Molecular anatomy of 2009 influenza virus A (H1N1).

Influenza A viruses are a major cause of morbidity and mortality worldwide and affect large segments of the population every year. The nature of their genome, formed by eight segments of single-stranded RNA, favors the constant evolution of the virus by two main mechanisms: the accumulation of single nucleotide mutations in the viral genes introduced by an error-prone viral RNA polymerase and the reassortment of genes between two strains of different origin. The viral genome encodes 11 proteins. Most have been shown to play a role in shaping the virulence scenario of influenza A viruses, including the adaptation of infection and transmission into new host species, the ability to modulate the host immune response, and the capacity to replicate efficiently at low temperature. On the surface of the virus particles there are two principal polypeptides, the hemagglutinin (HA) and the neuraminidase (NA), which are the target for the neutralizing antibodies immune response. There are 16 HA and 9 NA different subtypes in the influenza A virus that circulate in humans and animals. When a virus strain with a new HA or NA subtype appears in the human population by genetic reassortment, it usually causes a pandemic because there is no preexisting immunity against the new virus. This was the case for the three pandemics that occurred during the last century (1918, 1957, and 1968) and also for the first pandemic of the 21(st) century, caused by the currently circulating A (H1N1) 2009 virus, which was generated by gene reassortment between a virus present in pigs of North America and a virus that circulates in the swine population of Euroasia.