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Avian flu and influenza pandemics in human populations.

including pigs, horses, ducks, chickens, and seals. In most of these species the virus produces an acute infection. In wild ducks and other aquatic birds the virus primarily infects the gut and the birds do not appear to have physical symptoms. Ducks may remain infected for 2 to 4 weeks and during this time they shed the virus in their faeces which makes them potentially a major reservoir of infection. The pool of virus present in other species is an important genetic reservoir for the generation of new flu viruses that infect humans. In considering strategies for controlling flu pandemics in human populations the presence of an animal reservoir has to be taken into account. There are three groups of flu viruses, influenza, A, B, and C. Type A viruses are able to infect a wide variety of warm-blooded animals. Analysis of their genomes indicates that all strains of influenza A originated from aquatic birds. By contrast type B and C are mostly confined to humans. At any one time a number of different strains of virus may be circulating in the human population. The genome of flu viruses consists of negative sense single-stranded RNA which means that it must be first copied to a complementary positive sense strand of RNA before it can be translated into protein. The genome is segmented and consists of seven or eight fragments of RNA encoding approximately 14 proteins. The viral RNA is enclosed by nucleoproteins to make a ribo-nucleoprotein complex which is contained in the central core of the virus called the capsid. The viral envelope is a lipid bilayer formed from the plasma membrane of the host cell that produced the virus. The viral envelope contains two virus encoded proteins viz. haemagglutinin and neuraminidase. The virus uses haemagglutinin to attach to the cell that it will infect. Haemagglutinin can bind to a sialic acid containing polysaccharide, glycophorin, which is present on the surface of a variety of cells. Neuraminidase can cleave sialic acid residues from polysaccharides. It has a role in clearing a path in the surface of the target cell prior to infection, and it promotes release of the budding virus from host cell after infection. Inside the host cell new viral genomes are produced from a complementary strand of RNA which is positive sense but structurally slightly different from the parent mRNA. Viruses which contain RNA are flexible and can mutate rapidly. When this property is combined with a segmented genome that allows recombination easily there can be a variety of genetic diversity in nature. Only a few subtypes H1N1, H1N2, and H3N2 circulate in mammalian hosts, but a wide variety of subtypes circulate freely in wild birds mixing and exchanging gene segments though rarely in association with disease. The structures of influenza B and influenza C are more or less similar to that of Type A, although in influenza C the functions of the haemagglutinin and neuraminidase are combined in a single molecule, haemagglutinin esterase. Influenza C does not normally cause clinical disease or epidemics. In humans, pigs and horses flu viruses circulate through the population at regular intervals. Flu is endemic in tropical regions and seasonal in winter months in temperate countries. Sporadic epidemics also occur in sea mammals and poultry. In these species high mortality is typical. The influenza virus accumulates a number of genetic mutations during its replication resulting in what is called antigen drift which brings about progressive changes in the molecules present on the surface of the virus. This means that the immune response which was effective at recognizing and eliminating the virus from the previous year is less effective against the strain of the current year. More worrisome is major genetic change occurring at irregular intervals called antigenic shift. The process occurs in only influenza A virus at intervals of 10 to 30 years, and results in major pandemics. The pandemic strains are designated according to their surface antigens e.g. Spanish flu (H1N1) in 1918, Asian flu (H2N2) in 1957, and Hong Kong flu (H3N2) in 1968. Research on victims of the 1918–19 pandemic which killed 20 million–50 million people around the world showed that in the 1918 virus the haemagglutinin adapted to human sialo-polysaccharide in a different way from adaptation in subsequent pandemics. This suggests that the virus can jump the species barrier from birds to humans in more ways than have been realized. Major human influenza outbreaks since 1918 and the animal species implicated are listed in Table 1. In 1997 a new strain of influenza A, H5N1, was identified in Hong Kong. The strain was widespread in poultry but a small number of people also became infected with high mortality. The epidemic was contained by a mass cull of poultry. Whether H5N1