Some like it hot: human nose too cold for bird flu

Friday, May 15, 2009 — It’s now widely known that influenza type A viruses that usually infect ducks and other water birds can jump species to infect the human respiratory tract. Such transmission from birds to humans remains rare and tends to happen when some of the 16 subtypes of avian influenza manage to mutate by applying proteins on their surfaces taken from human flu viruses.

So why is a tricky mutation the key to making the interspecies leap? It may be that bird flu likes it hot. A new study by scientists from the University of North Carolina at Chapel Hill School of Medicine and Imperial College, London, in the U.K suggests that avian influenza finds the temperature in the human nose too cold a place to infect and replicate.

The study, published Friday, May 15, 2009 in the on-line, public access journal PLOS Pathogens, points out that avian influenza viruses are adapted for growth at 104 degrees Fahrenheit (40 degrees Celsius). This is the gut temperature of host birds. But the human nose and throat, which are “the likely site of initial inoculation by influenza viruses, are maintained at a cooler temperature 32°C or 89.6°F, suggesting that zoonotic transmission may be limited by temperature differences between the two hosts,” the authors write.

The research included growing cells from the human airway and infecting them with different human and avian influenza viruses, including H5N1, to see how well the viruses grew and spread. “The human influenza viruses grew equally well in the cells whether they were maintained at 37 degrees Celsius, our core body temperature, or at 32 degrees Celsius, the temperature of the nose. In contrast, the four avian influenza viruses tested grew well at 37 degrees Celsius but grew very slowly at 32 degrees Celsius,” the authors write.

And when they created a mutated human influenza virus by adding a protein from the surface of an avian influenza virus, the mutated virus “struggled to thrive at 32 degrees Celsius”. This suggests that a mutated bird flu virus “would need to undergo further changes in order to adapt to the conditions in the human body,” the authors conclude.

Lead author of the study was Margaret A. Scull, a graduate student working in the lab of senior author Raymond Pickles, Ph.D., of the UNC Cystic Fibrosis/Pulmonary Research and Treatment Center and associate professor of microbiology and immunology.

Support for the research came from the National Institutes of Health

School of Medicine contact: Les Lang (919) 966-9366 or llang@med.unc.edu

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