As the world focused on the bird flu that killed hundreds of people in Asia, another bird flu strain infected pigs. It mixed with two kinds of flu from swine and a fourth kind that came from people. The resulting concoction spread among pigs, then recently started infecting humans. Scientists say they are unable to predict what this new swine flu will do next.
Since late March, it has sickened hundreds of people in 30 U.S. states and nations across the globe, including Canada and Mexico, where there have been 19 confirmed deaths.
"It's impossible to say with any assurance what's going to happen," said 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, because scientists have yet to identify which features help it spread or kill, said Dr. Scott Layne, an epidemiologist at the University of California at Los Angeles' School of Public Health.
"The microscope doesn't tell you anything," Layne said. "What are the genetic correlates of virulence? Unknown. Transmissability? 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 recognize.
Flu research has accelerated since the Asian bird flu spread to humans in 1997. But the more scientists study flu, the more questions they have.
"I know less about influenza today than I did 10 years ago," said Michael Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota.
So what should people worry about? History and ongoing research hold the key.
Why it mutates
The eight genes that make up all Type A flu viruses - the most dangerous kind - consist of RNA, not DNA, so they don't copy themselves reliably and are prone to mutation.
How it attacks
The virus' outer shell is studded with the protein hemagglutinin (H) that allows flu particles to attach to respiratory tract cells. The virus takes over the host cell and makes copies. Those flu particles use the protein neuraminidase (N) to break off to find new targets.
As the H and N change shape, the immune system fails to recognize them, and an infection can result. If two or more viruses - even from two species - infect the same host at the same time, they create a novel strain of flu. The name (H1N1) The combination of H and N proteins gives a flu strain its name. This swine flu is an H1N1 variety, the same label as the 1918 strain. This strain, though, is a new variation of an H1N1 virus. How easily does it spread?
Scientists are now getting their hands on samples of this strain and using it to infect laboratory animals. Researchers will see whether direct contact is needed for transmission and whether small flu droplets can spread easily from cage to cage. That will provide clues about how easily the virus spreads and how deadly it is.
Why Mexico?
Perhaps the genetic code of the Mexican version is slightly different, said Dr. Christopher Olsen, a molecular virologist who studies swine flu. "It can take as little as a single amino acid change to have a substantial difference in pathogenicity." Mexicans may have had longer exposure and may be more vulnerable to secondary infections.
How serious is it?
Dr. Peter Palese, a leading flu researcher at New York's Mount Sinai Medical School, said the new virus appears to be similar enough to other common flu strains that "we probably all have some type of immunity. There is no real reason to believe this is a more serious strain."
How common is it?
It may not be rare. A 2007 study compared swine flu exposure in farmers, their spouses and a control group. Compared with 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. The history The Spanish flu infected up to 40 percent of the world's population and killed more than 50 million. Swine flu was the first culprit, but scientists now blame a bird flu strain.
The bad news
Compared to the seasonal flu, the 1918 pandemic killed a disproportionate number of people ages 20 to 40. "The mortalities occurred in healthy people in their 20s, which is what we're seeing in Mexico," said Barry Bloom, a professor at Harvard School of Public Health. "That's a bit of a worry."
The good news
The movement of troops and refugees in WWI created a unique breeding ground for the virus. New research suggests that most deaths were caused by bacterial infections in weakened respiratory systems. If today's flu did reach such magnitude, antibiotics would save many of the infected.
The history
Swine flu was identified when about 200 soldiers at Fort Dix, N.J., got sick and one died. Genetic strands showed that it was similar to the 1918 virus.
The lesson
President Gerald Ford authorized a mass inoculation program, and almost 25 percent of the population were vaccinated. Guillain-Barre syndrome, which causes the immune system to attack the body's nerves, began appearing in patients who had received the flu shots. About 500 cases were linked to the vaccine; 32 died. But there was no swine flu epidemic, just a handful of cases.
Sources: The Washington Post; Los Angeles Times; Bloomberg News; U.S. Centers for Disease Control and Prevention; Centers for Infectious Disease Research & Policy, University of Minnesota; The Associated Press
