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The science behind the H1N1 virus is key to understanding why it is so difficult to produce effective anti-viral treatments.
Influenza is caused by members of the same family of RNA viruses, called orthomyxoviridae (1). These are not the same virus that causes the common cold, despite many of the symptoms of infection being quite similar. Flu viruses can infect mammals and birds, although different strains of the virus are generally predominantly found in certain species. The Influenza A subtype mainly infects birds, influenza B is mostly found in humans, and influenza C, the least common of the subtypes, mostly infects dogs, pigs and humans (2). Virus StructureAll three virus types have a very similar structure and are made up of the same components. They are usually spherical, and consist of a spherical outer envelope, with a diameter of around 100 nm (about a ten-thousandth [0.0001] of a millimetre), surrounding the genetic material in the centre (2). While the best-known genetic material is DNA, these viruses instead have RNA. The genes on the RNA encode the components of the virus particle itself, so that it can replicate once inside a host cell.This RNA actually reverse-codes for DNA; once a virus particle has invaded a cell, it can utilise the cells own machinery to make strands of DNA out of its RNA. The host cell then makes the protein components of the virus in the normal way, from the newly produced DNA. Classification of VirusesInfluenza A viruses are classified according to two classes of glycoproteins – proteins that contain chains of sugar - on the surface of the envelope: hemagglutinin (HA) and neuraminidase (NA). HA mediates the attachment of the virus to the surface of the cell it is about to infect. It is variants of these that determine the name of the virus (2). Avian subtypes of influenza A include H1 to H15 and N1 to N9, while human subtypes include H1N1, H3N2, H1N2 and H2N2 (3). Why Are There No Reliable Treatments?Anti-virus treatments work by tagging proteins on the surface, so that they are then recognised by the immune system as targets for destruction. This relies on the surface proteins being relatively stable and unchanging, as even a single point mutation stops the treatment from recognising the virus. However, viruses have a tendency to mutate. In fact, the flu virus can mutate 50% of its proteins and still remain functional (1). This means that it is very difficult to design a treatment that will recognise a virus for very long. Variation Aids EvasionSubtle differences in the proteins that lie on the surface of the 'flu virus particles determine their ability to infect different species, and also help these microorganisms to evade detection and destruction by the immune system. References
The copyright of the article The Science of Swine Flu in Human Infections is owned by Lindsay Napier. Permission to republish The Science of Swine Flu in print or online must be granted by the author in writing.
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