printable versionBird flu fears can be traced to 1918 pandemic
BY KRISTA CONGER
An Army hospital at Camp Funston in Kansas in 1918 is filled with the initial victims of the Spanish influenza pandemic that eventually would kill approximately 50 million worldwide.
My great-great-grandmother Anna was 64 years old in 1918 when she dug up the body of her 22-year-old son. It had been delivered home to rural Kansas from a military training camp in New Mexico in a sealed coffin. Forbidden to open it, Anna was haunted by the idea that the body her family had buried may not have been that of Aloysious.
Her backbreaking, heartbreaking work spanned several nights, and the reward was bitter. When she pried the lid from the coffin with a hay hook, she saw that no mistake had been made. Her son was one of the tens of millions of people who died that terrible fall and winter from what was then known as the Spanish influenza.
Anna's desperation can only truly be understood in a global context. One in three people in this country was infected with the virus. More than 500,000 died, adding to a worldwide total that has been estimated at about 50 million. Digging up a grave while bodies piled in the streets must have seemed inconsequential in a world dominated by death.
Recently, the 1918 flu virus was molecularly resurrected and used to infect mice. It clearly is more virulent than a typical virus that is currently found in humans. However, no one knows exactly what made the 1918 flu virus so deadly, or why young, healthy adults were most likely to die. What we do know is that we don't want it to happen again. Recent news and scientific reports suggest that the storm clouds of the next flu pandemic are again gathering on the horizon, and governments and world health organizations are readying themselves to fight the virus.
To better understand the threat, it's necessary to submit to a crash course in influenza biology. Flu viruses are separated into three types—A, B and C—each of which can cause human disease. Global epidemics, called pandemics, are caused by type A, which, although it can infect both humans and animals, naturally occurs in wild birds. Type A is divided into subtypes according to the versions of two main proteins that poke from its protein coat: hemagglutinin (HA) and neuraminidase (NA).
HA is an important molecule: It binds to species-specific structures on the host cell and allows the virus to slip inside and begin replicating. But it's also a red flag for the immune system, which begins marshalling its forces to fight the virus when it sees a version of HA made familiar by previous infection or vaccination.
There are 16 types of HA and nine types of NA, and aquatic birds can host viruses with every HA and NA combination. Until recently only three versions of HA have been known to infect humans: H1, H2 and H3. The 1918 virus that killed my great-grand uncle, for example, was an H1N1 subtype.
Unfortunately for us, the flu virus accumulates mutations from year to year that change the virus just enough to evade the immune responses we so carefully crafted to fight the previous year's foe. These small changes drive the annual flu epidemics and are the reason why new flu shots are offered every fall.
In contrast, pandemics are often caused by larger changes, or shifts, in the virus's disguise that can happen when two or more different strains infect the same cell. Like school kids trading sandwiches in the lunchroom, gene swapping is the name of the game inside the hapless cell, and some of the resultant viruses emerge cloaked with new-looking, but still deadly, versions of old proteins. This type of antigenic shift was responsible for the less-deadly flu pandemics that followed the 1918 pandemic: H2N2 in 1957 and H3N2 in 1968. Another mild pandemic in 1977 involved a less-virulent strain of H1N1 thought to have been accidentally released from a research laboratory or a military vaccine program.
So why is everybody so worried now? Well, for one thing, we're overdue for a natural pandemic, which usually occurs about every 30 years. For another, an avian flu strain in Asia known as H5N1 has recently shown a propensity to jump directly from birds to humans without any prerequisite for gene swapping — in the process causing a disease that has killed at least 63 people since December 2003. That strain is now spreading through wild bird populations in Asia and Eastern Europe.
Finally, recent research has shown that the deadly 1918 H1N1 flu is much more like its avian cousins than had previously been thought—supporting speculation that it also jumped from birds to humans with limited or no time infecting an intermediate animal, such as a pig. No antigenic shift was involved in the appearance of the 1918 virus in humans.
Fortunately so far, the H5N1 virus seems to only reluctantly infect people. Almost all cases of confirmed infection can be traced to close contact with birds, or, in a very few cases, with immediate family members infected with the virus. The situation would be much more dire should the virus find a way to spread directly from person to person while maintaining its remarkable virulence. The mortality rate in human cases has been around 50 percent so far, although with so few confirmed cases—a total of 124 reported as of this month—this number is probably inaccurate. Theoretically this event could happen either through the random accumulation of mutations or through gene swapping in some unfortunate person co-infected with both avian and human flu. If this were to occur, the distant drumbeat of worry we're hearing could quickly become a thundering call to action as nations scramble to prevent another 1918-like scenario. Even a "small" avian influenza epidemic could have global economic repercussions if borders were sealed to prevent its spread.
Yet the nearly 100 intervening years have left us with a lexicon of protection that would have been completely unfamiliar to my great-great-grandmother and her unfortunate son: surveillance, vaccination, antiviral drugs and hygiene. Although we must still be cautious and aware of the dangers of a potential pandemic, we now have the tools with which to write our own story. And perhaps we can avoid repeating the tragic ending that played out for my great-great-grandmother and the many others who lost loved ones.
