1992
DOI: 10.1099/0022-1317-73-2-359
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Construction of vaccinia virus recombinants expressing several measles virus proteins and analysis of their efficacy in vaccination of mice

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Cited by 70 publications
(36 citation statements)
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References 46 publications
(42 reference statements)
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“…The only cross-reacting antibody induced by the W recombinants was directed against the F protein. No cross-neutralizing antibodies for any of the MV proteins were observed (Wild et al, 1992). Furthermore, the same protection was observed when the animals were challenged 9 days after vaccination suggesting that a CMI response may be involved.…”
Section: Discussionmentioning
confidence: 69%
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“…The only cross-reacting antibody induced by the W recombinants was directed against the F protein. No cross-neutralizing antibodies for any of the MV proteins were observed (Wild et al, 1992). Furthermore, the same protection was observed when the animals were challenged 9 days after vaccination suggesting that a CMI response may be involved.…”
Section: Discussionmentioning
confidence: 69%
“…The VV recombinants expressing the HA, F, NP and M proteins of MV, VV HA, VV-F, VV NP and VV-M respectively, are as previously described (Drillien et al, 1988;Wild et al, 1992Wild et al, , 1993. Viruses were grown in HeLa cells and titrated on Vero cells.…”
Section: Methodsmentioning
confidence: 99%
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“…This gene, designated KIL according to the nomenclature of Rosel et al (1986) for open reading frames (ORFs) on the HindIII restriction map of VV, was shown to encode an early protein ofM r 30K (Gillard et al, 1986). Unexpectedly, when the K1L gene was deleted from wt VV, the virus retained the ability to multiply in human cells but lost the capacity to multiply in RKI3 cells Wild et al, 1992). This suggested that another gene functionally equivalent to K1L for multiplication in human cells was present in the VV genome.…”
mentioning
confidence: 99%
“…To construct a recombinant virus lacking both C7L and K1L chick embryo fibroblasts were co-infected with VVIV043 and VV-NP. K1L is deleted in the latter, giving rise to plaques on permissive cells in which cell aggregation is considerably less extensive than in wt VV plaques (Wild et al, 1992). Recombinant virus that retained both the modifications introduced into the parental viruses could be recognized, therefore, by visual screening for the plaque morphology typical of a K1L-defective virus and for the blue plaque phenotype.…”
mentioning
confidence: 99%