THE SCIENCE:Scientists say they are unable to predict what this new swine flu will do next, writes KAREN KAPLAN
SOME TIME in the past few years, as the world’s attention was focused on the bird flu that killed hundreds of people in Asia, another bird flu strain infected pigs. It combined with two kinds of flu that are endemic in pigs and a fourth kind that came from people. The resulting concoction spread among pigs, then recently – no one yet knows where or when – started infecting humans.
Scientists say they are unable to predict what this new swine flu will do next. “It’s impossible to say with any assurance what’s going to happen,” says Dr Christopher Olsen, a molecular virologist who studies swine flu at the University of Wisconsin’s school of veterinary medicine. “Influenza viruses can evolve quite quickly.”
Inspecting the virus itself is of little help, since scientists have yet to identify which features help it spread or kill, according to Dr Scott Layne, an epidemiologist at the University of California school of public health.
“The microscope doesn’t tell you anything,” he says. “What are the genetic correlates of virulence? Unknown. Transmissibility? Unknown.”
Among threats to public health, influenza poses an unusual challenge. People, pigs, birds and horses have developed unique strains of flu, which can easily mix and match into new strains that the human immune system is ill-equipped to recognise. And since the eight genes that comprise all type A flu viruses – the most dangerous kind – are made of RNA instead of DNA, they do not copy themselves reliably and are prone to mutation.
Flu research has accelerated since the Asian bird flu spread to humans in 1997. But the more scientists study it, the more questions they have. “I know less about influenza today than I did 10 years ago,” says Dr Michael Osterholm, director of the Centre for Infectious Disease Research and Policy at the University of Minnesota.
Yet for all its destructive power, the influenza virus is a straightforward organism.
Its outer shell is studded with a protein called haemagglutinin that allows flu particles to attach to cells lining the respiratory tract.
The virus then takes over the host cell and uses it to make hundreds of copies. Those new flu particles use another surface protein, neuraminidase, to break off from the host so they can search for new targets. There are 16 types of haemagglutinin, or H, and nine of neuraminidase, or N; the combination gives a flu strain its name. The swine flu involved in this outbreak is a H1N1 variety.
Scientists surmise that influenza originated in wild birds because they carry all types of H and N. Over thousands of years, the flu evolved into five major lineages – one each for humans, pigs and horses, and two for birds.
Swine flus were first detected in the 1930s, but pigs have probably had their own strains for hundreds of years, says Dr Greg Gray, director of the Centre for Emerging Infectious Diseases at the University of Iowa.
For a long time, swine flu was the suspected culprit in the 1918 Spanish flu pandemic that killed about 50 million people. Scientists now blame a bird flu strain, which probably infected pigs and humans, Gray says.
The pandemics of 1957 and 1968 both involved strains that contained a mixture of human and avian flu viruses.
Experts theorise that pigs were the mixing vessel in those cases, “but there’s no smoking gun to indicate that”, Olsen says.
Experts do not know why the current flu is more virulent south of the US border. Perhaps the genetic code of the Mexican version is slightly different, Olsen says. “It can take as little as a single amino acid change to have a substantial difference in pathogenicity,” he says.
Mexicans may have had longer exposure to the virus, and patients may also be more vulnerable to secondary infections, such as pneumonia.
The World Health Organisation estimates swine flu is fatal in 1 per cent to 4 per cent of cases. But it is impossible to know its true virulence since so many mild cases go unreported, experts say.
In fact, it may not be all that rare. A 2007 study in the Emerging Infectious Diseases journal compared swine flu exposure in farmers, their spouses, and a control group of university students, faculty and staff.
Compared to the controls, the farmers were 55 times more likely to have swine flu antibodies – a sign that their immune systems had tangled with the virus – and the spouses were 28 times more likely.
“There are probably a lot of infections that are totally missed from the medical system,” says Gray, who led the study.
Scientists are now getting their hands on samples of this swine flu strain to conduct tests that should provide clues as to how easily it spreads and how deadly it is.
“We don’t know what this virus will do,” says Osterholm. “It could burn itself out in the next four to six weeks and we never see it again.” But he says health officials cannot ignore the chance that it could sputter out in the spring and reappear in late summer with a vengeance, as in 1918. – (LA Times-Washington Post service)