Toxoplasma could be altering its hosts as a side effect of infection, not as an evolved adaptation. The authors note that another single-celled parasite called Eimeria also robs mice of their fear of cats, despite the fact that its life cycle takes it from mouse to mouse, not mouse to cat.

If natural selection really had been at work here, it would be necessary for manipulations to actually increase the number of offspring Toxoplasma produced. But no one has ever done a large-scale trapping experiment to see whether cats catch more Toxoplasma-infected prey than healthy ones. This sort of experiment has been done for other species. In an experiment on fluke-infected fish, researchers found they became easier targets for birds because they jumped around near the surface of the water.

On the other hand, some behaviors that seemed like they ought to make hosts more likely to be killed turned out not to. A tapeworm called Hymenolepis dimunata alternates between beetles and rats. When it infects beetles, they spend more time out in the open, where they ought to be easier for rats to find and eat. Despite such expectations, scientists found that infection didn’t actually raise the odds of a beetle getting killed. In the case of Toxoplasma, rodents may lose their fear of cat urine but might still avoid other scents from their predators, such as the smell of cat fur.

The Australian scientists also point out that Toxoplasma has a more flexible life cycle than it’s often given credit for. It has to get into cats in order to sexually reproduce. But it can also clone itself in other species. The parasite can even spread from mothers to their offspring. When scientists survey the DNA of Toxoplasma, they see evidence for a lot of cloning, and not a lot of mixing genes through sex. If the parasite isn’t moving much between cats and their prey, the natural selection for manipulation should be weak.

A lot’s been made of the fact that Toxoplasma winds up not just in rat brains, but in human brains. Some scientists have argued for a whole host of changes to behavior in people who carry the parasite. It’s tempting, for example, to see “cat ladies” as being in the thrall of cat-infecting parasites. The critics think all this speculation is completely unwarranted at this point.

“Given that research into human behavior is based at least partly on findings in rodents,” the authors conclude, “it is vital that we have a good understanding of how rodent behavior is affected by T. gondii, before we extrapolate to other species.”

I reached out to some of the scientists who have done the most prominent work advancing the manipulation hypothesis. While they all agreed that scientists should be careful to avoid assuming adaptations that may not actually exist, they dispute a lot of the claims made by the Australian critics.

“I firmly believe Toxoplasma is a clear case of actual manipulation and that their attempt to dismiss this is a little too naïve and simplistic,” says Joanne Webster of Imperial College. Webster herself is no “manipulation fundamentalist,” as it were–she was the one who did the beetle experiment that the Australian critics use as evidence against manipulations. But she thinks that the evidence for Toxoplasma is strong, and the criticism against its power to manipulate are weak.

Mathematical models of evolution, for example, show that it’s not necessary for there to be a huge boost in cat attacks in order for natural selection to favor manipulation. And while it’s true that Toxoplasma doesn’t need sex to reproduce, sexual reproduction in the long run has many advantages–such as mixing genes together into better combinations.

Webster agrees that it would be great to see whether cats are more likely to kill infects prey than uninfected ones, but that’s a hugely challenging undertaking for all sorts of reasons (such as the rules about animal welfare). Michael Eisen, a Berkeley researcher who has done experiments on Toxoplasma in mice in recent years, put it this way:

It’s an almost impossible experiment to do right. Are you going to infect mice and release them and a control group and see which get eaten? Where would you do that? How would you know the results wouldn’t be different in a different setting?

As for the different results from some studies on Toxoplasma infection, Webster argues that a lot of that may come down to the fact that scientists have run some experiments on lab rodents and others have studied wild ones. Lab animals have been bred for decades away from their natural threats–including cats. If these differences are accounted for, Webster still sees the evidence for manipulation as being strong.

Eisen, on the other hand, thinks that scientists have yet to do enough experiments to make any strong statements about Toxoplasma. “We’re still far away from having done truly definitive studies to characterize the behavior itself,” he said. “Let’s talk about this before we start calling Toxo the parasitic king of behavior manipulation.”

Still, he agrees with Webster that the critics make a weak case when they try to downplay the importance of cats to Toxoplasma’s long-term survival. If Toxoplasma can do so well without having sex inside of cats, he asks, why does it still carry so much genetic machinery for having sex and producing offspring? Eisen calls this argument from the critics “very poor evolutionary thinking.”

Finally, I got in touch with Ajai Vyas of Nanyang Technological University. He’s done some of the most detailed work on how Toxoplasma affects the brains of rodents, finding it zeroes in on emotional circuits. Vyas pointed out that scientists have debated for a long time how you can tell whether the effects of a parasite are an adaptation for manipulating their host. A few criteria have emerged. Is the effect complex? Is it something that well-fitted to a parasite? Does it turn up in different parasite species, suggesting natural selection has favored it repeatedly. By these standards, Vyas argues, it makes sense to look at Toxoplasma as a manipulator.

But it’s also important to bear in mind that the cats and rodents that we see today–even in the so-called wild–are living in a human-dominated world. Both predator and prey in this case have benefited from our company; we’ve moved them around the world, we’ve given them shelter, and we’ve given them–intentionally or not–an abundant supply of food. The manipulations that Toxoplasma originally evolved may have been less ambiguous before its hosts underwent so much rapid change.

“It could be a historical legacy rather than a present adaptation,” says Vyas. “I am not yet clear about this.”

When You’re A Naked Mole Rat, Why Stop At One Weapon Against Aging?

In June I wrote about the amazing longevity of naked mole rats. These rodents can live for thirty years, whereas their mice cousins can only live two years. One secret to their longevity may be the fact that they’ve never been documented with cancer. As I wrote back in June,  scientists at the University of Rochester found  a gooey protein in the tissues of the rodents that prevents cells from multiplying out of control.

But naked mole rats do more than just fight cancer. In addition to avoiding tumors, they also resist the overall decline seen in other aging mammals. A new study from the same Rochester team may reveal how they ward off aging: they’re very careful about making proteins.

Like other animals, naked mole rats carry DNA that encodes thousands of genes. To make a protein, the mole rat’s cells make a single-stranded version of the corresponding gene (called messenger RNA), which is then grabbed by a cellular factory called a ribosome, which is made up of RNA molecules and proteins. The ribosome reads the messenger RNA and uses the genetic code to pick out building blocks to attach to a growing protein.

If the ribosome picks the wrong building block, a protein may end up with a defective shape and can’t do its job properly. A big part of getting old is the accumulation of these defective proteins. Our cells end up getting worse and worse at all the things they excelled at when we were young. Collagen no longer stretches in our skin; our digestive enzymes no longer break down nutrients as efficiently as before. A number of studies have hinted that we can extend our healthy lifespans by boosting our ability to repair defective proteins.

The Rochester team took a look at how naked mole rats build proteins. They discovered something odd about their ribosomes. All living things use pretty much the same set of RNA molecules in this factory. One of these molecules is called 28S. Naked mole rats have a mutation to the gene for 28S RNA. Instead of producing a single RNA molecule, they break it in two.

To see if two 28S molecules worked differently than just one, the researchers compared how the naked mole rats make proteins to the process in mice. They engineered a gene and inserted it into both species. If a cell made an error at one site in the protein, the protein would give off a flash of light. A cell that always built perfect proteins would stay dark. A sloppy cell would glow.

The scientists found that the naked mole rat cells were much darker than those of mice. They built the engineered protein far more accurately, in other words. Naked mole rats, the scientists found, made anywhere from four to ten times fewer mistakes. Yet the naked mole rats can make their proteins as quickly as the sloppier mice.

The scientists were unable to directly examine the 28S RNA fragments in action, so they can’t say for sure that splitting 28S in two is the reason for the accuracy of naked mole rat proteins. Still, the results offer an intriguing hint that this ugly creature has more than one secret to long life. Whether we can borrow that secret is hardly clear. I for one wouldn’t volunteer to have my ribosomes shattered.

(Reference:  Jorge Azpurua et al.“Naked mole-rat has increased translational fidelity compared with the mouse, as well as a unique 28S ribosomal RNA cleavage.” PNAS 2013)

Paying The Extinction Debt: My New Column for the New York Times

The extinction crisis we’re experiencing today is hard to get our arms around. It can be tough even to just know when a species really has become extinct, and not just hiding from people. But scientists also want to know how species become extinct. Once we disturb a place, how long do we have to wait before the species there start to disappear? If we can understand the path towards extinction, we may be better able to stop the stampede. For this week’s “Matter” column in the New York Times, I  look at a rare opportunity to test out ideas of “extinction debt,” created by a dam in Thailand. It turns out that species can vanish from fragmented forests with startling speed. Check it out.

Ten Years!

On Monday I was at a meeting at MIT. When it broke up in the afternoon, I breathed a sigh of relief. The purpose of the meeting was to bring together lots of people who share science in one way or another–in museums, on Facebook, at street fairs, in books, and so on–and have them talk about what they saw in the future. Thankfully, I got to the end of the day without anyone stopping to say, “Now, we really need to talk about how blogging is going to change the landscape. Carl, maybe you could stand up and explain how blogs work?”

I had reason to dread this, because I’ve experienced variations of it over the years. People were wondering whether blogs were here to stay long after they had infiltrated the entire body of journalism. But it seems that, at long last, no one even thinks of blogs as something new and strange. And it felt particularly satisfying to me to go unbothered on that point this particular week. Because today marks the tenth anniversary of The Loom.

It’s hard to escape reflection when a ten-year anniversary rolls around. In 2003, starting a blog was still something people did as an experiment, or as a short-cut around traditional publishing, or as an open journal. Science blogs–the few that were around at that point, at least–were a mix of journal-club-like musings on new papers or righteous rants by scientists about bad reporting on science. As I got familiar with the software (because blogging is, when you get down to it, publishing software), I used it to write essays about science, toy with video, and find other ways to be a science writer than what I’d been doing up to then. (Like curating science tattoos.)

I don’t think many people blogging about science in 2003 would have guessed at the upheavals that would sweep across journalism in the years that followed. I certainly didn’t. And I was also surprised at the vague suspicion that somehow we science bloggers were to blame for the shuttering of newspaper science sections across the country. I was even more surprised to find myself in journalism classrooms where teachers asked me to explain the laws of good science blogging. When I said that blogging was software, and that you could make up your own rules, my answer did not satisfy. Clearly, blogging had achieved a cultural heft if rules were now required.

Its peculiarity dwindled as big publications established their own blogs. But the online world was also concocting new ways to communicate (or waste time, depending on your view of such things). Twitter and other outlets lured people away who wanted to have public conversations but didn’t want to learn WordPress. (I will spare you the “In my day, you had to build your blog from twigs and paper clips!” rant.) Recently, some high-profile blogs shut down, and so now we’re getting routinely exposed to think-pieces declaring that blogging is dead.

Does that mean that the Loom at ten is a zombie publication? I don’t think so. And I think the “blogging is dead” meme overlooks how bloggy all journalism has become. While blogging is just software, it has fostered certain social behaviors–an informality, a personal voice, a willingness to hear other voices such as commenters, an interest to respond to those voices, and a dedication to backing up claims with evidence in the form of links. Those behaviors now extend far beyond publications that we arbitrarily identify as blogs.

That’s not to say that these behaviors don’t pose their own challenges. Popular Science, for example, has gotten so tired of trolls in their comments that on Tuesday they simply shut down comments altogether on their stories. While I have no intention of shutting off comments on the Loom, I certainly appreciate how unpleasant a few commenters can make a thread with anti-scientific rants, insults, narcissism, and other conservational toxins. That’s why I keep an eye on comments and intervene when they break dinner-party rules. But I have always been well aware that I can always shut comments down–because blogging is software, and turning comments off is a feature of that software. I don’t think shutting down comments or banning trolls is automatically a cause for high dudgeon. After all, no one prevents even the nastiest trolls from starting a blog of their own for free. (“In my day, you had to pay for the privilege…” Oh, sorry again.)

For me, ironically, the biggest challenge for the Loom is that ever-expanding blogginess. In May, I started a weekly column for the New York Times, where I can write in a personal style about new developments in science that intrigue me. I write short essays sometimes for Slate or other publications. Ten years ago, by contrast, my options were stark. They were a) magazine features, b) newspaper articles, c) other. The Loom was the only place for Other. Now Other is everywhere.

So I’d love to hear from you about where you think I should steer the Loom in its next decade. The comment thread, after ten years, remains open.

 

Genetically Engineering the Wild

Back in April, I wrote in National Geographic about the provocative idea of bringing extinct species back to life. In the five months that have passed since then, I haven’t spotted any mammoths or saber-tooth lions drifting through my front yard. If “de-extinction” ever does become real, it won’t for quite a while.

What I have seen over the past five months is a new conversation. Part of the conversation has revolved around the specifics of de-extinction. Some people are open to the possibilities of rebuilding genomes and embryos of vanished species. Some people find it a flashy distraction from the real work of fighting the current wave of extinctions.

But the conversation is bigger than mammoths and saber-tooth lions. It makes us think about how much we could–or should–manipulate DNA of wild animals and plants. This question applies not just to extinct species that are gone, but to endangered species that are rolling down the road towards extinction. And with estimates that at least 15 to 40% of species will be effectively extinct by 2050, that road is wide indeed. Is it okay to use genetic engineering to save some of them?

In Nature today, a group of conservation biologists take this conversation much further. They report on a meeting they had this spring in New Mexico to discuss how the changing climate will push some species towards extinction and what can be done about it.

For a few years now, some conservation biologists have argued that we should move species to places where they’re more likely to survive. If Florida is too hot in 50 years for a tree to survive, move the tree to Virginia.

But what if we were to move genes instead? That’s the question that the scientists at the New Mexico meeting considered.

Their conversation was based on the fact that animals and plants have evolved genes that adapt them to their environments. As trees move into drought-stricken plains, natural selection may favor genes that help them conserve their water. When pathogens emerge, natural selection may favor genes that make hosts resistant. If Florida is going to become more like, say, Brazil, then maybe genes from Brazil will help species survive in Florida. (As for what genes we might give the species in Brazil…well, that’s hard to say.)

Farmers and livestock breeders have harnessed genetic variation for centuries. They’ve crossed different breeds to create a combination of traits they desire. Conservationists have sometimes used hybridization as well, to nurture endangered species.

In Florida, for example, the dwindling panther population became inbred, and they had less success producing cubs. Conservationists trucked in eight panthers from a related subspecies in Texas. It’s been a dozen years since this cross-breeding took place, and their genetic pool now has more variation.

Hybridization can be very effective, but it’s also slow and inefficient. It jumbles together lots of DNA in lots of different ways; breeders then pick out the crosses that seem to perform best. In recent decades, genetic engineering has made it possible to move individual genes from one subspecies to another, or even one species to another. It might be possible to move genes into wild species to help them thrive. The scientists from the New Mexico meeting point to gene variants in rainbow trout, discovered earlier this year, that help the fish survive in warm water. Those variant could be inserted into other trout that are going to be threatened by rising river temperatures.

The scientists call wildlife genetic engineering “facilitated adaptation.” While they’re ready to give it a name, they don’t want to launch into it without a lot of consideration, however. They want to make sure facilitated adaptation doesn’t cause harm to species that are already on the brink of extinction. Genes often carry out more than one function, and so even if an imported gene has one beneficial effect, it might have others that are dangerous.

The scientists also worry that facilitated adaptation might sap the energy for fighting the causes of today’s extinction crisis. If scientists tell us we can just engineer penguins to live in warm temperatures, then who needs to do anything about climate change?

Even if we stopped warming the planet tomorrow, though, endangered species would still face other threats, some of which genetic engineering might help. We humans move pathogens around the planet, bringing new diseases to new places. A fungus from Europe has killed millions of bats in the United States and show no sign of slowing down. If scientists can determine why bats in Europe don’t die of the fungus, they might be able to insert their gene variant into American bats and make them resistant.

And if this seems like wishful thinking, consider the case of the American chestnut. As I wrote on the Loom, another fungus has nearly annihilated the tree. Fungus-fighting genes from other plants are now bringing it back.

I’ll be very curious to see how this new stage of the conversation plays out in weeks to come. (Feel free to leave your thoughts on the comments below.) But I also hope it doesn’t veer over ideological guard rails.

Opponents may argue that the very act of moving genes from one organism to another is a violation of nature’s diversity. But this is a romantic, pre-genomic view of life. Genes have flowed from species to species for billions of years.

Some supporters of genetic engineering may consider this an easy fix for our extinction crisis. But for many species, genetic engineering won’t help, I expect. You can’t tweak an elephant’s gene to make it bullet-proof. And even for those species that could be helped, scientists know precious little about the genes that could help them. Scientists have started to gather together what little they know about life’s genetic diversity, but they have only started. And unfortunately, for a lot of species, they’re running out of time.

MERS At One: The Deadly Virus Drizzle

We have the dubious privilege of observing a new disease in the midst of being born. The disease could go on to spread around the world, stall out as a minor, local blight, or disappear altogether. Scientists have been observing its emergence for a year now, and while they know more than they did in 2012, they still can’t predict quite what will happen. Part of their uncertainty stems from the fact that they still don’t know much about its past.

The disease I speak of is Middle Eastern Respiratory Syndrome–MERS for short. Last fall, doctors began recognizing this pneumonia-like disease in people who either lived in or passed through Saudi Arabia. Virologists soon isolated a virus common to them all, which they named MERS-CoV. Now, a year after its discovery, people are still getting infected with MERS, and many of the infected are dying. The World Health Institute reported on Friday that, from September 2012 to date, they’ve been notified of 130 people with laboratory-confirmed MERS-CoV infections, the vast majority of whom are in Saudi Arabia. Out of those 130 people, 58 have died.

Some scientists are scrambling to test out MERS vaccines and anti-viral drugs that can fight the pathogen. Others are acting as the virus’s historians, trying to figure out where it came from. Back in March, I wrote about the preliminary investigations into the origins of MERS. Now, six months later, researchers have looked at some of the viruses from newer cases, using powerful methods for statistically comparing the genes in the viruses. They’ve carried out the biggest genetic study of MERS so far.

The new study, from a team of Saudi and British scientists, appears in the journal The Lancet. (It’s free if you register. Or get it free without registering here.) The researchers isolated genetic material from viruses taken from 21 people sick with MERS. Many of them had become ill during a hospital outbreak in May 2013 in eastern Saudi Arabia. The scientists sequenced the full genome of 13 of the viruses, and got a third or more of the genetic material of the other eight. They compared the viruses to one another, as well as to other viruses that have been found earlier.

The differences between virus genes can tell scientists how the viruses spread to their victims. Each time a virus replicates inside a host, there’s a chance that its genes will mutate. Its descendants will inherit that mutation, and as more mutations stack up, they can create a fingerprint-like identifier for different lineages.

Reading these viral fingerprints isn’t easy, however, in part because viruses mutate fast. It’s possible for the same mutation to arise in two different lineages, or for a second mutation to reverse an earlier one, erasing a virus’s genealogical tracks. Scientists take on this challenge with statistics. Based on what they know about how viruses mutate–which mutations are more common and which less, for example–they can calculate the most likely evolutionary tree to explain the genetic diversity in a group of viruses.

Scientists can then overlay other kinds of information on this tree to probe the virus’s history. They can estimate how long ago the viruses all split from a common ancestor by adding up their mutations and comparing that figure to the rate at which the viruses mutate.

They can also trace the spread by looking at the geography of infection, noting where different lineages of the virus infected people. It’s even possible in some cases to get clues about how an outbreak spreads from person to person by tracking the mutations carried the viruses in each patient. (In January described this new method in this feature for Wired about a deadly bacterial outbreak.)

What’s striking about the new results is the difference between different groups of the MERS viruses. The scientists found that the viruses fell into distinct genetic clusters, suggesting that they’ve been diverging from other clusters for a long time. One virus isolated from a patient from Riyadh on October 23, 2012 was on a separate branch from another virus isolated from another Riyadh patient a week later. That suggests that two virus strains were circulating in the city at that time.

That’s not to say that all of the viruses were distantly related to each other. Some of the viruses in the May 2013 hospital outbreak were very similar, genetically speaking–so similar, in fact, that the scientists could track their spread from one patient to another. Nevertheless, even in the hospital outbreak, some of the viruses were distantly related to the others.

When the scientists looked at all the genetic diversity of the viruses in their study, they concluded that their common ancestor emerged in July 2011, over a year before MERS was identified. There are a couple possible scenarios in which MERS viruses could have evolved this way.

Hypothetically, MERS might have leaped from an animal to a human over two years ago and then spread from one person to another, splitting into genetically distinct branches. The researchers find this unlikely. If that were true, you’d expect that doctors would have encountered a lot more sick people along the virus’s path.

The alternative is that the virus has been jumping again and again from animals. They’ve been circulating in some animal host for the past couple years, splitting into different lineages. Those different lineages have independently infected humans. Once the viruses cross over, people may bring them to cities, such as Riyadh, and from there to other parts of the country. Along the way they sometimes spread the virus to other people–especially in hospitals, where the virus encounters sick people with weakened immune systems.

Back in March, I noted that MERS closely resembles viruses in bats on other continents. Researchers at Columbia University identified short fragments of MERS virus in Saudi bats, but a number of virologists find the results far from conclusive. Even if MERS did get its start in bats (which happened with other human diseases like SARS and Nipah virus), people may not be getting sick from direct contact with them. One possibility scientists are investigating is that camels or other livestock have picked up MERS from bats, and are now passing it on to people.

These results got me wondering. Should we feel comforted by these results, or freaked out, or warily mindful? We might take comfort from the fact that all of the people sick with MERS do not seem to form a single human-to-human chain of infection. Instead, they form many chains, most of which may have few human links. That pattern might mean that MERS is lousy at spreading among people and a poor candidate for a new scourge.

On the other hand, perhaps we should feel a chill up our spines when we consider that MERS is peppering our species boundary, implying that there’s a big supply of the viruses in close contact with us in some unknown species, and one of them may manage to get through and evolve into a fast-spreading human scourge.

Hoping for a little clarity, I got in touch with Andrew Rambaut of the University of Edinburgh, one of the co-authors of the new paper. Rambaut has studied a number of these boundary-crossing viruses, including influenza, SARS, and HIV.

To Rambaut, success for a cross-over virus is largely a matter of luck. “It is down to a virus with the right properties getting into an adequately connected network to allow sustained transmission,” he told me.

HIV, for example, probably infected a lot of people in rural west central Africa over many years without reaching sustained transmission. Only when it happened to get from the bush into the city of Kinshasa in the mid-1900s did it take off. SARS, likewise, exploded once it got into the urban regions of southern China.

The research Rambaut and his colleagues have carried out on MERS shows that the virus is indeed mutating. But even in the hospital outbreaks, they haven’t seen any clear evidence that those mutations are favored by natural selection for spreading among humans. And Rambaut sees little opportunity for MERS to undergo that transformation.

“Natural selection requires time and numbers,” says Rambaut. “It can’t pull a rabbit out of a hat.”

In other words, a virus needs a big population and many generations for natural selection to allow a mutation to rise to dominance. Rambaut estimates that MERS has infected hundreds of people at most. If one virus inside a person gains a mutation that increases its spread among humans, the odds that it will be the one that gets the chance to infect another human is tiny.

For now, in Rambaut’s view, MERS is a virus that relies on chronically ill people to spread. In hospitals, it can find lots of new hosts, and so it can sustain its population. Outside of hospitals, it fares poorly and will be unlikely to do better.

Of course, Rambaut warns that this conclusion is based on what he calls “wildly inadequate information.” This recent article by Helen Branswell provides an excellent survey of what scientists have learned after a year of studying MERS, and it’s a small fraction of what was learned after a year of studying SARS. Basic epidemiology has yet to be carried out on MERS, according to Branswell’s sources, and we don’t even know what animals are hosting the virus yet. The latest study on the history of MERS brings it into sharper focus, but a lot of blurriness remains.

 

Retro Report Looks At the Afterlife of Thalidomide

A couple weeks ago I wrote about the great work at Retro Report in looking back at news stories that were in the headlines decades ago. It was especially gratifying to see all the science they’ve delved into. This morning, they unveiled another fascinating look at the history of science. It’s on the drug thalidomide, which caused dramatic birth defects to children’s arms and legs in the 1950s and led to the modern regulation of medicine.”The Shadow of Thalidomide” features interviews  with the victims of the drug and scientists who discovered new medical uses for it.

Thalidomide’s unexpected benefits actually go beyond medicine. It can also reveal hints about the mystery of how arms and legs develop normally. I wrote about this research for the New York Times.

Here’s the video:

Rising Seas, Burrowing Worms, and Nasty Jaws: Weaving Together Animal Evolution

Just over half a billion years ago, the animal kingdom went through a remarkable flowering that lasted somewhere in the neighborhood of 20 million years. During the so-called Cambrian Explosion, the first known fossils of many major groups of living animals appear. It’s a chapter of evolutionary history that has captivated many scientists ever since Darwin. And in recent years researchers have gathered a lot of fresh evidence about different factors that might have been the trigger to this evolutionary big boom. Today in the New York Times, I talk to Paul Martin, the director of the Oxford Museum of Natural History, who has co-authored a new synthesis of ideas about the Cambrian Explosion. Rather than looking for just one cause–such as rising sea levels–he argues for a tangled web of feedback loops. Check it out.

Chimeras and Mosaics: My New York Times Feature on Our Personal Genome*s*

In a mosaic portrait, many tiles, each a little different from the other, add up to an entire person. Genetically speaking, we can be living mosaics, too. As our cells divide, they sometimes mutate, creating distinct populations within us. Many of us carry the genomes of other people inside our bodies.

Scientists have known about these phenomena for a long time, but it was hard to know whether they were more than odd flukes. Now that scientists can sequence genomes from individual cells, they can now start to get at an answer. They are more widespread than was previously thought. The growing significance of chimeras and mosaicist has implications for our sense of genetic identity, as well as for treating diseases. Our many personal genomes are the subject of a feature I’ve written for today’s New York Times. Check it out.

 

How Did Life Begin? It’s Not About the Planets So Much As the Chemistry

At the end of August, I got a press release saying that a chemist named Steven Benner was going to deliver a lecture in Italy in which he broached the idea that we might descend from Martians.

I met Benner ten years ago. He was sitting in a coffee shop in Cambridge, Massachusetts, working out what it would take to make life from scratch. Helping him in this exercise was Jack Szostak, a Nobel-prize winning Harvard biochemist whom he had known for years. In the midst of their conversation, Dr. Benner abruptly turned to me and asked, “How much do you think it would cost to create a self-replicating organism capable of Darwinian evolution?”

As a journalist, I’m not accustomed to such questions. “Twenty million dollars?” I blurted.

“Ridiculous,” I thought to myself. But Benner just tilted his head, looked away, and nodded in thought.

“That’s what Jack says,” he said.

Benner, a distinguished fellow at the Westheimer Institute at the Foundation for Applied Molecular Evolution in Florida, has balanced his career between two ways of doing science. On the one hand, he is a data-driven chemist who publishes papers with heart-stopping titles like, “Labeled nucleoside triphosphates with reversibly terminating aminoalkoxyl groups.” On the other hand, he is the sort of scientist who enjoys trying to draw up Frankenstein’s budget, or investigating whether life could exist in the liquid methane oceans of Saturn’s moon Titan.

So I knew that he’d have something interesting to say in his talk about Mars.

Not surprisingly, many reports have gone for the Little-Green-Men angle. But when I caught up with Benner, we ended up talking not about alien life, but about the philosophy of science–about how to investigate the origin of life when it happened so long ago and we still have so much left to learn about it. That conversation is the subject of my new “Matter” column for the New York Times. Check it out.