Evolutionary arms race turns ants into babysitters for Alcon blue butterflies

In the meadows of Europe, colonies of industrious team-workers are being manipulated by a master slacker. The layabout in question is the Alcon blue butterfly (Maculinea alcon) a large and beautiful summer visitor and its victims are two species of red ants, Myrmica rubra and Myrmica ruginodis.

The Alcon blue is a ‘brood parasite’ – the insect world’s equivalent of the cuckoo. David Nash and European colleagues found that its caterpillars are coated in chemicals that smell very similar to those used by the two species it uses as hosts. To ants, these chemicals are badges of identity and so similar are the caterpillars that the ants adopt them and raise them as their own. The more exacting the caterpillar’s chemicals, the higher its chances of being adopted.

The alien larvae are bad news for the colony, for the ants fawn over them at the expense of their own young, which risk starvation. If a small nest takes in even a few caterpillars, it has more than a 50% chance of having no brood of its own. That puts pressure on the ants to fight back and Nash realised that the two species provide a marvellous case study for studying evolutionary arms races (which I’ve blogged about before here).

Theory predicts that if the parasites are common enough, they should be caught in an ongoing battle with their host, evolving to become more sophisticated mimics, while the ants evolve to become more discriminating carers. The two species make a particularly good model for this because their geographical ranges overlap in a fractured mosaic.

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Mud time capsules show evolutionary arms race between host and parasite

Evolution can sometimes be seen as a futile contest. Throughout the natural world, pairs of species are locked in an evolutionary arms race where both competitors must continuously evolve new adaptations just to avoid ceding ground. Any advantage is temporary as every adaptive move from a predator or parasite is quickly neutralised by a counter-move from its prey or host. Coerced onward by the indifferent force of natural selection, neither side can withdraw from the stalemate.

These patterns of evolution are known as Red Queen dynamics, after the character in Lewis Carroll’s Through the Looking Glass who said to Alice, “It takes all the running you can do, to keep in the same place.”

These arms races are predicted by evolutionary theory, not least as an explanation for sex. By shuffling genes from a mother and father, sex acts as a crucible for genetic diversity, providing a species with the raw material for adapting to its parasites and keep up with the arms race.

Watching the race

We can see the results of Red Queen dynamics in the bodies, genes and behaviours of the species around us but actually watching them at work is another matter altogether. You’d need to study interacting species over several generations and most biologists have neither the patience nor lifespan to do so.

But sometimes, players from generations past leave behind records of the moves they made. Ellen Decaestecker and colleagues from Leuven University found just such an archive in the mud of a Belgian lake.

Is a virus responsible for the disappearing bees?

A group of scientists have found that a virus – IAPV – may be responsible for Colony Collapse Disorder, the mysterious condition that’s emptying the hives of European and American beekeepers.

In 2006, American and European beekeepers started noticing a strange and worrying trend – their bees were disappearing. Their hives, usually abuzz with activity, were emptying.

Like honeycombed Mary Celestes, there was no trace of the workers or their corpses either in or around the ghost hives, which still contained larvae and plentiful stores of food. It seemed that entire colonies of bees had apparently chosen not to be.

The cause of the aptly named ‘Colony Collapse Disorder’, or CCD, has been hotly debated over the last year. Fingers were pointed at a myriad of suspects including vampiric mites, pesticides, electromagnetic radiation, GM crops, climate change and poor beekeeping practices. And as usual, some people denied that there was a problem at all.

But a large team of US scientists led by Diana Cox-Foster and Ian Lipkin have used modern genomics to reveal the main villain in this entomological whodunnit – a virus called Israeli Acute Paralysis Virus or IAPV.

Foul-tasting ant parasitises the colonies of other species

An ant nest is sheltered, well defended and stocked with food, but one that takes time to build and protect. Which is why some species of ants don’t bother to do it themselves – they just squat in the nests of others.

These ants are ‘social parasites’ – they don’t feed off their hosts’ tissues, but instead steal their food, sleep in their homes and use their resources. They’re like six-legged cuckoos

An ant colony is too dangerous a target to victimise lightly and the social parasites use several tricks to stop their hosts from ripping them apart. Some escape reprisal by chemically camouflaging themselves, either by mimicking their hosts’ odour, or by acquiring it through contact.

This specialised strategy ties the parasite’s fates into those of its host. Both are caught in an evolutionary arms race, with the hosts becoming more discriminating and the parasites’ deception becoming more accurate. But Stephen Martin from the University of Sheffield has found one ant species with a completely different and more flexible strategy – it tastes really, really bad.

An entire bacterial genome discovered inside that of a fruit fly

Bacteria have the ability to transfer genes to one another. Now, scientists have found that one species, Wolbachia, has managed to transfer its entire genome into that of a fruit fly. These extreme gene transfers could be more common than we thought, and they have important consequences for genome-sequencing projects.

A humble species of fruit fly is the genetic equivalent of a Russian doll – peer inside its DNA and you will see the entire genome of a species of bacteria hidden within.

The bacteria in question is Wolbachia, the most successful parasite on earth and infects about 20% of the world’s species of insects. It’s a poster child for selfishness. To further its own dynasty, it has evolved a series of remarkable techniques for ensuring that it gets passed on from host to host. Sometimes it gives infected individuals the ability to reproduce asexually; at other times, it does away with an entire gender.

Now, Julie Dunning-Hotopp from the J. Craig Venter Institute and Michael Clark from the University of Rochester have found an even more drastic strategy used by Wolbachia to preserve its own immortality – inserting its entire genome wholesale into that of another living thing.

Butterflies evolve resistance to male-killing bacteria in record time

Six years ago, the males of a Samoan butterfly were being killed off by a bacteria and made up only 1% of the population. Now, the males have returned in a dramatic comeback and the sex ratio is equal again. In just ten generations, they evolved resistance to the parasite, a powerful example of natural selection in action.

In our world, there is (roughly) one man for every woman. Despite various social differences, our gender ratio remains steadfastly equal, so much so that we tend to take it for granted. Elsewhere in the nature, things are not quite so balanced.

Take the blue moon butterfly (Hypolimnas bolina). In 2001, Emily Dyson and Greg Hurst were studying this stunningly beautiful insect on the Samoan islands of Savaii and Upolu when they noticed something strange – almost all the butterflies were females. In fact, the vastly outnumbered males only made up 1% of the population.

Male-killers

The cause of this female-dominated world was an infection, an inherited bacterium called Wolbachia. Wolbachia is a strong candidate for the planet’s most successful parasite for it infects a huge proportions of the world’s arthropods, themselves a highly successful group. And it does not like males.

Wolbachia has an easy route of infection – it can be passed to the next generation through the eggs of an infected female. But it can’t get into sperm, and for that reason, male insects are useless to it and it has a number of strategies for dealing with them.

Sometimes, it allows females to reproduce without male fertilisation. At other times, it forces males to undergo sex changes to become females. But in cases like the blue moon butterfly, it simply kills the males outright before they’ve even hatched from their eggs.

In 2001, Dyson and Hurst noted that the islands with the fewest males were the ones with the most prevalent Wolbachia infections.

The butterflies fight back

But by 2005, things had changed. Sylvain Charlat from University College London, along with Hurst and others, found that males were increasing in number all around Upolu Island. A year later, a formal survey confirmed the males’ amazing comeback.

On Upolu, they equalled in the females in number. Within just 10 generations, the male butterflies had gone from being outnumbered a hundred to one to an equal footing with the females. “To my knowledge, this is the fastest evolutionary change that has ever been observed,” said Charlat.

Charlat found the same story at a site on Savaii Island close to neighbouring Upolu. On the other side of the island, the males were still in the minority and many failed to hatch. But at 7% of the population, they were doing better than they had done in five years before.

All the butterflies were still infected with the same Wolbachia strain that had slaughtered their males just a few years back. And the bacteria themselves had not changed – when Charlat mated infected females with uninfected males from a different island, the parasite’s male-killing nature resurfaced within a few generations.

Evolution in action

Charlat believes that the Upolu butterflies had gained a resistance gene (or several) that allowed them to shrug off the male-killing bacteria. It either evolves the trait itself, or gained it from South-east Asian populations that had already become resistant.

Whatever the origin, the mutation spread like genetic wildfire across the Upolu and onto neighbouring Savaii. Most mutations carry small benefits and spread slowly. But by levelling a populations sex ratio, a mutation that resists Wolbachia clearly provides a huge advantage.

Surviving males who carry the gene(s) would have had their pick of females, since most of their competition lay dead in their eggs. And females, that picked up the mutation would have had twice the number of surviving young.

Arms race

Charlat’s work highlights just how powerful an influence parasites have in the course of evolution. Just how powerful parasites can be in the course of evolution. Events like this may be very commonplace, but at such speed, they may have happened before researchers could spot them.

The butterflies’ newfound resistance is also marvellous example of the Red Queen hypothesis, where parasites and hosts are caught in an evolutionary arms race. Each is forced to acquire new adaptations and counter-adaptations just to stay in the same place.

In this particular arms race, the butterflies have won the battle against Wolbachia. But the war isn’t over. The parasite now faces renewed pressures to find innovative ways of doing away with the dead-end males. How long will it be before it evolves a retaliatory strike?

More on evolution in action:
Natural selection does a handbrake turn – quick evolution at work
Of flowers and pollinators – a case study in punctuated evolution

More on parasites and evolutionary arms races:
Parasites can change the balance of entire communities
Viruses evolve to be more infectious in a well-connected population
Beetle and yeast vs. bee – how American bees are losing the evolutionary arms race

More on animal sex and reproduction:
Virgin birth by Komodo dragons
When the heat is on, male dragons become females
Chimerism, or How a marmoset’s sperm is really his brother’s
Aphids get superpowers through sex

 

Reference: Charlat, Hornett, Fullard, Davies, Roderick, Wedell & Hurst. 2007. Extraordinary flux in sex ratio. Science 317: 214.

 

 

Technorati Tags: butterfly, Wolbachia, male-killing, sex ratio, blue moon butterfly, Sylvain Charlat, Gregory Hurst, evolutionary arms race

Photos by Sylvain Charlat and Comacontrol

Parasites can change the balance of entire communities

By changing the behaviour of their hosts, parasites can change the face of entire habitats. Now, scientists have demonstrated how a tiny flatworm can alter the structure of a tidal habitat by infecting small marine snails.

Conspiracy theories, TV thrillers and airport novels are full of the idea that the world is secretly run by a hidden society. We have come up with many names for this shadowy cabal of puppet-masters – the Illuminati, the Freemasons, and more. But a better name would be ‘parasites’.

Every animal and plant is afflicted by parasites. The vast majority are simple, degenerate creatures, small in size and limited in intelligence. They affect our health and development, and even our behaviour and culture. And by pulling the strings of key species, parasites can change the face of entire habitats.

In a typical school textbook, an ecosystem consists of plants that feed plant-eaters, who in turn, line the bowels of predators. But parasites influence all of these levels, and as such, they can change the structures of entire communities.

The idea that nature is secretly manipulated by these tiny, brainless creatures is unsettling but manipulate us, they do.

Chelsea Wood and colleagues from Dartmouth College found compelling evidence for the influence of parasites by studying small animals that live on the coasts of the North Atlantic.

Snails and flukes

These tidal boundaries are home to the common periwinkle (Littorina littorea; below), a type of marine snail. It invaded America’s shores about two centuries ago and has spread successfully along the eastern seaboard. It acts as this habitat’s equivalent of cattle, grazing the ephemeral algae that grows in rocky tidal pools.

But they are not alone. The periwinkles are unwitting passengers for the parasitic fluke Cryptocytole lingua (above), a kind of flatworm. In most parts of the coast, the flukes are relatively rare, but in some parts of New England where seabirds are plentiful as many as 90% of periwinkles can be infected.

Like most parasites, the fluke has an amazingly complicated life cycle. Snails become infected by accidentally eating eggs spread in the droppings of seabirds. The larvae develop in their bodies by eating the snails inside out. They eventually give rise to a free-swimming creature that finds and infects fish, which are then eaten by seabirds, completing the cycle.

Infected snails lose their appetites

By devouring the snails’ internal organs, the flukes wreck their hosts’ digestive and reproductive systems. Wood reasoned that the neutered and malnourished snails must be have altered feeding habits and tested this idea in the lab and the field.

She found that the flukes put infected snails on an involuntary diet, and they ate far less algae than uninfected ones. While many parasites can directly alter their hosts’ behaviour, Wood believes that nixing the periwinkles’ appetities is not part of Cryptocytole’s plan.

It’s just an incidental side effect of infection and happens because the snails’ crippled digestive glands could not cope with the normal amount of food. And because the parasites trashed their reproductive systems and several other organs, they needed less energy to begin with.

Even so, by reducing the snails’ feeding, the parasites could potentially affect the entire tidal community. Wood demonstrated this by setting up cages in the tidal zone containing uninfected snails or infected ones. Sure enough, after a month or so, cages that housed infected snails had about 60% more algae than those with uninfected ones.

In the long-term, these effects are likely to be even larger as the fluke castrates its unfortunate hosts and lowers their life expectancy. Over time, this would reduce the size of the whole snail population and give the algae an even greater chance to grow.

Ripple effects

These snails’ lost appetites ripple out through the entire habitat. Infected snails mean more algae, which provide more food for other invertebrates. The algae also crowd out the rocky real estate that barnacles attach themselves too, and the loss of barnacles reduces the numbers of blue mussels that coexist with them.

Even though it never comes into contact with these other tidal players, the fluke indirectly influences all of them. Nestled within the body of a snail, it pulls the strings of the entire ecosystem.

This is one of the few instances where the effects of parasites on ecosystems have been carefully documented. Millions of similar dramas must play out all over the world, for half of the planet’s species are parasitic. It’s not our world, it’s theirs.

Find out more: Carl Zimmer’s superb book Parasite Rex is an amazing journey through the world of parasites, how they affect other animals, and how they change entire habitats.

Reference: Wood, Byers, Cottingham, Altman, Donahue & Blakeslee. 2007. Parasites alter community structure. PNAS 104: 9335-9339.

Images: by Chelsea Wood and James Byers

Technorati Tags: parasites, periwinkle, Cryptocytole, fluke, trematode, parasite effects

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Beetle and yeast vs. bee – how American bees are losing the evolutionary arms race

In America, the parasitic small hive beetle has gained the upper hand in its evolutionary arms race against the honeybee. It has formed an alliance with a type of yeast, and together, they use the bees’ own chemical communications against them.

Bee hives, with their regularly arranged honeycombs and permanently busy workers may seem like the picture of order. But look closer, and hives are often abuzz with secret codes, eavesdropping spies and deadly alliances.

African honeybees are victimised by the parasitic small hive beetle. The beetles move through beehives eating combs, stealing honey and generally making a mess. But at worst, they are a minor pest, for the bees have a way of dealing with them.

They imprison the intruders in the bowels of the hive and carefully remove any eggs they find. In turn, the beetle sometimes fools the bees by acting like one of their own grubs, and gets a free meal instead of imprisonment. In Africa, both species have found themselves in an evolutionary stalemate.

But in 1998, American beekeepers spotted the beetle in hives of their local European-descended honeybees. These insects are gentler versions of their aggressive African relatives, and in them, the beetles found more vulnerable victims.

In the last decade, they have spread through hives on the East Coast, causing much more destruction than they normally get away with. In some cases, the damage is so severe that the bees are forced to abandon their hive. As the bees suffer, so do the economically vital crops they pollinate.

Now, scientists from the International Centre of Insect Physiology and Ecology and the University of Florida have uncovered the secrets behind the beetle’s destructive ability.

Small hive beetles (right) hunt down beehives by hijacking their communications. When bees are stressed or confronted by threats, they release alarm pheromones into the air to alert their hive-mates of impending danger. But the beetles can also detect these chemical signals and use the bees’ own early warning system to locate their hives.

Baldwyn Tonto and colleagues found that the beetles are sensitive to much lower levels of these pheromones than the bees themselves are, and can detect a much wider ranger of airborne chemicals from the hive. With their superior senses, the beetles can home in on beehives before the bees themselves can sense the alarm.

But that’s not the whole story. Tonto found that honeycombs infested by beetles, but free of worker bees, were emitting a strange smell. It mimicked the bees’ alarm pheromones and strongly attracted even more beetles. But it wasn’t coming from the parasites themselves.

Instead, the source of the smell was a type of yeast that hitches a ride with small hive beetles into the bees’ home. Tonto found that the fungus was fermenting the pollen collected by the bees, and releasing chemicals that closely mimic the beetle-attracting alarm pheromones.

The beetles’ keen sensitivity to the bees’ chemical messages allows them to initially home in on a hive. As they arrive, they bring the yeast along for the ride and distribute it among the hive’s pollen stores. The yeast ferments the pollen and releases chemicals that mimics the bee’s alarm pheromone, attracting even more beetles .

Soon, the infection reaches critical mass, and the bees are forced to abandon their homes. They leave behind a sizeable store of pollen and honey, ideal breeding grounds for the unwitting partnership of yeast and beetle.

But the yeast also exists in Africa, where it is similarly spread to hives by hive beetles. Why does the alliance not wreak such havoc there? Tonto believes that domestication is the answer. Because of years of selective breeding, the European honeybee is a slightly dopier version of the African bee – more docile and less prone to swarming.

It faces a larger number of pests and problems that prevent it from concentrating on imprisoning invading beetles. And its poor sensitivity to its own alarm chemicals allows the beetle-yeast alliance to gain a strong foothold before the bees recognise the threat.

With bee populations mysteriously dying off across America, the threat of the small hive beetle and its fungal partner may be even more pressing than before.

 

Reference: Torto, Boucias, Arbogast, Tumlinson & Teal. 2007. Multitrophic interaction facilitates parasite-host relationship between an invasive beetle and the honey bee. PNAS 104: 8374-8378.

Image: Photo of small hive beetle by Jeffrey Lotz

Technorati Tags: Small+hive+beetle, honeybee, beetle, symbiosis, introduced+species, bee, science

Related stories about parasites and symbiosis:
Aphids get superpowers through sex
Hatena: when two cells are better than one
Too few genes to survive – a bacteria with the world’s smallest genome
Parasites can change the balance of entire communities

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The secret of drug-resistant bubonic plague

The bacterium that causes bubonic plague can pick up drug resistance from common bacteria responsible for food poisoning.

The plague, or the Black Death, is caused by a microbe called Yersinia pestis (right). In the 14^th century, this microscopic enemy killed off a third of Europe’s population.

While many people consign the plague to centuries past, this attitude is a complacent one. Outbreaks have happened in Asia and Africa over the last decade and the plague is now recognised as a re-emerging disease.

In 1996, two drug-resistant strains of plague were isolated from Madagascar. One of these, was completely resistant to all the drugs that are used to control outbreaks.

Any scientist currently studying tuberculosis can attest to the ability of bacteria to evolve resistance to drugs. In the case of drug-resistant plague, the secret to its powers is a plasmid – a small free-floating ring of DNA, that carries drug resistance genes.

Bacteria can trade plasmids across individuals, transferring genes between each other in ways that humans can only achieve with technology.

The worry is that common and less harmful bacteria could transfer drug-resistance plasmids over to Yersinia, resulting in new resistant strains.

Timothy Welch and colleagues from the United States Department of Agriculture showed that this concern is well-founded. They found that the plague plasmid is virtually identical in parts to plasmids from an increasingly common strain of Salmonella (left) that is also resistant to multiple drugs.

They even found related plasmids were in other drug-resistant bacteria isolated from meat samples across the USA during quality control checks.

A word of caution – this doesn’t mean that people risk contracting plague from eating meat. Even though the plasmids are strikingly similar, the bacteria involved are very different.

But it does mean that the plague bacterium could potentially gain drug resistance from other common resistant bacteria, if they should both find themselves in the same human or flea host.

Despite this scary scenario, Welch’s study also provides us with a silver lining. We are aware of the threat and we know how to monitor for it, by searching for the plasmid.

Monitoring is especially important because the plague has all the qualities you would look for in a potential biological weapon – a high fatality rate, no vaccine and possible air-borne transmission.

If the worst happens, we will want to be prepared.

 

Reference: Welch, Fricke, McDermott, White, Rosso, Rasko, Mammel, Eppinger, Rosovitz, Wagner, Rahalison, LeClerc, Hinshaw, Lindler, Cebula, Carniel& Ravel. 2007. Multiple antimicrobial resistance in plague: an emerging public health risk. PLOS ONE.

Technorati Tags: bubonic plague, plague, black death, Yersinia, drug resistant, science,

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Genetically-modified mosquitoes fight malaria by outcompeting normal ones

Genetically-engineered mosquitoes that are resistant to the malarial parasite could be the key to reducing the burden of malaria. In laboratory experiments, they are stronger and fitter than their normal peers and rapidly dominate the population.

Fighting malaria with mosquitoes seems like an bizarrely ironic strategy. But that’s exactly what many scientists are trying to do.

Malaria kills one to three million people every year, most of whom are children. Many strategies for controlling it naturally focus on ways of killing the mosquitoes that spread it, stopping them from biting humans, or getting rid of their breeding grounds.

But the mosquitoes themselves are not the real problem. They are merely carriers for the true cause of malaria – a parasite called Plasmodium. It suits neither mosquitoes nor humans to be infected with Plasmodium, and by helping them resist it, we may inadvertently help ourselves.

With the power of modern genetics and molecular biology, scientists have produced strains of genetically engineered mosquitoes that cannot transmit the malarial parasite.

These ‘GM-mosquitoes’ carry a modified gene – a transgene – that produces chemicals which interfere with Plasmodium’s development. Rather than becoming suitable carriers, the modified mosquitoes are death for any invading Plasmodium.

But scientists can’t very well change the genes of every mosquito in the tropics. To actually reduce the burden of malaria, the genetic changes that induce malaria resistance need to be spread throughout the mosquito population. The easiest way to do this is, of course, to let the insects do it themselves.

And Mauro Marrelli and colleagues from the Johns Hopkins University have found that they are more than up to the task.

They kept cages full of equal numbers of engineered and normal mosquitoes and fed them on the blood of mice infected by Plasmodium. After nine generations, they found that the engineered insects had become proportionally more common, making up about 70% of the total population.

Like most parasites, Plasmodium affects the health of its host. So mosquitoes that are parasite-resistant are stronger and fitter than their infected peers. Marrelli found that they were about 25% less likely to die early, and had more young, with every female laying an average of 60 eggs compared to 43.

With these advantages, the transgenic mosquitoes outlasted and out-bred normal ones, and quickly established a majority in the population.

But if the advantages to resistance are so great, why haven’t naturally-resistant mosquitoes replaced non-resistant ones? Other studies have shown that resistant mosquitoes fight off Plasmodium with the help of hyperactive immune systems, but have no evolutionary advantages over carriers.

Marrelli thinks that because chronic immune responses produce health problems of their own, that cancel out the advantage of not carrying Plasmodium. In contrast, the transgenic mosquitoes are simply expressing a gene that is mostly harmless. The gene also kills Plasmodium early on in its life cycle, well before it triggers the body’s own immune system.

Even though a single transgene copy does not affect the modified insects’ health, it appears that two copies might have some as-yet-unknown health consequences. This may explain why the resistant mosquitoes in Marrelli’s experiments did not totally dominate the population, but plateaued at 70%. The strongest mosquitoes are those with just one copy of the gene.

This means that introducing the engineered mosquitoes into the wild would not completely wipe out their disease-spreading cousins. But it would still drastically cut their numbers. Considering that malaria infects over 400 million people a year, reducing this number by 70% would be a monumental victory for international health.

Nonetheless, Marrelli is cautious about the future of malaria-resistant strains. These experiments are a proof-of-principle and their results may not bear out as planned in practice.

In the field, only a relatively small proportion of mosquitoes become infected, and he expects the spread of the transgene to be slower. But if it becomes established, it could complement other programmes for controlling malaria, by making it very hard for the parasite to re-colonise a cleared area after it has been eradicated.

 

Reference: Marrelli, Li, Rasgon & Jacobs-Lorena. 2007. Transgenic malaria-resistant mosquitoes have a fitness advantage when feeding on Plasmodium-infected blood. PNAS 104: 5580-5583.

Images: Plasmodium image by Ute Frevert

Technorati Tags: malaria, mosquitoes, genetically engineered, GM, genetic engineering,

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Viruses evolve to be more infectious in a well-connected population

We still don’t know enough about how viruses evolve to predict what would happen in a twenty-first century viral pandemic. New research in insects provides a clue – in a well-connected and well-travelled world, we would expect viruses to evolve to become more infectious.

If the media is to be believed, we are under the constant threat of a deadly viral pandemic. While bird flu certainly poses a very real threat if it evolves the ability to pass between humans, it is still difficult to say whether the doom-mongering is justified. At this stage, we don’t know enough about how viruses evolve over time to predict what would actually happen.

A virus, like any other carrier of genetic information, is only successfully if its offspring can infect new hosts. Its host must live to infect again, and the virus that kills its host prematurely signs its own evolutionary death sentence.

So over time, we might expect that the ideal virus would evolve to never kill any of its hosts – it would have zero ‘virulence’. It would also evolve to successfully infect every host it comes into contact with it – it would have a hundred per cent ‘infectivity’. In this way, a virus would turn any hosts it meets into long-lived virus factories.

But this expectation is based on a model with overly simple assumptions. It only holds true if the virus’s potential hosts are evenly-distributed and ignores questions of distance. In this artificial scenario, once one person in a population carries the virus, every other person has an equal chance of being infected.

Obviously, this is not the case – humans, for example, are concentrated in certain areas, be they villages or cities. And even highly infective viruses can only be spread to new hosts within easy reach.

In this more realistic world, highly infective viruses would soon infect every possible host in the local area, exhausting themselves of potential carriers. Strains that were less infective would then gain an advantage.

On the face of it, this model makes sense, but testing it can be difficult. Needless to say, ethics committees might frown upon infecting people with viruses and constraining them to different locations to see what happens. Insects are another rmatter.

Michael Boots and Michael Mealor at the University of Sheffield have studied virus evolution using the larvae of the moth Plodia interpunctella, and the virus that infects it, PiGV. Plodia larvae can be easily reared in a solid and nutritious jelly, which they spend their young lives in, slowly eating their way around.

By changing the viscosity of the jelly, Boots and Mealor could slow down or speed up the moth’s movements, and they used this to study the effects of population movements on viral transmission.

In softer jellies, the highly mobile moths could spread over large areas, and the viruses they carry have a wide choice of future hosts. But in harder jellies, moths are more likely to bump into the same individual again and again, and local transmission becomes more important.

After forty weeks and eight generations, Boots and Mealor compared the viruses carried by moths living in hard and soft jellies. They found that those infecting the concentrated hard-jelly larvae were three times less infective than those living from the free-roaming soft-jelly moths.

This provides direct evidence in populations with low movement rates, evolution drives viruses to become less infective. Even very subtle changes in a host population led to strong differences in viral characteristics.

Imagine then, what large changes would lead to. Our world is becoming more and more connected. Air travel is easy and cheap while foreign holidays are becoming par for the course. As our populations mix and local interactions become less important, we would be wise to expect viruses to react accordingly.

Boots and Mealor’s results suggest that globalisation will lead to the rise of even more infective strains of viruses and other parasites, and larger epidemics.

Boots and Mealor. 2006. Local interactions select for lower pathogen infectivity. PNAS 315: 1284-1286.

Technorati Tags: viruses, virus evolution, infectious diseases, globalisation, epidemics, science

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Worms track us down with a chemical trail

Parasitic worms infect millions of people in the developing world, by following chemical trails to their hosts. Isolating the substances that attract them is the key to finding cheap and practical ways of preventing infection.

Throughout the day, our skins are constantly sending out messages that we can neither see nor hear. The message is written in chemical form and it says, “Here I am. Come and get me”. We neither see nor hear these signals. But to those that can, they act as shining beacons, sending them crawling, swimming and slithering in our direction.

These creatures are nematodes, a group of worms that are some of the most common animals on the planet. The vast majority of nematode species are parasites, and hundreds of species count humans among their potential hosts.

In the developing countries of the tropics and sub-tropics, these parasites pose a major health problem, causing illness, stunted physical and mental development, anaemia and more. Just two species, the hookworms Ancylostoma duodenale and Nector americanus, infect over 600 million people around the world

Unlike bacteria or viruses, nematodes actively seek out their hosts, rather than waiting to be transferred by water, a sneeze or a bite. Unfortunately, we know very little about how these parasites track down their prey, giving us few options for preventing infections.

This may be because they are a relatively minor problem in the world’s affluent nations. But mostly, our lack of knowledge reflects how difficult it is to study these animals. Human experiments are out of the question, and animal tests are largely impossible since most human nematodes do not equally infect other species.

The threadworm Strongyloides stercoralis is an exception. It can be relatively easily raised in laboratory conditions and also affect primates and dogs. Daniel Safer and colleagues from the University of Pennsylvania have exploited these traits to work out how this species finds a potential victim.

Safer found extracts prepared from the skins of host animals, like dogs and gerbils, had a magnetic attraction for Strongyloides, drawing the worms from distances many times greater than their own body length. Extracts prepared from non-host species, like cats had no effect.

By separating the chemicals in these extracts into more and more specific fractions, Safer eventually identified the substance that was attracting the worms – urocanic acid.

Urocanic acid is found in animal skin where it acts as a natural sunscreen. But it is most common on the sole of the foot, where where levels can be five to ten times higher than other body parts. Each of our footsteps creates a trail of this acid that leads the soil-dwelling Strongyloides to the part of our body closest to the ground.

This acid is not the only substance that attracts Strongyloides. Temperatures within those of mammalian bodies summon them too, as do the high carbon dioxide levels in the air we exhale. But while we cannot control our body heat or the gases we breathe out, we can do something about urocanic acid.

Urocanic acid sticks to metal ions, and Safer reasoned that this could be a way of stopping the parasites from tracking it. Sure enough, adding manganese, calcium or magnesium successfully hid otherwise attractive extracts from the sniffing worms.

This is encouraging news. It means that applying creams containing these metals to vulnerable body parts like feet, could provide a cheap and practical way of preventing Strongyloides infection.

Foiling this species along would have great implications for global health, and doing so cheaply and easily would be ideal for the developing countries where the worms pose the greatest threat. Currently, over 300 million people are infected every year. Strongyloides can cause anaemia, but in people with weakened immune systems, the worms can breed to a point where they become fatal.

Drugs can kill the adult worms, but do nothing against the scores of larvae that travel through infected bodies. Preventing infection is best option. Safer’s work provides hope for a breakthrough, and for finding molecules that other parasites use to track their hosts.

Safer, Brenes, Dunipace & Schad. 2006. PNAS 104: 1627-1630.

Technorati Tags: parasites, worms, threadworm, urocanic acid, third world diseases, science

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