Avian influenza virus H7N9, which killed several dozen people in China earlier this year, has not yet acquired the changes needed to infect humans easily, according to a new study by scientists at The Scripps Research Institute (TSRI). In contrast to some initial studies that had suggested that H7N9 poses an imminent risk of a global pandemic, the new research found, based on analyses of virus samples from the Chinese outbreak, that H7N9 is still mainly adapted for infecting birds, not humans.
“Luckily, H7N9 viruses just don’t yet seem well adapted for binding to human receptors,” said Ian A. Wilson, the Hansen Professor of Structural Biology and chair of the Department of Integrative Structural and Computational Biology at TSRI.
Study showed that H7N9 is still mainly adapted for infecting birds, not humans.
“Because publications to date have implied that H7N9 has adapted to human receptors, we felt we should make a clear statement about this,” said James C. Paulson, chair of TSRI’s Department of Cell and Molecular Biology.
The Wilson and Paulson laboratories collaborated on the study, which is reported in the December 6, 2013 issue of the journal Science.
A Worrisome Outbreak
H7N9 flu viruses infect birds, apparently causing them few or no symptoms. Until this year these strains had never been reported in humans. However, starting in February in two urban areas of eastern China, dozens of people began to come down with H7N9 flu. Most became severely ill. By the end of May, when the outbreak had mostly subsided, there were 132 laboratory-confirmed human cases and 37 deaths—a nearly 30% case-fatality rate.
The outbreak understandably alarmed public health officials, and across the globe dozens of laboratories began studying H7N9 isolates from infected patients. The big question was whether these strains were capable of spreading only in a limited, sporadic way from birds to humans—many of the cases were linked to poultry exposure—or if they had truly “jumped the species barrier.” If the latter were true, and H7N9 could now spread from human to human, the Chinese outbreak might be the start of a global pandemic.
Some prominent early studies came to worrisome conclusions. For example, most of the H7N9 isolates from the outbreak turned out to have acquired a notorious flu-virus mutation that substitutes the amino acid leucine for glutamine in the part of the virus that grabs receptors on host cells. The same mutation, in other influenza virus subtypes, was apparently a key enabler of pandemics that killed an estimated one million people worldwide in 1968-69 (the “Hong Kong flu”) and two million during 1957-58 (the “Asian flu”). Initial studies of the new H7N9 isolates in mice, ferrets and monkeys also suggested that they had at least a limited ability to spread among mammals.