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item Suarez, David

Submitted to: American Association of Veterinary Laboratory Diagnosticians
Publication Type: Abstract Only
Publication Acceptance Date: 9/1/2003
Publication Date: 10/1/2002
Citation: Suarez, D.L. 2002. Avian influenza virus as a zoonotic agent. American Association of Veterinary Laboratory Diagnosticians.

Interpretive Summary:

Technical Abstract: Type A influenza viruses are common pathogens of humans, pigs, horses, chickens, and turkeys. Although the virus is endemic in a number of different species, all type A influenza viruses originate in wild birds, primarily ducks, gulls and shorebirds. Influenza viruses have eight gene segments, with six segments coding for conserved internal proteins and two coding for extremely diverse surface proteins, the hemagglutinin (HA) and neuraminidase (NA) proteins. Influenza viruses are generally promiscuous and many replicate in both birds and mammals. Introductions of influenza viruses from the reservoir host probably occurs frequently, but rarely do these viruses replicate or transmit well enough in the new host to cause either disease or become endemic. On rare occasions an influenza virus may contain the right constellation of genes to allows sufficient replication and transmission for the virus to become established in a new species. These viruses may cause disease and are characterized by a high evolutionary rate as the virus becomes adapted to the new host species. If a virus continues to replicate in the new host species, enough genetic changes accumulate so that it will no longer replicate well in the original host species. For zoonotic spread to humans, 3 models of spread have been proposed. The first is direct spread of virus from wild birds to humans. Few examples of this model have been documented. The second model is spread through an intermediary host. Several examples of avian influenza viruses infecting poultry that have spread to humans have been documented, including recent outbreaks of H5N1 in Hong Kong and H7N7 in the Netherlands. The third model of spread is the mixing vessel hypothesis where an intermediary host susceptible to two different influenza viruses can allow the reassortment of viral genes between the two viruses with the creation of progeny virus with new virulence characteristics. For example, the human H3N2 influenza virus, first observed in 1968, was a reassortant virus with both avian-like viral genes including the hemagglutinin gene, and human H2N2 influenza viral genes. This reassortant virus could replicate and transmit well in humans, and because immunity to influenza is primarily by antibodies to the hemagglutinin protein, the human population was very susceptible to this new H3 virus. This 'antigenic shift' led to a human pandemic. Experts predict that the human population is overdue for another antigenic shift, and many unique hemagglutinin genes are present in the wild bird reservoir.