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Origin of current influenza H1N1 virus by Vincent Racaniello on 2 March 2009 influenza-oligonucleotide-mapInfluenza viruses of two subtypes, H1N1 and H3N2, have been causing respiratory infections in humans since 1977. Before that year, it was believed that only one human subtype circulated each flu season. How did this unusual situation come about? Major changes in the surface glycoproteins of influenza virus – called antigenic shift – lead to worldwide epidemics of influenza known as pandemics. There have been six instances of antigenic shift since 1889. In that year, H2N2 viruses circulated, followed by H3N8 in 1900, H1N1 in 1918, H2N2 in 1957, H3N2 in 1968, and H1N1 in 1977. Each pandemic strain carries HA and NA proteins that have been absent in humans for many years, and therefore immunity is either very low or nonexistent. Influenza viruses of the H3N2 subtype were still circulating in humans in May of 1977 when H1N1 viruses were isolated in China and then Russia. In the winter of 1977-78 the H1N1 viruses caused epidemic infection throughout the Northern Hemisphere. The results of serological tests indicated that the HA and NA glycoproteins of the 1977 H1N1 viruses were very similar to those from viruses of the same subtype which circulated in 1950. Palese’s group compared viral RNA of one 1977 isolate, A/USSR/90/77, with RNA from a virus isolated in 1950. To their surprise, the two viral RNAs were highly related. In contrast, there was less similarity between viral RNAs from the 1977 H1N1 virus and H1N1 viruses that circulated in humans between 1947 and 1956. Why were the viral genomes of the 1977 H1N1 isolate and the 1950 virus so similar? If the H1N1 viruses had been replicating in an animal host for 27 years, far more genetic differences would have been identified. The authors suggested several possibilities, but only one is compelling: …it is possible that the 1950 H1N1 influenza virus was truly frozen in nature or elsewhere and that such a strain was only recently introduced into man. The suggestion is clear: the virus was frozen in a laboratory freezer since 1950, and was released, either by intent or accident, in 1977. This possibility has been denied by Chinese and Russian scientists, but remains to this day the only scientifically plausible explanation. The close genetic identity between the 1950 and 1977 H1N1 strains was revealed by oligonucleotide mapping. In this technique, purified viral RNA is cleaved with an enzyme, RNAse T1, that cuts the RNA after every G base. The oligonucleotides are labeled at the 5′-end with 32P, separated by two-dimensional gel electrophoresis, and detected by exposing the gel to X-ray film. The oligonucleotides form a pattern (’fingerprint’, pictured) that can reveal genetic differences between virus isolates. This technique is more sensitive than serologic assays, but only provides information on about 10-15% of the viral RNA. However, the larger oligonucleotides are a representative sample of the entire genome. The authors calculated that there was a minimum of 8 bases changes among the large oligonucleotides of the RNAs of the 1950 and 1977 H1N1 viruses. In contrast, the RNA of the 1977 H1N1 isolate had 38 base changes compared with a 1947 H1N1 isolate. Oligonucleotide mapping was used to study the genome of the 1977 H1N1 viruses because nucleotide sequencing was not yet in widespread use. Because nucleotide sequencing is now routine, oligonucleotide mapping is no longer used – as scientists like to say, it has been relegated to the museum of obsolete experimental methods.
Swine Flu, a Disease of Young Adults When A/H1N1 "swine flu" broke out in North America and then the world in 2009, initial reports suggested it may have been following the pattern of the 1918 flu. In its first update on 2009 A/H1N1 swine flu, dated April 24, the World Health Organization reported: "The majority of these cases have occurred in otherwise healthy young adults. Influenza normally affects the very young and the very old, but these age groups have not been heavily affected in Mexico." It further noted that the fact that young adults were heavily affected was "of high concern." The A/H1N1 swine flu has turned out to be far less deadly than was initially feared. Yet as the pandemic has progressed, a peculiar pattern has emerged: the elderly are not catching it, by and large. Why do older people seem to be immune to swine flu? Why are the Elderly Immune? A possible answer to this puzzling question was published as a report in the journal Science in May 2009: The elderly may have already been exposed! To understand how this is possible, it is necessary to know the history of the H1 component of influenza A. H1 is a subtype of the virus protein hemagglutinin. The H1 in both swine flu and human flu has a common ancestor. Between the 1918 and 1957 influenza pandemics, H1 circulated in humans, evolving continuously. H1 then became inactive, replaced by other subtypes of hemagglutinin such as H3. H1 in humans reappeared in 1977 and has been a dominant subtype of human flu ever since. It has evolved significantly from 1977 to the present. One could call this version "New H1." In pigs, meanwhile, the H1 has evolved very little. Swine flu H1 has been very similar to the "original" 1918 and 1930 versions of H1. One could call this version "Old H1." To the immune system, Old H1 is very different from New H1. It may be speculated that most people born before 1957 were exposed to human H1 influenza, which at that time was similar to Old H1. Their immune systems produced antibodies to Old H1. Since Old H1 has not been seen in humans in many years, younger people do not have antibodies to Old H1. Meanwhile, the H1 in 2009 A/H1N1 swine flu — as in all H1 swine flu — is very close to Old H1. Since most older people probably have antibodies to Old H1, they are immune to this new swine flu. Younger people are not so lucky, and this is why swine flu mainly affects younger adults. Read more: www.brighthub.com...
Originally posted by angelx666
1977 'swine flu' was pollonium poisoning