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Three types of influenza virus are recognized: A, B and C. The influenza virus is a spherical or filamentous enveloped virus. Haemagglutinin (H), a surface glycopeptide, aids attachment of the virus to the wall of susceptible host cells at specific receptor sites. Cell penetration, probably by pinocytosis, and release of replicated viruses from the cell surface is effected by budding through the cell membrane facilitated by the action of the enzyme neuraminidase (N) which is also present on the viral envelope. ISH subtypes (H1-H15) and nine N subtypes (N1-N9) have been identified for influenza A viruses but only H1, H2, H3 and N1 and N2 have established stable lineages in the human population since 1918.
Influenza A is generally responsible for pandemics and epidemics.
Influenza B often causes smaller or localized and milder outbreaks, such as in camps or schools.
Influenza C rarely produces disease in humans.
Antigenic shift describes the capacity of influenza A to develop new antigenic variants at irregular intervals. This results from genetic recombination of the RNA of the virus (which is arranged in eight segments) with that of an animal orthomyxovirus.
Antigenic drift (minor changes in influenza A and B viruses) results from point mutations leading to amino acid changes in the two surface glycoproteins, haemagglutinin (H) and neuraminidase (N), which induce humoral immunity.
Thus, changes due to antigenic shift or drift render the individual's immune response less able to combat the new variant.
Major shifts in the antigenic make-up of influenza A viruses provide the necessary conditions for major pandemics, whereas minor antigenic drifts give rise to less severe epidemics because immunity in the population is less blunted.
The most serious pandemic of influenza occurred in 1918, and was associated with more than 20 million deaths world-wide. In 1957, a major shift in the antigenic make-up of the virus led to the appearance of influenza A2 type H2-N2, which caused a world-wide pandemic. A further pandemic occurred in 1968 owing to the emergence of Hong Kong influenza type H3-N2, and minor antigenic drifts have caused outbreaks around the world ever since. In 1997, avian H5-N1 strain of influenza A was found in humans and represented a major change in viral surface antigens. Avian flu re-emerged in 2004-5.
Purified haemagglutinin and neuraminidase from recently circulating strains of influenza A and B viruses are incorporated in current vaccines.
Sporadic cases of influenza and outbreaks among groups of people living in a confined environment are frequent. The incidence increases during the winter months. Spread is mainly by droplet infection but fomites and direct contact have also been implicated.
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