Replication of Two Influenza Virus Strains and a Recombinant in HEF and LEP Cells

Ghendon, Y. Z.; Tučková, Eva; Vonka, V.; Klimov, Alexander; Ginzburg, V. P.; Markushin, S. G.

doi:10.1099/0022-1317-44-1-179

Cited by 7 publications

(3 citation statements)

References 11 publications

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“…Impairment in cleavage of the HA polypeptide under non-permissive conditions may be due to a mutation in the neuraminidase since there are data available suggesting involvement of the neuraminidase in the haemagglntinin cleavage (8,28). That virions of the mutant are not formed under non-permissive conditions (2, 5) is unlikely to be associated with the impMrment in haemagglutinin cleavage since this defect normally does not prevent formation of virions, although being noninfectious (16,18,22).…”

Section: Discussionmentioning

confidence: 98%

Functional defects of fowl plague virus temperature-sensitive mutant having mutation in the neuraminidase

Ghendon¹,

Markushin²,

Ginzburg³

et al. 1983

Archives of Virology

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A fowl plague virus (FPV) temperature-sensitive mutant ts 5 having mutation lesions in the gene coding for the neuraminidase has been obtained. The mutant induced synthesis of cRNA, vRNA and proteins in cells under non-permissive conditions, but formation of virions including non-infectious ones was defective. The neuraminidase and haemagglutinin synthesized under non-permissive conditions possessed functional activity and could migrate from the rough endoplasmic reticulum into plasma membranes; however, cleavage of the haemagglutinin was reduced. In ts 5-infected cells under non-permissive conditions the synthesis of segments 5 and 8 of cRNA and vRNA was predominant both early and late in the reproduction cycle, and the synthesis of P1, P2, P3, HA and M proteins was reduced after approximately 3 hours. The data obtained suggest that involvement of the neuraminidase in the formation of infectious virions may have no direct association with the enzymatic activity of this protein, and that the mutation in the neuraminidase may affect regulation of replication and transcription processes.

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Section: Discussionmentioning

confidence: 98%

Functional defects of fowl plague virus temperature-sensitive mutant having mutation in the neuraminidase

Ghendon¹,

Markushin²,

Ginzburg³

et al. 1983

Archives of Virology

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“…Therefore the CR43-3 hr mutant is not a td-hr mutant, but simply a hr mutant. Host range mutants that are not td-hr mutants have been associated with polymerase genes (Almond, 1977) or with the HA and NA genes (Schulman and Palese, 1977;Ghendon, et al, 1979;Bosch, et aZ., 1979). The CR43-3 hr mutant is independent of the HA and NA genes, but as noted earlier in the CR55 reassortants, the NP and RNA3 genes from the CR43-3 parent co-reassorted with the aberrant NS gene.…”

Section: Fig 2 Genotype Determination Of Rna4-8 For Cr43 Reassortamentioning

confidence: 99%

“…(1) those involving cleavage of the HA gene due to the presence of a particular NA gene (Schulman and Palese, 1977;Ghendon et aL, 1979;Nakajima and Suigiura, 1980) or due just to the presence of a particular HA gene (Bosch et al, 1979); and (2) hr mutants with an extended host range due to a mutation in a polymerase gene (Almond, 1977). Polymerase genes were also involved in the td-hr mutants (Scholtissek and Murphy, 1978;Israel, 1980).…”

Section: Introductionmentioning

confidence: 99%

Characterization of an influenza a host range mutant

Maassab¹,

DeBorde²

1983

Virology

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A mixed infection of primary chick kidney cells at 38 degrees with A/Ann Arbor/6/60 cold adapted virus and A/Alaska/6/77 wt virus yielded a cold-reassortant virus, CR43-clone 3, which had a host range different from that of either parent. It does not produce detectable virus when grown in Madin-Darby canine kidney cells, while growing normally in primary chick kidney cells at 33 degrees. Both parents, however, grow well in either cell type at 33 degrees C. Genotypic analysis of viral RNA electrophoresed in polyacrylamide gels has shown that CR43-clone 3 virus has an aberrant NS gene different from the NS gene of either parent virus. Reassortant viruses made between CR43-clone 3 virus and A/California/10/78 (H1N1) virus in primary chick kidney cells at 33 degrees showed the same host range restriction only if the NS gene was derived from the CR43-clone 3 virus. A mixed infection with these same parents, but in Madin-Darby canine kidney cells at 33 degrees C, produced reassortants that always contained the A/California/10/78 NS gene instead of the CR43-clone 3 NS gene. Ferrets inoculated intranasally with the CR43-clone 3 reassortant do not become sick or infected, based on the lack of symptoms: no rhinitis, coryza, or fever; and no detectable virus recovered from nasopharyngeal swabs, turbinate, or lung tissues at 48 hr after infection. Thus, CR43-clone 3 virus contains an aberrant NS gene and manifests a restricted host range phenotype in Madin-Darby canine kidney cells and ferrets.

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Mutants of Influenza Virus

Mahy¹

1983

Genetics of Influenza Viruses

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Replication of Two Influenza Virus Strains and a Recombinant in HEF and LEP Cells

Cited by 7 publications

References 11 publications

Functional defects of fowl plague virus temperature-sensitive mutant having mutation in the neuraminidase

Functional defects of fowl plague virus temperature-sensitive mutant having mutation in the neuraminidase

Characterization of an influenza a host range mutant

Mutants of Influenza Virus

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