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      The Pause on Avian H5N1 Influenza Virus Transmission Research Should Be Ended

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          ABSTRACT

          A voluntary 60-day pause on avian H5N1 influenza virus transmission research was announced in January 2012 by the international community of influenza scientists engaged in this work to provide time to explain the benefits of such work and the risk mitigation measures in place. Subsequently, the pause was extended to allow for time for review of the biosafety and biosecurity conditions. After almost 8 months, these conditions have been met in some countries and are close to being met in others. Because H5N1 virus transmission studies are essential for pandemic preparedness, researchers who have approval from their governments and institutions to conduct this research safely under appropriate biosecurity conditions should resume this important work.

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          Airborne transmission of influenza A/H5N1 virus between ferrets.

          M Linster, Thomas A Smith, Martin Linster … (2012)
          Highly pathogenic avian influenza A/H5N1 virus can cause morbidity and mortality in humans but thus far has not acquired the ability to be transmitted by aerosol or respiratory droplet ("airborne transmission") between humans. To address the concern that the virus could acquire this ability under natural conditions, we genetically modified A/H5N1 virus by site-directed mutagenesis and subsequent serial passage in ferrets. The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. The transmissible viruses were sensitive to the antiviral drug oseltamivir and reacted well with antisera raised against H5 influenza vaccine strains. Thus, avian A/H5N1 influenza viruses can acquire the capacity for airborne transmission between mammals without recombination in an intermediate host and therefore constitute a risk for human pandemic influenza.
          Article 0 comments Cited 195 times – based on 0 reviews     Review now
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            Experimental adaptation of an influenza H5 haemagglutinin (HA) confers respiratory droplet transmission to a reassortant H5 HA/H1N1 virus in ferrets

            Masaki Imai, Tokiko Watanabe, Masato Hatta … (2012)
            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 since it mediates virus binding to host-specific cellular receptors 1–3 . Here, we therefore assessed the molecular changes in HA that would allow an H5 HA-possessing virus to transmit among mammals. We identified a reassortant virus with H5 HA possessing four mutations in a 2009 pandemic H1N1 virus backbone 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 it was not highly pathogenic and did not cause mortality. These results suggest that H5 HA can convert to an HA that supports efficient viral transmission in mammals. However, we do not know whether the four mutations in the H5 HA identified in this study would render a wholly avian H5N1 virus transmissible. The genetic origin of the remaining seven viral genes may also critically contribute to transmissibility in mammals. Nevertheless, as H5N1 viruses continue to evolve and infect humans, receptor-binding variants of H5N1 viruses with pandemic potential, including avian-human reassortant viruses as tested here, may emerge. Our findings emphasize the need for pandemic preparedness for H5 HA-possessing viruses and will help individuals conducting surveillance in regions with circulating H5N1 viruses to recognize key residues that predict the pandemic potential of isolates, which will inform the development, production, and distribution of effective countermeasures.
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              The potential for respiratory droplet-transmissible A/H5N1 influenza virus to evolve in a mammalian host.

              Colin A Russell, Judith M Fonville, André E X Brown … (2012)
              Avian A/H5N1 influenza viruses pose a pandemic threat. As few as five amino acid substitutions, or four with reassortment, might be sufficient for mammal-to-mammal transmission through respiratory droplets. From surveillance data, we found that two of these substitutions are common in A/H5N1 viruses, and thus, some viruses might require only three additional substitutions to become transmissible via respiratory droplets between mammals. We used a mathematical model of within-host virus evolution to study factors that could increase and decrease the probability of the remaining substitutions evolving after the virus has infected a mammalian host. These factors, combined with the presence of some of these substitutions in circulating strains, make a virus evolving in nature a potentially serious threat. These results highlight critical areas in which more data are needed for assessing, and potentially averting, this threat.
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                Author and article information

                Journal
                Journal ID (nlm-ta): mBio
                Journal ID (iso-abbrev): MBio
                Journal ID (hwp): mbio
                Journal ID (pmc): mbio
                Journal ID (publisher-id): mBio
                Title: mBio
                Publisher: American Society of Microbiology (1752 N St., N.W., Washington, DC )
                ISSN (Electronic): 2150-7511
                Publication date (Electronic): 9 October 2012
                Publication date Collection: Sep-Oct 2012
                Volume: 3
                Issue: 5
                Electronic Location Identifier: e00358-12
                Affiliations
                Viroscience Lab, Erasmus MC, Rotterdam, The Netherlands [ a ];
                Department of Microbiology, Department of Medicine, Division of Infectious Diseases, Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, New York, USA [ b ];
                Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin, USA [ c ];
                Division of Virology and International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan [ d ]; and
                ERATO Infection-Induced Host Responses Project, Saitama, Japan [ e ]
                Author notes
                Address correspondence to Ron A. M. Fouchier, r.fouchier@ 123456erasmusmc.nl .
                Article
                Publisher ID: mBio00358-12
                DOI: 10.1128/mBio.00358-12
                PMC ID: 3484389
                PubMed ID: 23047750
                SO-VID: a5d1dd06-6015-4ce3-8229-b97d29641b8d
                Copyright © Copyright © 2012 Fouchier et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                Pages: 2
                Categories
                Subject: Commentary
                Custom metadata
                cover-date September/October 2012

                ScienceOpen disciplines: Life sciences
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                ScienceOpen disciplines: Life sciences

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