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Avian Influenza

Bill Wiggin: To ask the Secretary of State for Environment, Food and Rural Affairs whether a flock will be slaughtered if it is (a) found to be positive to avian influenza (i) High Path and (ii) Low Path and (b) not positive but in (A) a slaughter zone and (B) a movement restriction zone. [26889]

Mr. Bradshaw: Powers to slaughter in the event of an outbreak of avian influenza are contained in Section 16A and Schedule 3 of the Animal Health Act 1981 (as amended).

This allows the slaughter of:

    (i) any diseased poultry;

    (ii) any poultry suspected of having disease; and

    (iii) any poultry with a view to preventing the wider spread of avian influenza. This power can be exercised whether or not the poultry is affected with avian influenza or suspected of being so affected.

These powers apply to both poultry with HPAI and LPAI.

Any action taken to control avian influenza would be proportionate and decided upon in the light of an overall assessment of the risks, costs and benefits in a particular situation. However, it is a requirement under EU obligations that poultry on an infected premises must be slaughtered.
Mr. Paterson: To ask the Secretary of State for Environment, Food and Rural Affairs whether her Department has identified strains of avian influenza closely
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related to H5N1 already in England; and what assessment she has made of the epidemiological implications of co-infection with H5N1 in a single host. [24009]

Mr. Bradshaw: The last H5 avian influenza virus to be isolated in England was the H5N1 virus responsible for the outbreak of highly pathogenic avian influenza in turkeys in Norfolk in 199192. This virus is genetically distinguishable from the H5N1 viruses currently causing the problems in East Asia and the virus isolated recently in quarantine birds in Essex.

The genetic material (RNA) of influenza viruses is segmented into eight distinct genes, which code for 10 proteins. Because this viral RNA is segmented, genetic reassortment can occur in mixed infections with different strains of influenza A viruses. This means that when two viruses infect the same cell, progeny viruses may inherit sets of eight RNA segments made up of combinations of segments from either of the parent viruses. The epidemiological significance of this for humans is that in theory if, for example, an H5N1 virus and a human influenza virus infect the same animal and same cell a reassortant virus could emerge that possessed the virus genes that enabled it to be transmissible in humans, but with the H5 haemagglutinin gene, which would mean that humans had no immunity to this virus. This mechanism is thought to have been the way the H2N2 and the H3N2 pandemic viruses emerged in 1957 and 1968 respectively.