欧盟发布一份猪及猪肉等可能作为H1N1流感病毒饮食来源的科学报告

This report describes the genetic make up and presumed swine origin of the novel (pandemic) 2009 H1N1 influenza virus that has caused a sustained infection and pandemic in humans. Swine are readily infected upon experimental inoculation with human nH1N1 isolates and infected humans have occasionally transmitted the virus to swine in the field. However, swine-to-human transmission has not been reported so far. Turkeys became infected after experimental inoculation via the reproductive tract, but not via the respiratory route, and there have been a few outbreaks of nH1N1 in turkey breeder hens in the field. The infections in swine and turkeys as food-producing animals have raised questions about the possibility that food or food products from these animal species could pose a risk of foodborne infection in humans.

This possibility was analysed on the basis of specific pathogenetic features of nH1H1 infection in swine and turkeys and on the basis of biological and physico-chemical characteristics of type A influenza viruses in general. The different requirements for a virus infecting food-producing animals to cause a foodborne infection in humans were discussed and applied to nH1N1 influenza virus.

So far, reverse zoonosis with humans serving as a source of infection for swine, has been described in several countries, but zoonotic transmission from pigs or turkeys to humans has not been reported. This does, however, not exclude food as a possible source of infection for humans. It was shown repeatedly that nH1N1 infection in pigs only involves the respiratory tract and that there is no viraemia or dissemination to other organs. nH1N1 virus does not reach muscles and thus does not colonize meat. Low titre virus contamination of pork or pork products by respiratory excretions at slaughter or at processing cannot be excluded.

The nH1N1 virus, when ingested, would have to overcome different hurdles upon arriving in the gastro-intestinal tract. Mammalian influenza viruses are susceptible to acid pH and to bile salts, both of which may exert an inactivating effect. There is no evidence that the gastro-intestinal tract of humans can serve as a portal of entry or target organ for influenza viruses of swine and this premise can be extrapolated to nH1N1 virus. So, nH1N1 virus if and when ingested with contaminated food products, particularly when present at low titres or when the food is eaten raw, is highly likely to become inactivated prior to arrival in the intestines.

Virus that has been swallowed, possibly at high titres e.g. with respiratory secretions in infected pigs, does not replicate in the intestines. Furthermore, in contrast to typical enteric human viruses known to cause foodborne infections, the infectivity of influenza viruses is poorly resistant to physical and chemical agents. Influenza viruses are susceptible to heat and threshold values obtained with the frequently studied avian influenza viruses can be applied to all influenza viruses, including nH1N1, because their inactivation kinetics at increasing temperatures are similar. Heating at 70°C and thus moderate cooking inactivates high virus titres within seconds, even when the virus is embedded in meat products or in by-products. While less is known about the pathogenesis of potential nH1N1 infection in turkeys, the same rules would apply.

Most disinfectants used for disinfecting equipment that is possibly contaminated with influenza virus during food processing, easily destroy these viruses, as do the common lipid solvents, which act on the lipoprotein outer envelope of the virion.

All these factors were discussed and, based on this evaluation, it was concluded that pork or pork products or turkey meat possibly contaminated with nH1N1influenza virus are not a foodborne threat.