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Titolo:
FINE MECHANISMS OF ECTROMELIA VIRUS THYMIDINE KINASE-NEGATIVE MUTANTSAVIRULENCE
Autore:
KOCHNEVA GV; URMANOV IH; RYABCHIKOVA EI; STRELTSOV VV; SERPINSKY OI;
Indirizzi:
NPO VECTOR,INST MOLEC BIOL KOLTSOV RUSSIA
Titolo Testata:
Virus research
fascicolo: 1, volume: 34, anno: 1994,
pagine: 49 - 61
SICI:
0168-1702(1994)34:1<49:FMOEVT>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
VACCINIA VIRUS; EXPRESSION; VIRULENCE; GENE; RECOMBINANTS; PROTEIN; VECTOR; INVIVO; MICE;
Keywords:
ECTROMELIA VIRUS; TK- MUTANT; BETA-GALACTOSIDASE ESCHERICHIA COLI; VIRULENCE; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
22
Recensione:
Indirizzi per estratti:
Citazione:
G.V. Kochneva et al., "FINE MECHANISMS OF ECTROMELIA VIRUS THYMIDINE KINASE-NEGATIVE MUTANTSAVIRULENCE", Virus research, 34(1), 1994, pp. 49-61

Abstract

Three independently selected spontaneous thymidine kinase-negative mutants (TK(-)phenotype) and a recombinant with Escherichia coli beta-galactosidase gene (LacZ(+) phenotype) inserted in the viral thymidine kinase gene (tk) were derived from a plaque-cloned isolate of K-1 ectromelia virus strain (TK+ phenotype). Dramatically decreased virulence of TK- variants was observed for all routes of mouse inoculation. The kinetics of TK+ and TK- variants in various target organs indicated a significant decrease of production and dissemination of TK- mutants andrecombinant in the organs of mice. In the spleen and liver of intranasally or intracerebrally infected mice TK- virus was not detected during the entire period of observation. Analysis of organs homogenates ofmice intranasally infected by a mixture of recombinant with TK(-)LacZ(+) phenotype and parental isolate with TK(+)LacZ(-) phenotype on the monolayers of TK- cells indicated that only white plaques (LacZ(-)) with the TK+ phenotype appeared from liver and spleen homogenates. Thus,the mouse acts as a live filter much more efficiently than any other selective systems. Ultrastructural studies showed that viral damage inanimals infected by TK- variants was far less than that observed in mice, infected with wild type of ectromelia virus and pathological lessions were slight and reversible. Replication of ectromelia virus TK- variants was blocked at the viroplasma stage in cells with a high levelof differentiation in contrast to TK+ variants. Most likely, such restriction of target cells assortment is the general reason of reduced virulence in the case of tk-gene inactivation.

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Documento generato il 29/11/20 alle ore 10:36:12