The model and images of the influenza virus A/H1N1

Influenza viruses belong to the Orthomyxoviridae family. These viruses are pathogenic to humans, a number of other mammals and many birds. In humans and mammals, the virus infects the upper respiratory tract, whereas in birds, the infection affects mainly the bowel. The characteristics of these viruses include a high variability and a wide range of hosts. Influenza periodically causes epidemics and pandemics. The severity and nature of the disease varies depending on virus strain. The influenza virions are pleomorphic; however, the most prevalent shape is spherical. The diameters of the virions range from 80 to 170 nm [1]. The viral particles are covered with a lipid membrane, which is comprised from the host cell membrane and contains hemagglutinin (HA) and neuraminidase (NA) proteins. To date, 16 HA (H1-H16) and 9 NA (N1-N9) subtypes have been identified in influenza virions. These proteins facilitate binding of the virus to host cell receptors, subsequent endosomal fusion and viral release from the cells [2]. The membrane also contains M2-protein channels, which play a critical role in the early phase of infection leading to the uncoating and release of viral RNP [3]. The swine virus subtype A/H1N1 caused most of the cases of influenza in the United States and Europe in the autumn of 2009. This variant of the influenza virus is characterized by approximately the same virulence and pathogenicity as seasonal strains. The seasonal human influenza virus also continues to circulate and cause disease. Currently, it is not entirely clear what mutations allowed the swine flu to infect humans. Swine subtype A/H1N1 is resistant to remantadin but sensitive to oseltamivir (Tamiflu) [4].