Influenza A viruses occur naturally in a wide variety of waterfowl. Due to their high genetic flexibility, they can adapt to the new host when transferred to another species, leading to animal diseases and influenza pandemics. H5N1, H7N7, H9N2, and H2N2 viruses are pathogens with a high pandemic potential due to proven human pathogenicity and the lack of immune protection in the population. However, the unexpected outbreak of an H1N1 pandemic in 2009 shows that the reliability of such predictions is limited. Host specificity, pathogenicity, and transmissibility of the influenza a is based on the complex interaction of the viral proteins with cellular factors. Receptor specificity and fusion activity of hemagglutinin play central roles,
Ecology of Influenza A
The diversity of the influenza a virus is most clearly reflected in a large number of haemagglutinin (HA) and neuraminidase (NA) subtypes (H1–H17, N1–N9). While only some of these subtypes have been observed in humans, pigs, horses, and several other mammals, almost the entire spectrum can be found in birds. Today we can assume that waterfowl (goose, duck, seagull) are the natural hosts of the influenza A viruses. More than 100 different HA and NA combinations were discovered in these animals.
Most avian influenza viruses cause no or only mild symptoms in their natural host species. These low pathogenic viruses must be distinguished from the highly pathogenic avian influenza viruses, also known as avian influenza. The highly pathogenic pathogens arise when low pathogenic viruses of subtypes H5 and H7 are transferred from waterfowl to chickens and then mutate in the new host. As a rule, highly pathogenic viruses do not occur naturally in waterfowl, but the retransmission of H5N1 viruses from chickens to waterfowl seems to have happened a few years ago.
The fact that the host barrier is not an insurmountable obstacle is also reflected in the fact that viruses are transmitted not only between bird species but also from birds to mammals. Most of the time, these transmissions are transient, so the burst dies quickly. In rare cases, however, it adapts to the new host and forms a new virus line. The adaptation is based on numerous mutation processes and gene exchange with other influenza viruses.
Although direct transmission of viruses from water bowls to humans does occur, it is assumed that other animal species usually play an essential role as intermediate hosts. There is evidence that viruses originating from ducks acquire receptor specificity for human cells when they multiply in chicken or quail as intermediate hosts. These viruses are then able to infect human tissue. The ability to reproduce in humans is finally optimized through further mutations or gene exchange with a human virus. Another intermediate host could be the pig, where avian viruses acquire mutations in the hemagglutinin and possibly the internal proteins that facilitate transmission to humans. Alternatively, the pig could serve as a mixing vessel in which gene sorting between human and avian viruses occurs, resulting in the formation of a new human virus. Each of these pathways can lead to a virus with new surface glycoproteins, thus significantly altering antigenicity.