What happened to avian flu?

Health and medicine explained.
April 28 2009 4:40 PM

What Happened to Avian Flu?

It never really went away. We just forgot about it.

Click here to read more from Slate on swine flu.

Should we still be worried about avian flu? Click to expand.
Should we still be worried about avian flu?

Before swine flu reared its head, we thought that the next global pandemic would come from the birds. In 1996, in the southern Chinese province of Guangdong, some geese that fell ill and died were found to have carried a new avian influenza virus. Designated H5N1, this virus can be thought of as the grandparent for an incredibly widely distributed, very virulent strain of influenza, responsible for the death of millions of birds and some mammals, including a fair number of humans.

Over the next few years, similar viruses popped up repeatedly in Hong Kong poultry markets, leading to the killing of millions of birds and infecting 18 humans, six of whom died. But it was after 2003 that the disease really took off, spread mostly by wild waterfowl, which are often able to carry the disease and transmit it without becoming sick themselves.

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In the years since then, the avian flu virus has been spreading and spreading. Through the middle of 2005, the disease was confined to Asia, moving from China to Vietnam, Thailand, Indonesia, and Japan. By July, birds were dying in Russia; by October, the virus had spread to Turkey and Eastern Europe. Soon after, it appeared in Africa, the Middle East, and India. Outbreaks among domestic poultry—spread by infected migrating birds—were detected in Western Europe. To this day, small outbreaks are reported in Asia, Europe, the Middle East, and Africa. Fortunately, geography and favorable bird migration patterns have so far protected the Americas.

As the disease was spreading among birds, there were more and more reports of spillover into the human population, especially in developing countries where small-scale agriculture keeps farmers in close contact with the birds they raise. So far, more than 100 people in Vietnam, 60 in Egypt, 140 in Indonesia, and more than 30 in China are known to have contracted avian flu; the total is now up to 421 known human cases worldwide, and more than 60 percent of those who acquired it have died (a percentage which has remained remarkably constant over time). According to the World Health Organization, 21 human cases of avian flu have been confirmed in 2009 (including a few that apparently began in December 2008); Egypt has seen four human cases, three of them young children, since late February.

In short, although we stopped paying attention, avian flu never really went away. But—fortunately—the virus has not yet acquired the ability to infect humans easily or to be passed efficiently from person to person. The general population, very panicky and anxious in 2005, seems to have become blasé about avian flu. Because of the great virulence of this virus, however, public-health workers still go to bed at night clutching their blankets and staring up at the ceiling, dreading the possibility that this virus might become humanized.

It is still not entirely clear why humans are so rarely infected with avian flu yet are so easily infected with human influenza virus. It may have to do with where the different forms of flu attach themselves in the human respiratory tract. Human flu tends to bind to cells in the nose and throat such that coughing and sneezing spreads the infection through droplets in the air. Avian flu binds to sites in the lungs, deep in the human respiratory tract; these sites are generally inaccessible to inhaled droplets.

Most new influenza strains arise as a result of a small, random mutation in the genome of the virus that makes our anti-influenza immunities unable to protect us. The new virus has a selective advantage and is likely to spread. Small changes like this are often called "antigenic drift," signifying the minimal differences in the immunologic characteristics of the new virus type. But sometimes the immunologic change is more dramatic—"antigenic shift," which occurs when an animal cell (maybe a bird's, maybe that of a mammal) becomes infected with two influenza viruses from different sources and the genetic information gets mashed together. When that happens, it is relatively easy for viral strands from each of the different original viruses to become mixed up and packaged together in a new virus.

That is the scenario we've all been dreading and preparing for. But it ended up coming from an animal source and country we hadn't anticipated: a swine flu * originating in Mexico, not Asia. Our stockpiled avian flu vaccine will be useless against this threat, but our pantry full of anti-viral medications will probably be helpful.

The avian flu scare had one other benefit: It led to extensive planning and preparations for an influenza pandemic that could be hugely beneficial in preventing the vast human disaster we've seen before when very virulent and highly infectious new flu viruses appeared. (I'm thinking, of course, of the great epidemic of 1918.) These preparations include plans for the distribution of anti-viral medicines; triage and providing health care in a medical system that could easily become overloaded; and setting out new, rational schemes to help contain and limit the spread of newly emerging dangerous strains of influenza. What kinds of quarantines are appropriate? How to best provide medical services to the ill without adding to the risk of spread? How to address the panic that people may feel in the midst of an epidemic? These are the kinds of preparations that developed as we have been thinking about avian flu. If this is the big one—and it's too early to tell whether it is—perhaps our earlier panic will enable us to dodge the bullet.

Correction, April 29, 2009: This article originally and incorrectly noted that the Mexican swine flu is a mix of pig, human, and avian flus. Though the strain's genetic material came from pig, human, and avian flu, the virus came only from a pig. ( Return to the corrected sentence.)

Sydney Spiesel is a pediatrician in Woodbridge, Conn., and clinical professor of pediatrics at Yale University's School of Medicine.

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