1980
DOI: 10.1139/m80-227
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The complete neuraminidase of influenza A/PR8/34 (H0N1) is not detectable in its recombinant virus

Abstract: The neuraminidase located on the influenza virus recombinant A/Eq (Heq1) x A/PR8 (N1) was relatively a poor antigen (NI titre less than 10) as compared with the enzyme present on the parent virus A/PR8/34 (H0N1) (NI titre 160). This difference in the antigenic behavior of the neuraminidase of A/PR8/34 (H0N1) virus was explored. Results obtained showed that rabbit anti-A/PR8/34 (H0N1) serum contained two distinct types of antineuraminidase antibody and only one type of antineuraminidase antibody was precipitabl… Show more

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Cited by 4 publications
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“…In a special case, by using ts mutants of NA and NP genes, Thierry & Spring (1980) detected intragenic complementation of NA and NP proteins. It has also been reported that the structure of the NA protein of a reassortant virus is different from that of the parental virus (Arora & Hill-Schubert, 1980). These reports suggested that NA structure and NA activity could be affected by other viral gene products.…”
Section: Discussionmentioning
confidence: 99%
“…In a special case, by using ts mutants of NA and NP genes, Thierry & Spring (1980) detected intragenic complementation of NA and NP proteins. It has also been reported that the structure of the NA protein of a reassortant virus is different from that of the parental virus (Arora & Hill-Schubert, 1980). These reports suggested that NA structure and NA activity could be affected by other viral gene products.…”
Section: Discussionmentioning
confidence: 99%
“…Alternatively,j point mutations may have occurred in one or more genes during the in vitro recombination event and, although subsequent cloning may yield variants with gene segments of identical parental origin, they would be genetically different. Such mutants may arise readily on sequential passage of virus (Brand & Palese, 1980) and have been noted to occur during recombination (Erickson & Kilbourne, 1980;Arora & Hill-Schubert, 1980). Whether the variations in the haemagglutinin and gene 2 product are responsible for the virulence differences of clones DC 2 and DC 9 cannot, however, be deduced from the limited information available.…”
Section: Virulence Comparisons Of Recombinant Clones With Genetic Commentioning
confidence: 99%