It sounds like the plot of a Hollywood disaster movie: scientists tinker with a flu virus to make it more deadly, only for the mutant strain to escape and trigger a pandemic.

Yet flu scientists are currently at loggerheads over experiments to make the H7N9 bird influenza virus that emerged in China earlier this year even more dangerous.

Some argue that “gain of function” experiments to make the virus more infectious, more deadly and drug resistant in ferrets – the best available test animal for human flu – offer up vital information that could help us defend against a pandemic.

Other scientists are concerned that deliberately creating a supervirus could provide a weapon to bioterrorists. What’s more, they point out, existing biosafety measures – such as requiring researchers to wear special safety suits and go through decontamination chambers when leaving the lab – may not be enough to prevent the virus spreading.

Now, a team led by , at Icahn School of Medicine at Mount Sinai, New York, has devised a genetic failsafe that would switch off mutant strains if they escaped from the lab and infected humans.

Genetic tag

tenOever’s team tweaked an H3N2 flu strain, a common cause of seasonal flu, by tagging it with a single strand of microRNA, a sequence of genetic material that when paired with a complementary sequence, can switch genes on and off.

The microRNA put into the virus is chosen so that when it is met by a matching strand in its host organism, the virus’s replication genes get shut down.

By using a microRNA that exists in human and mice lung cells but not in ferrets, tenOever and his team developed a modified virus that could replicate in ferrets during their experiments but not in mice or humans, if it ever escaped the lab.

The study comes shortly after a by Ron Fouchier of the Erasmus Medical Center in Rotterdam, the Netherlands, and 23 colleagues, defending such research on the basis that the best way to prevent a worst-case scenario is to provoke one.

The letter was intended to prevent a similar furore to the one that erupted in late 2011 surrounding gain of function experiments, which Fouchier also led, on another avian influenza strain, H5N1. It resulted in the publication of the work being delayed by nine months.

tenOever says that Fouchier’s H5N1 research was key in identifying mutations that would make the bird virus start to spread between mammals. “This knowledge was critical to focus our surveillance efforts to monitor the virus and predict when the risk of disease justifies vaccine development.”

Unpredictable consequences

at the Harvard School of Public Health in Boston is unconvinced. He considers gain of function studies highly risky. And the genetic failsafe proposed by tenOever’s team may itself be volatile, he says. “Engineering the restrictive sequence is a change with unpredictable consequences, which could make experiments even harder to interpret and also provide a false sense of security”.

at University of Michigan in Ann Arbor agrees. “My concern is that the microRNA target on the viral genome will just mutate in the same way that a virus develops drug resistance.”

tenOever says that the modified viruses grow and infect cells in a similar way to non-mutated strains, suggesting that the biology of the virus has not been altered. On sequencing the altered viruses, they found no mutations.

Yesterday, the was reported in the Guangdong province of China. According to the World Health Organization, .

Last week, the BMJ reported the – a father and his daughter – although this doesn’t seem to be common.

Journal reference: Nature Biotechnology,

It’s enough to give a camel the hump. Camels have been accused of infecting humans with Middle East respiratory syndrome (MERS), the deadly coronavirus that emerged last year in the Arabian peninsula.

The only thing scientists know for sure about MERS is that it has so far killed 46 of the 94 people it has infected. Where the virus came from, how it is transmitted and whether it could become more contagious in future are still open questions.

Although the virus can spread between people, the chain of transmission quickly peters out, suggesting that something other than humans is the natural host. And it looks like camels might be the culprit.

Marion Koopmans at the National Institute for Public Health and the Environment in Bilthoven, the Netherlands, and colleagues, looked for antibodies to MERS in the blood of sheep, cattle, goats and camels in Oman, Spain, the Netherlands and Chile.

All of the 50 Omani camels, and 15 per cent of the 105 Spanish camels tested had antibodies to the virus, but none of the species in the other countries did. This implies that the camels must have been exposed to the virus at some point for their bodies to have mounted an immune response.

The discovery came as a surprise, says Koopmans, because until then, bats had been the prime suspect. Bats harbour SARS (severe acute respiratory syndrome) and other coronaviruses similar to MERS, and last month .

However, because most people have little contact with bats, an intermediate host seems likely, says Koopmans. Camels are still a common sight in the Middle Eastern countries such as Saudi Arabia where MERS has been found.

Camel contact

This is the first real clue, of how the virus might spread to humans, says Anthony Mounts of the World Health Organization’s MERS response team in Geneva, Switzerland. “While there is a limited amount that you can tell about a virus from the antibody – essentially they are tracks in the sand – for the first time, it offers a clear direction in which to work”.

The next step is to look for the virus itself by studying stool samples and nose or throat swabs from the camels. This won’t be easy, says Koopmans, because coronaviruses are short-lived and don’t circulate in the host for long. “Even if you find the virus in camels, it still doesn’t tell you how people get infected,” says Mounts. “In most cases of MERS, people had no direct contact with camels.”

However, eating camel meat and drinking the milk is common in some countries in the Middle East, as is racing the animals and using them to transport goods, all occasions during which humans and camels would be in close contact.

Understanding the route of transmission will require studying newly infected people, to find out what contact they have had with animals, if they didn’t catch the virus from another person.

“If camels are indeed the source of human MERS infection, specific measures can be taken to prevent interspecies transmission from infected animals to humans” says of Erasmus University in Rotterdam, the Netherlands. For now, however, WHO advice remains unchanged, says Mounts.

Journal reference: The Lancet Infectious Diseases, DOI:

at the University of Illinois, Urbana-Champaign, and her colleagues looked for genetic differences between bees from US colonies that have suffered CCD and bees that were sampled before colony collapses shot up in 2006. CCD killed off about a third of US honeybees in 2007 and 2008.

The team found 65 genes that were distinctly different in CCD bees. They also discovered unusual snippets of genetic material that are typical of infection with the RNA viruses known as picorna-like viruses. They found no evidence to suggest that pesticides or bacterial infection are the primary cause of CCD. Berenbaum thinks picorna-like viruses may be the root cause, making the bees highly vulnerable to other viruses, pesticides and bacteria.

The team want to use the genetic fingerprint to investigate reports of CCD from other countries that believe their bees are also dying of the disorder. This could provide evidence as to how prevalent the problem is.

Screening for the genetic fragments could act as an early warning system for beekeepers, says Berenbaum. “This could open a new avenue for colony monitoring,” says Peter Neumann at the Swiss Bee Research Centre in Switzerland.

Journal reference:

Mirror neurons fire both when we perform an action and when we see someone else doing it. The theory is that by simulating action even when watching an act, the neurons allow us to recognise and understand other people’s actions and intentions.

However, at Harvard University and colleagues say their research suggests this theory is flawed.

Neurons that encounter repeated stimulus reduce their successive response, a process called adaptation. If mirror neurons existed in the activated part of the brain, reasoned Caramazza, adaptation should be triggered by both observation and performance.

Theory ‘overturned’

To test the theory, his team asked 12 volunteers to watch videos of hand gestures and, when instructed, to mimic the action. However, fMRI scans of the participants’ brains showed that the neurons only adapted when gestures were observed then enacted, but not the other way around.

Caramazza says the finding overturns the core theory of mirror neurons that activation is a precursor to recognition and understanding of an action. If after executing an act, “you need to activate the same neurons to recognise the act, then those neurons should have adapted,” he says.

Caramazza’s results support similar findings by Ilan Dinstein at New York University and his team in 2007.

However, mirror neuron researcher , at the University of California, Los Angeles, thinks the study’s basic assumption is flawed. “There is no evidence that mirror neurons adapt,” he says.

Journal reference: (DOI: 10.1073/pnas.0902262106)