The influenza virus constantly changes form, thereby eluding the protective antibodies that target populations (swine, avian or human) may have developed in response to previous exposures to influenza or to influenza vaccines. Every two or three years the virus undergoes minor changes. But at intervals of roughly a decade, after the bulk of the world's population has developed some level of resistance to these minor changes, it undergoes a major change that enables it to easily infect populations around the world, often infecting hundreds of millions of people whose antibody defenses are unable to resist it. The influenza virus has also been known to change form over a much shorter period of time. For instance, during the Spanish flu pandemic, the initial wave of the disease was relatively mild, while the second wave of the disease a year later was highly lethal.
The first identification of an influenza virus as a cause of disease in pigs occurred in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, novel viruses of three different subtypes and five different genotypes emerged as agents of influenza among pigs in North America. In 1997-1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2. In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.
The H1N1 form of swine flu is one of the descendants of the Spanish flu that caused a pandemic in humans in 1918–1919. As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza. However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005.
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