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Highly pathogenic avian H5N1 influenza A viruses occasionally infect humans, but currently do not transmit efficiently among humans. The viral haemagglutinin (HA) protein is a known host-range determinant as it mediates virus binding to host-specific cellular receptors1, 2, 3. Here we assess the molecular changes in HA that would allow a virus possessing subtype H5 HA to be transmissible among mammals. We identified a reassortant H5 HA/H1N1 virus—comprising H5 HA (from an H5N1 virus) with four mutations and the remaining seven gene segments from a 2009 pandemic H1N1 virus—that was capable of droplet transmission in a ferret model. The transmissible H5 reassortant virus preferentially recognized human-type receptors, replicated efficiently in ferrets, caused lung lesions and weight loss, but was not highly pathogenic and did not cause mortality. These results indicate that H5 HA can convert to an HA that supports efficient viral transmission in mammals
Whether or not the H5N1 viruses currently circulating in the world can easily acquire the additional mutations needed to cause a pandemic is an open question, according to Kawaoka: "It is hard to predict. The additional mutations may emerge as the virus continues to circulate."
In December 2011, a National Institutes of Health advisory panel, the National Science Advisory Board for Biosecurity (NSABB), recommended redacting critical information from the Kawaoka lab's report, as well as from a similar study conducted in Holland. The unprecedented request was to withhold the methodologies used to make the virus transmissible and to not identify the mutations needed to make the virus transmissible in mammals. This month, the NSABB reversed itself, citing new information and manuscript revisions that more explicitly state the public health rationale for the work as well as the safety and security precautions in place in the labs in Wisconsin and Holland.