Birds of Hong Kong - The Monster at Our Door: The Global Threat of Avian Flu - page 19

ways in California and Minnesota suggested to scientists that it originated in ducks and other waterfowl.
Like all influenza, HPAI is essentially mysterious: it flares up unexpectedly among chickens and turkeys
in different countries, continents, and hemispheres. Until recently, it has been relatively rare, with fifteen
localized outbreaks between 1959 and its sudden appearance in Hong Kong in 1997. HPAI in all of these
instances was caused by influenza subtypes containing either H5 or H7; researchers believe that these
hemagglutinins contain extra basic amino acids at their cleavage sites that amplify virulence by allowing
viruses to invade a broader variety of tissues and, possibly, species. 75 But there was no evidence at all to
suggest that these avian superviruses posed any threat to humans, not even to the poultry workers who
tended the ill birds and cleaned up in the aftermath of HPAI's carnage. “In fact,” Hong Kong researchers
emphasized, “attempts to transmit experimentally a number of avian virus subtypes directly to humans
were not successful.” The species barrier was believed to be insurmountable. 76
After agricultural authorities killed off the remaining sick chickens in April, HPAI seemingly disap-
peared, with extensive testing failing to reveal any further traces of H5N1 in New Territory chicken farms
or Hong Kong's live-poultry markets. Veterinary scientists relaxed. Then in mid-May a three-year-old
boy—previously in perfect health—was admitted to Queen Elizabeth Hospital in Kowloon with a sore
throat, fever, and abdominal pain. Despite top-flight intensive care, his condition deteriorated catastroph-
ically, and he died on 21 May. Physicians and nurses were appalled by the relentless cascade of disasters
that wracked his tiny body: viral pneumonia, acute respiratory distress syndrome (ARDS), Reye's syn-
drome, and finally, kidney and liver failure. The local department of health ran tests on secretions from
the dead child's throat and found an unusual influenza subtype that it could not identify; frozen samples
were sent off in June to two of WHO's four collaborating centers (CDC in Atlanta and NIMR in London),
as well as to the National Influenza Center in Rotterdam.
In retrospect, influenza experts would applaud the vigilance of Hong Kong health officials. The city,
with its world-class medical community, is the sentinel for influenza surveillance in the south China re-
gion, where interspecies transmission of viral strains is believed to be most frequent and intense. If the
three-year-old had died in neighboring Guangdong, or for that matter, in any of the poorer countries of
southeast Asia, it is unlikely that the identification of his pathogen would have been pursued with such
vigor. 77 The team in Rotterdam was the first to uncover the lethal strain's identity. As Davies recounts,
the Dutch worked throughout July in an unsuccessful attempt to match the Hong Kong virus against their
reference archive of human and swine influenzas. Baffled by the failure of the virus to react with any of
their antisera, in early August they tested it against a long-shot H5N1 reagent that been brought back from
the Memphis laboratory of the famous influenza authority Robert Webster. To the consternation of the
Rotterdam team, it was a positive match. 78
The Dutch result was soon confirmed by Atlanta and London, but no one was yet ready to accept that
H5N1 had actually vaulted the species barrier and killed the child in Hong Kong. It seemed more plaus-
ible that Hong Kong public-health scientists had unwittingly submitted a contaminated sample. Leaving
nothing to conjecture, the Dutch, followed by the CDC and WHO, sent experts, including Webster, to
double-check conditions in the Hong Kong lab. They soon discovered that the Chinese had been scrupu-
lous in their procedures—there was no contamination. H5N1 was indeed the killer, and as Webster later
discovered, it was almost identical to the strain that had killed the chickens in March. A slight hemagglu-
tinin mutation—a difference of only three amino acids—had apparently allowed the bird virus to open the
lock on human cells and infect the child. 79
It was a staggering, paradigm-shifting discovery. This H5N1 was not a reassortant, as textbooks pre-
dicted, but an avian virus that had come to roost in the human body with a little help from genetic drift.
Having made such a seemingly impossible species leap, moreover, there was no theoretical reason why
H5N1 could not subsequently reassort with human flu genes in the lungs of a co-infected human; pigs