Temperature-sensitive mutants of influenza A/Udorn/72 (H3N2) virus III. Genetic analysis of temperature-dependent host range mutants

Analysis of influenza A virus temperature-sensitive mutants with mutations in RNA segment 8

“…SPC45 and ICR1629 formed group H1, whereas ICR516 and UV1841 belonged to group H2, This result is in agreement with the genome structure of segment 8, which encodes two polypeptides. It should be noted, however, that ICR516 is a double-lesion mutant, having another lesion or lesions in RNA segment 3 (encoding the internal polymerase protein, PA) (Shimizu et al, 1983). Both lesions contributed to the ts phenotype as revealed by the complementation test.…”

“…In contrast, the reproduction of the virus is not impaired in mutants which have an extensive deletion at the C-terminal region of the NS1 protein (Buonagurio et al, 1984;Norton et al, 1987). Previously Shimizu et al (1982aShimizu et al ( , b, 1983 reported the isolation and characterization of ts mutants of influenza virus strain A/Udorn/72 which were classified into eight recombination groups, each corresponding to one genomic RNA segment on RMK cells. Mutants of recombination group H had ts lesion(s) in RNA segment 8, as indicated by segregation analysis, and were classified into four complementation groups on RMK cells (Shimizu et al, 1982b).…”

Studies of a Recombinant which Inherited the Haemagglutinin from the Human Influenza Virus A/Hong Kong/1/68 (H3N2) and Other Genes from Influenza Virus A/duck/Ukraine/1/63 (H3N8)

“…In the present case, this property may be due to the ability or inability of haemagglutinin to be cleaved into heavy and light chains (Klenk et al, 1982). At the same time it is possible that an hd phenotype of haemagglutinin may be associated with other properties of this protein (Shimizu et al, 1983), e.g. with properties of the haemagglutinin site responsible for attachment to a cell.…”

“…Such mutations could be the main barrier preventing the transfer of the haemagglutinin from the population of avian influenza viruses to that of human influenza viruses. According to the data available, hd mutations are likely to occur in any of the eight genes of influenza virus (Shimizu et al, 1983). Therefore, one cannot rule out the possibility that such a barrier may prevent the transfer of other genes of influenza virus from one population to another as well.…”

“…It was also shown that manifestation of the host-dependent (hd) phenotype of influenza viruses might involve the genes coding for the haemagglutinin (Klenk et al, 1982), PB2 protein (Almond, 1977) and, probably, any of the eight genes of influenza virus (Shimizu et al, 1983). Hence, one cannot rule out the possibility that host dependence may prove the main barrier hindering the transfer of genes of animal influenza viruses to the population of human influenza viruses, and vice versa.…”