The Disease in Birds: Impact and Control Measures
Avian influenza is caused by Type A strains of the influenza virus. First identified in Italy more than 100 years ago, the disease occurs worldwide. All birds are thought to be susceptible, although some species are more resistant to infection than others. Infection causes a wide spectrum of symptoms, ranging from mild illness to a highly contagious, rapidly fatal disease resulting in severe epidemics. The latter is known as "highly pathogenic avian influenza."
Fifteen subtypes of influenza virus are known to infect birds, thus providing an extensive reservoir of influenza viruses. To date, all outbreaks of the highly pathogenic form have been caused by Influenza A viruses of subtypes H5 and H7.
Migratory waterfowl--most notably wild ducks--are the natural reservoir of avian influenza viruses, and these birds are also the most resistant to infection. Domestic poultry, including chickens and turkeys, are particularly susceptible. Direct or indirect contact of domestic flocks with wild migratory waterfowl has been implicated as a frequent cause of epidemics. Live-bird markets have also played an important role in epidemics.
Recent research has shown that viruses of low pathogenicity can, after circulating in a poultry population for sometimes short periods, mutate into highly pathogenic viruses. During a 1983-1984 epidemic in the United States, the H5N2 virus initially caused low mortality, but within six months became highly pathogenic, with mortality approaching 90 percent. Control of the outbreak required destruction of more than 17 million birds at a cost of nearly $65 million.
In the absence of prompt control measures backed by good surveillance, epidemics can last for years. An epidemic of H5N2 avian influenza that began in Mexico in 1992 started with low pathogenicity, evolved to the highly fatal form, and was not controlled until 1995.
A Constantly Mutating Virus: Drift and Shift
All Influenza A viruses, including those that cause seasonal epidemics of influenza in humans, are genetically labile and well adapted to elude host defenses. Influenza viruses lack mechanisms for the "proofreading" and repair of errors that occur during replication. As a result, the genetic composition of the viruses changes as they replicate in humans and animals, and the existing strain is replaced with a new antigenic variant. These constant, permanent, and usually small changes in the antigenic composition of Influenza A viruses are known as antigenic "drift."
The tendency of influenza viruses to undergo frequent and permanent antigenic changes necessitates constant monitoring of the global influenza situation and annual adjustments in the composition of influenza vaccines. Both activities have been a cornerstone of the World Health Organization (WHO) Global Influenza Programme since its inception in 1947.
Influenza viruses have a second characteristic of great public health concern: Influenza A viruses, including subtypes from different species, can swap or "reassort" genetic materials and merge. This reassortment process, known as antigenic "shift," results in a novel subtype different from both parent viruses. As populations have no immunity to the new subtype, and as no existing vaccines can confer protection, antigenic shift has historically resulted in highly lethal pandemics.
Conditions favorable for the emergence of antigenic shift have long been thought to involve humans living in close proximity to domestic poultry and pigs. Because pigs are susceptible to infection with both avian and mammalian viruses, including human strains, they can serve as a "mixing vessel" for the scrambling of genetic material from human and avian viruses.
Recent events have identified a second possible mechanism. Evidence is mounting that, for at least some of the 15 avian influenza virus subtypes circulating in bird populations, humans themselves can serve as the "mixing vessel. …