If flu viruses have favoured hook-up spots, then pig pens would be high on the list. Their airways contain molecules that both bird flu viruses and mammalian flu viruses can latch onto. This means that a wide range of flu strains can infect pigs, and if two viruses infect the same cell, they can shuffle their genes to create fresh combinations.
This process is called reassortment. In 2009, it created a strain of flu that leapt from pigs to humans, triggering a global pandemic. If we needed proof that pigs are “mixing vessels” for new and dangerous viruses, the pandemic was it.
Now, scientists have found a new strain of flu in Korean pigs that remphasises the threat. It’s an H1N2, subtly different to the H1N1 virus behind the recent pandemic. But it’s got all the makings of a serious problem. It can kill ferrets – the animal of choice for representing human flu infections. And it spreads through the air between them. I’ve written about this new strain for Nature News, so head over there for more details.
Image by US Dept of Agriculture
You have a sculpture, an intricate piece of modern art, covered in bulges and blisters. Your task is to weave a cover for it. The fit must be exact. You have to fill in every dent and wrap around every lump. Here’s the catch: you have to make this faultless shroud from a single piece of string that must automatically weave itself into the right three-dimensional shape.
This is the challenge that Sarel Fleishman, Timothy Whitehead and Damian Ekiert from the University of Washington have just overcome. Their “sculpture” is a protein called haemagglutinin, or HA, which sits on the surface of flu viruses. Their “shroud” is another protein designed to perfectly fit onto the contours of HA and neutralise it. They have found a way of fashioning these designer proteins on a computer – a feat that could make it easier to create the next generation of anti-flu drugs.
In the film Slumdog Millionaire, Jamal Malik, a teenager from Mumbai’s slums, wins India’s version of Who Wants to be a Millionaire? As the film continues, flashbacks reveal how events in Jamal’s life inadvertently furnished him with the knowledge to answer all fifteen questions and net the top prize. The film illustrates how some of life’s most useful events have no apparent value at first; their true worth lies in allowing us to exploit future opportunities. It’s a lesson that evolution also teaches, time and time again.
One such lesson has just been narrated by Jesse Bloom from the California Institute of Technology and stars the H1N1 flu virus. One of our main defences against this dangerous infection is the drug oseltamivir, better known as Tamiflu. The drug was generally effective against the H1N1 swine flu from last year’s pandemic, but it doesn’t work against seasonal strains of H1N1 that naturally circulate among humans. In 2007, the first signs of resistance emerged and within a year, virtually all strains of seasonal H1N1 were shrugging off Tamiflu. And we’ve only just worked out why this happened.
Sex might be fun but it’s not without risks. As your partner exposes themselves to you, they also expose you to whatever bacteria, viruses or parasites they might be carrying. But some animals have a way around that. Ekaterina Litvinova has found that when male mice get a whiff of female odours, their immune systems prepare their airways for attack, increasing their resistance to flu viruses.
Litvinova worked with a group of mice that were exposed to bedding that had previously been soiled by females in the sexually receptive parts of their cycle. She compared them to a second more monastic group that were isolated from female contact.
Male mice use smells to track down females who are ready to mate. They’ll follow markings of faeces and urine and when they actually find the female, they’ll continue sniffing her nose and genitals. Each of these nasal encounters could be a source of infection. She then pitted both groups against a flu virus. Influenza doesn’t affect wild populations of house mice, so the virus in this case is acting as more of an indicator of the animals’ defences, rather than a representative of a real threat.
Both groups of mice lost a bit of weight, but at certain doses of virus, those that had been exposed to female aromas kept more of their grams on. They also fared better in the long run – just 20% of them died, compared to 46% of those that had only smelled male odours.
A friend of mine recently got onto a train and found a group of four seats that were empty except for one woman who was sitting face down. She looked asleep and he looked forward to a quiet journey. As soon as he sat down, the woman lifted her head to reveal streaming, puffy eyes and started sneezing profusely. This happened a few weeks after swine flu first began to dominate the headlines but being English, he was bound to the socially awkward choice of staying in his seat for the sake of avoiding social awkwardness.
Many of us probably have similar stories. At a time when fears of a flu pandemic dominate the headlines, does an innocuous sneeze make people fear the worst? Perhaps, but a new study suggests that hearing someone else sneeze plays with our minds far beyond exaggerated worries about pandemics. They can make us more worried about completely unrelated threats like heart attacks, crime and accidents. They can even affect our political attitudes.
On May 7, 2009, when swine flu had spread to at least 24 countries, a group of researchers from the University of Michigan took it upon themselves to sneeze in front of passers-by on their campus. Led by Spike Lee (no, not that one), the team approached 26 people who had heard the sneeze and 24 controls who hadn’t, and asked them to complete a questionnaire for a class project.
Compared to the control group, those who had heard the sneeze felt that “average Americans” were more likely to contract a serious disease, citing risks of 41% compared to just 27%. More surprisingly, they also gave significantly higher estimates for the risk of dying from a heart attack by the age of 50 or of dying from crime or accidents. They even had slightly less faith in US healthcare, although this difference wasn’t statistically significant.
Later on in the month, when almost twice as many countries had been infected, Lee performed a similar experiment in a shopping mall. This time, the experimenter asked passers-by to take part in a one-minute survey. Twenty-four of the volunteers received the form without much ado. Another 23 were handed the form by an experimenter who pretended to cough and sneeze at the same time, while covering her mouth with her forearm.
The first question asked people if they would prefer the federal government to allocate $1.3 billion towards the production of flu vaccines or the creation of green jobs. Faced with a sneezing, coughing researcher, almost half (48%) of the volunteers chose to finance the vaccine. Without the symptoms, only 17% did.
Of course, it’s possible that being handed a form by a spluttering individual just put the volunteers in a negative and grumpy mindset. But Lee thinks not – a second question about the general direction of the country showed that both groups of volunteers were, on the whole, equally ambivalent about it.
Lee suggests that a minor, everyday event (like a sneeze) can heighten our worries about a whole range of unrelated hazards because it brings to mind a prominent threat (like a flu pandemic). Our emotions are affected by our ability to assess risks, regardless of what those risks are. In this way, the feelings elicited by one threat can feed into our evaluation of others, and sneezing in a pandemic climate can make people more worried about unrelated hazards from heart disease to crime.
Obviously, there’s more work to be done. Lee’s team haven’t actually demonstrated that sneezing in a pandemic era makes people more worried about that specific threat. It would also be interesting to see if the effect they found waxes and wanes over time, and how that related to the amount of concurrent media coverage .
Nonetheless, one thing is clear. Like many aspects of our minds, people are completely unaware of this effect. When asked later, the volunteers didn’t twig to the aims of the experiments. And while they assumed that a sneeze could make them overestimate the risk of flu, they didn’t think it would make them think differently about the odds of other threats.
Reference: Psychological Science, in press.
More on our bizarre minds:
People infected with the bird flu virus – influenza A subtype H5N1 – go through the usual symptoms of fever, aching muscles and cough. The virus is so virulent that 60% of infected humans have died. But according to a study in mice, the infection could also take a more inconspicuous toll on the brain, causing the sorts of damage that could increase the risk of diseases like Parkinson’s and Alzheimer’s many years after the virus has been cleared.
The link between influenza and Parkinson’s disease is hardly old but certainly controversial. Previous studies have found no traces of flu genetic material in Parkinson’s patients, but one of the strongest pieces of evidence for a link comes from analysing an outbreak of von Economo disease following the 1918 flu pandemic.
To date, 433 people have been infected with H5N1, and a few cases have shown problems with their nervous system, running the gamut from inflammation of the brain to coma. For the survivors, it’s too early to say if their brief time with the virus could lead to neurological problems later on in life. Instead, Haeman Jang from St Jude’s Children’s Research Hospital turned to mice for answers.
He clearly showed that the H5N1 virus can infect mouse neurons within a few days, where it causes certain proteins to gather in the sorts of clumps that are so strongly associated with neurodegenerative disease. It kills off important cells, triggers symptoms reminiscent of Parkinson’s like tremors, and even stimulates an over-the-top immune response that lasted for months after the original infection was cleared.
Jang thinks that this long-lasting immune response may be how the virus leads to a higher risk of chronic diseases long after it has left its host. It’s a hit-and-run strategy, where the initial infection paves the way for something else to come along later on in life and make a “second hit”. According to this model, the flu virus doesn’t directly cause Parkinson’s or related diseases, but it primes the neurons for other things that do. This could also explain why scientists have been unable to detect influenza RNA in Parkinson’s patients.
The swine flu pandemic (S-OIV) currently sweeping the world is the result of an influenza H1N1 virus that made the leap from pigs to humans. But this jump is just the latest leg of a journey that has taken over 90 years and shows no signs of finishing.
Today’s pandemic is a fourth-generation descendant of the 1918 flu virus that infected around a third of the world’s population. This original virus is an incredible survivor and one that has spawned a huge legacy of daughter viruses. By importing and exporting its genes, it has contributed to several new strains that have been responsible for at least three further pandemics, including the current one.
In an editorial in the New England Journal of Medicine, David Morens says, “We are living in a pandemic era that began around 1918.” This is one of two papers that narrate the incredible story of the 1918 virus and its descendants – a thrilling tale of survival, adaptation, extinction and resurrection.
All influenza A viruses contain 8 different genetic segments that they can freely exchange with one another. Morens beautifully compares each virus to a squad of eight players, rather than a single entity. For the viral team to be successful, its eight-person genetic team has to work together. Their individual skills become more or less useful with time and the team will often swap its members for fresh faces that add something new to the mix. In technical terms, they “reassort”.
To do that, viruses need to infect the same cell and they find communal ground in the internal passages of birds, pigs and humans. Animal bodies are essentially viral networking events where different squads can meet and exchange players.
In 1918, one such squad of players went on an infamous world tour. H1N1 influenza viruses had been around for a long time, but the story of the current “pandemic era” really begins in that year. While H1N1 was busy killing humans in our millions, pig farmers at the Cedar Rapids Swine Show in Iowa also noticed something unusual. Even though H1N1 had never been described in pigs before, their herds were suffering from an unusual respiratory illness, whose symptoms were very similar to those afflicting the world’s humans. Swine flu had landed.