If you’re fretful about bird flu, you might not want to linger on the shoreline with the loons
MY CATACLYSMIC, STEPHEN KING-STYLE screenplay (soon to become a major waste of time) graphically depicts the arrival of avian flu in Minnesota via the bowels of the common loon. North Country residents drive south in droves as deliriously infected loons come to shore, pecking out the eyeballs of children and the elderly, poisoning water sources, and strafing high-traffic public areas with a horrific, deadly cough and a bad case of the runs. My agent is pushing it as The Andromeda Strain meets Jurassic Park, and also as an engaging public-service announcement. ¶ I chose the loon to be the evil viral vector not only because of the delicious irony of Minnesota being laid siege by its state bird, but because it’s scientifically accurate: avian flu viruses are typically disseminated by wild water birds like swans, geese, and ducks. Waterfowl make perfect hosts because they migrate great distances, and because they’re rarely sickened when infected by avian flu. This allows them to continue to go about their birdy business while shedding millions of copies of the virus in their feces, including in the ponds where they swim. When wild and domesticated birds commingle (often by sharing a common water source), all it takes is one chicken not practicing good bill-washing before dinner, and bam! the virus moves on.
Avian influenza may seem new, but it’s not. Here in the United States, there have been more than a dozen outbreaks in poultry in just the last 10 years. Some have been bad, and some haven’t. Strains of avian influenza can come in a “low pathogenicity” form, wherein infected birds display mild clinical symptoms such as lowered egg production and, as the Centers for Disease Control and Prevention (CDC) reports, “ruffled feathers.” It also can present in a highly pathogenic form that can kill a barnful of our feathered entrées in just 48 hours.
So although there are many avian flu viruses, practically speaking we’ve titled this virus known to scientists as “Influenza A subtype H5N1” as “The bird flu.” H5N1 first resurfaced in 1997, killing umpteen chickens and six humans in Hong Kong—a species-jumping feat that garnered far more media attention than the farmers who bulldozed dead chickens into an open pit. Since that initial outbreak, H5N1 has given all of us the creeps by creeping its way out of Southeast Asia. Human cases have been reported as far west as Iraq, Egypt, and Turkey, and the virus is showing itself to be highly lethal, with human death rates higher than 50 percent.
The good news is that, so far, the vast majority of human infections have been in people who’ve had direct contact with H5N1-stricken poultry, and poultry raising is much more intimate in Asia than it is in the factory farms of the United States. There’s no evidence that one can become ill by eating a properly cooked infected bird, but according to the CDC, at least two people in Vietnam became infected through the consumption of uncooked duck blood. Yum.
A small number of the few hundred reported cases of human avian flu seem to have developed from human-to-human transmission—people who got sick by taking care of the sick. Whether doing shots of duck blood, eating or handling an infected carcass, or taking care of an infected person, victims seem to require fairly high exposure to the virus to actually contract the illness.
Why is this? An article in the March 2006 edition of Nature suggests that it may be that to enter and infect a cell, a virus must bind to a very specific molecule. A virus and a bullet can both be lethal, but the bullet isn’t species-specific—it’ll kill whatever it runs into. If a virus can’t find an appropriate binding receptor, it’s harmless. According to the article, the standard human flu virus requires a binding receptor concentrated in the mouth, sinuses, and upper airways of the lungs, whereas avian flu’s target molecule is concentrated deep within the lungs—in the air sacs where oxygen is exchanged. This may be why humans do not easily contract H5N1: it must be deeply inhaled to have a chance at infecting a cell. A standard human influenza virus has easier access to binding molecules and, replicating in the upper airways, is more easily converted to an aerosol mist with a “haaaachoo” or a cough—the viral version of a mass mailing.
What scientists fear is that the H5N1 virus will pick up this human-cell entry code—the ability to bind to the standard human virus receptor molecule—and transform itself into a virus that is highly lethal and highly infectious. How do you spell “P-A-N-D-E-M-I-C”?
If avian flu breaks our code, it will likely do so via a process called “reassortment.” Influenza has eight separate gene segments, allowing a virus to mix and match genes with other viruses and give itself a whole new look. One reassortment possibility would be if a human already infected with a common influenza strain also happens to become infected with the H5N1 bird flu. Replicating in the same body, in the same cells, gene segments from the standard human flu virus could get “resorted” and reassembled with segments from avian flu. The same process could occur in a pig that is simultaneously infected with an avian flu virus and a human influenza virus.
Reassortment could produce a virus capable of infecting humans, but with a “face” (defined by the proteins displayed on its surface) no human would recognize. Viruses have two major surface proteins: H for hemagglutinin and N for neuraminidase (hence the bird flu being subtyped H5N1). Up to now, human flu strains have been exclusively H1, 2, or 3. H5 is a new face in town, and an infected person’s immune system would be starting from scratch. It would need time to identify the virus and make appropriate antibodies, but for a virus as pathogenic as the bird flu, there appears to be little time before the body is overwhelmed.
Distinctly different new viruses like H5N1 have pandemic potential because there’s no pre-existing immunity in the community. Compare this to a newly mutated H2 flu virus: it might have its own distinct fingerprint, but antibodies created against previous H2 infections can exhibit some cross-reactivity to this newly reconfigured H2. These “old” antibodies might not be a dart to the heart, but they’ll put up some immunological resistance and buy time while more specific antibodies are being created.
If we have the H5N1 virus isolated, why don’t we take it to the lab and make a vaccine? Actually, we have. The vaccine works, but there are problems.
First, annual human influenza vaccines are given in small doses because they’re boosters; most of us have some baseline immunity and just need a refresher. This isn’t the case with a novel virus like H5N1, so larger doses—three to six times the standard dose—are required to stimulate an effective immune response.
Which leads to the second problem: ramping up our production capacity to create the usual influenza vaccine, plus three-to-six times that amount to cover H5N1 vaccination. Our current production technology, which involves growing viruses in live chicken embryos—is clunky and laborious. Remember 2004, when contamination in a British facility cut our vaccine supply in half? Not only would the volume required to prepare for the possibility (not certainty) of an H5N1 outbreak be huge, but it would also leave us extremely vulnerable should an entirely different but equally deadly influenza strain suddenly emerge.
Because viruses are genetic slot machines, constantly rolling over their genes looking for winning combinations, we need to develop a vaccine program that can react quickly to a breakout virus and produce the vaccine in massive quantities.
In the meantime, let’s keep a wary eye on our state bird, the common loon. You cover the front door, I’ll get the back.
Craig Bowron is a Twin Cities internist.