Pathways of evolution of influenza A (H1N1) viruses from 1977 to 1986 as determined by oligonucleotide mapping and sequencing studies.

The evolutionary relationships of epidemic influenza A (H1N1) viruses isolated between 1982 and 1986 have been examined by oligonucleotide mapping and partial DNA sequencing. The T1 mapping studies confirmed our previous report that the evolution of the influenza virus genome generally results in an average of four to six oligonucleotide changes per year. Between 1982 and 1986, however, two apparent exceptions to this finding occurred. H1N1 antigenic variants (including the A/Chile/83 and A/Victoria/83 reference strains) that caused influenza outbreaks and epidemics from 1983 to 1984 differed by 20 to 30 oligonucleotides from viruses isolated during the previous influenza season. T1 mapping of individual RNA segments and sequencing revealed that all six internal genes of a representative 1983 A/Chile-like virus were more closely related to genes of non-reassortant H1N1 viruses that circulated from 1977 to 1982 than to genes of H3N2 viruses. Therefore, the 1983 variant viruses were not H1N1-H3N2 reassortants. The A/Taiwan/86-like H1N1 antigenic variants that emerged in south-east Asia in the spring of 1986 and caused epidemic activity the following winter also exhibited changes of 20 to 30 oligonucleotides from the A/Chile/83-like or A/Victoria/83-like H1N1 viruses that circulated during the previous influenza season. Fewer oligonucleotide changes were observed between the 1986 A/Taiwan/86-like and H1N1 viruses isolated before 1983, however, suggesting that the former evolved from viruses that circulated before the 1983 antigenic variants became the predominant H1N1 epidemic virus strains. This was confirmed by sequencing the HA1 domain of the haemagglutinin genes of three A/Taiwan/86-like viruses. These studies provide evidence that other genes of influenza A viruses, in addition to the haemagglutinin gene, may evolve concurrently along two or more separate pathways.