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.
The swine flu pandemic is well under way. With the WHO citing almost 60,000 laboratory-confirmed cases at the time of writing, the race is truly on to understand more about the virus. Now, two new studies have painted a fresh but partly contradictory picture about two of the virus’s most important aspects – its infectivity (its ability to spread from host to host) and its virulence (its ability to cause disease in a host). These two traits will largely determine the threat that the virus poses, especially in relation to more familiar garden varieties of seasonal flu.
Both groups, one based in the US and the other in the Netherlands, tested the virus’s behaviour in ferrets. These animals are affected by flu viruses in much the same way as humans, mimicking both the severity of our infections and ease of our viral transmission.
Both studies found that the new swine flu virus takes a slightly greater toll on its host’s health than the usual strains of seasonal flu. These strains limit their infections to a ferret’s nasal passages but the new swine flu virus makes its way into the lungs too. The Americans, led by Taronna Maines at the CDC, even found traces of the virus in the ferrets’ gut.
This helps to explain the unusual profile of symptoms associated with swine flu. Most patients experience typical mild flu symptoms but an unusually large proportion (around 40% or so) have also suffered from unusual symptoms like vomiting and diarrhoea. Some have also been hospitalised due to severe pneumonia and respiratory failure, occasionally with fatal consequences. A flu virus that is unusually good at infecting the lungs and gut certainly make sense of these cases.
However, when it came to the virus’s ability to spread, the two research teams disagree. The Americans found that swine flu is less easily transmitted from ferret to ferret than other seasonal viruses of the same H1N1 subtype. However, the Dutch team, led by Vincent Munster from the Erasmus Medical Center, found that the new virus transmits just as easily as its seasonal counterparts.
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.