The use of T1 oligonucleotide mapping to determine that the emergence of Canadian 1973-like and 1974-like H3N2 strains in 1984 was the result of laboratory contamination.
Influenza undergoes extensive antigenic variation in nature. These new antigenic variants invariably supplant the preceding antigenic type that then disappears. In apparent contrast to this, two H3N2 strains that were forwarded to the Laboratory Centre for Disease Control, Ottawa, in 1984 from a Canadian public health laboratory for reference analysis were shown to be most closely related to 1973 and 1974 strains. Laboratory contamination on isolation by the regional public health laboratory was the most likely explanation for the occurrence of these strains, since one of the isolates (RV/76/84) was identical by T1 mapping to an A/Eng-like isolate being grown in the laboratory of isolation. The two isolates, RV/74/84 and RV/76/84, were shown to be distinct from each other and from prototype H3N2 strains by RNase T1 oligonucleotide mapping, SDS-PAGE, peptide mapping of hemagglutinin, and hemagglutination inhibition assay. RV/74 and RV/76 appeared to have been genetically stable for the 10 to 11 years preceding 1984; this is consistent with laboratory frozen storage for this period of time. This paper demonstrates the utility of RNase T1 mapping for the characterization of novel or spurious influenza isolates.
D006801:Humans; D053122:Influenza A Virus, H3N2 Subtype; D009980:Influenza A virus / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification; D009710:Nucleotide Mapping; D009975:Orthomyxoviridae / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification; D010449:Peptide Mapping; D012367:RNA, Viral / Q000032:analysis*; D006163:Ribonuclease T1
D012367:RNA, Viral; D006163:Ribonuclease T1