Opinion - Swine Flu H1N1

The latest animal to human virus mutation, the Mexican Swine Flu or H1N1 again demonstrates the capacity of viruses to mutate and literally jump species with relative ease. New Scientist (2 May 2009) points out that the virus was genetically stable until 1976 as a mild, purely swine flu. In that year it affected people at a military camp in New Jersey and by 1998, the virus had hybridised with human and bird flu viruses. The current version of H1N1 in Mexico has surface proteins from Swine flu virus, five swine flu genes, two avian flu genes and one human flu gene (shown above). The surface protein being the swine version means that human antibodies will not recognise it.

The other matter which comes to mind is the use of antibiotics in animal husbandry - the use of antibiotics is widespread in farming and while it prevents animals from becoming sick, it does not prevent initial infection nor the transmission of disease. Connected to this aspect is the potential risk of an infection becoming antibiotic resistant as large scale farms become in effect, incubation laboratories.

An example which springs to mind is 'Golden staph' or Staphylococcus aureus which is mostly associated with hospital acquired infections, mainly post-operative. Since the mid 1990s antibiotic resistant 'Golden Staph' has been detected in abattoirs in the meat and livestock industry and also in site sampling in the general community.

The high use of antibiotics with animals has been in use for decades but with some bacterium common to various species and also humans and some viruses developing the capacity to leap between species, how long will it be before such a step takes place and humans face an infection (viral or bacteria), created in farming and resistant to any treatment?