AVAIN FLU: IT's TOO COLD IN THE HUMAN NOSE THAT H5N1 CAN SPREAD

Avian flu: It's too cold in the human nose that H5N1 can spread
While all the media attention at the moment is focused towards the H1N1 influenza A (also known as swine flu), researchers continue to try to understand how the H5N1 avian influenza. In an article published in the journal free online access PLoS Pathogens (reference below), an Anglo-American study reveals that a likely reason why the H5N1 avian influenza infects human with difficulty is the relatively low temperature (32 ° C) environment of the proximal human airway. It is possible that the epidemic of avian influenza (H5N1) in Southeast Asia was in 2007, which inter-species transmission has remained sporadic, never ever be transformed into a human pandemic because the mutations that might have made virus infection in humans have not occurred.

Temperature difference between distal and proximal human airway
Because previous studies showing that the H5N1 virus infecting the more distal (bronchi) that the proximal side (nose, throat) of the human airway, scientists from the University of North Carolina at Chapel Hill (U.S.) and Imperial College London (United Kingdom) have hypothesized that the temperature difference between the two areas have been crucial to prevent zoonosis (transmission of animal disease to humans and vice versa). To provide some answers to their hypothesis, the U.S. and British researchers have used an in vitro model of human ciliated cells from the airways, they were seeded at temperatures of 37 ° C or 32 ° C ( to mimic the existing conditions of distal or proximal). In the first case, the two types of human and avian viruses infecting cell cultures efficiently, while at 32 ° C, only the human virus demonstrated efficiency of infection of cells in culture. These results are consistent with the fact that the infection in birds takes place in the intestine, and then at 40 ° C.

The important role of glycoproteins in the adjustment to room temperature
It is furthermore known that the influenza virus present at position 627 in the PB2 polymerase (element responsible for the replication of influenza virus genome in the host cell), an amino acid plays a crucial role in Adaptation of virus to the environmental temperature within the same host. The replacement of this residue of the human virus by that of avian virus but did not explain the difference between the infectious properties of both viruses at different temperatures. The researchers then used two types of human viruses, the H3N2 and H1N1, and replaced some of their surface proteins (glycoproteins, see box) by surface proteins of influenza virus. The human viruses as amended showed reduced ability to infect human cells ciliated cells cultured at 32 ° C, suggesting an important role of these glycoproteins in the adjustment to room temperature, and therefore a crucial role in limited transmission of H5N1 influenza viruses in humans and in the inter-human contagion.

The study, funded by the Medical Research Council (MRC Council for Medical Research) in the United Kingdom and by the NIH in the United States is important because in the words of Professor Wendy Barclay, Imperial College London,

"It is impossible to develop vaccines against the 16 subtypes of avian viruses [...]. By studying a range of viruses, we can nevertheless determine what changes come to significantly increase the risk of zoonoses and contagion in the human species. "

The Influenza Virus
The influenza virus belongs to the family Orthomyxoviridae, enveloped viruses with single-stranded RNA and having a spherical shape 80 to 100 nm in diameter. There are three types of influenza viruses named A, B and C. Their surface is studded with surface proteins or glycoproteins, also known as surface antigens. Viruses A and B have two types, the hemagglutinin (H) and neuraminidase (N). The hemagglutinin is responsible for virus attachment on a sialic acid residue on the surface of cells of the ciliated epithelium of the respiratory tract, and the fusion of viral and cellular membranes during the penetration phase virus. Neuraminidase, in turn, allows the release into the host cell virions pre-formed, and the posting of the hemagglutinin (and therefore the virus particle) of the cell membrane of the host.

Reference:
Article: Avian Influenza Virus Glycoproteins Restrict Virus Replication and Spread Through Human Airway Epithelium at Temperatures of the Proximal Airways
Authors: Margaret A. Scull, Laura Gillim-Ross, Celia Santos, Kim L. Roberts, Elena Bordonali, Kanta Subbarao, Wendy S. Barclay, Raymond J. Pickles
Published Journal: PLoS Pathogens
DOI: 10.1371/journal.ppat.1000424

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Source: BE UK number 97
http://www.bulletins-electroniques.com/actualites/59855.htm