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Titolo:
Determinants of pantropism of the F1-R mutant of Sendai virus: specific mutations involved are in the F and M genes
Autore:
Okada, H; Seto, JT; McQueen, NL; Klenk, HD; Rott, R; Tashiro, M;
Indirizzi:
NatlnInst Infect Dis, Dept Viral Dis & Vaccine Control, Tokyo 2080011, Japa Natl Inst Infect Dis Tokyo Japan 2080011 ne Control, Tokyo 2080011, Japa Calif State Univ Los Angeles, Dept Biol & Microbiol, Los Angeles, CA USA Calif State Univ Los Angeles Los Angeles CA USA iol, Los Angeles, CA USA Univ Marburg, Inst Virol, D-3550 Marburg, Germany Univ Marburg Marburg Germany D-3550 Inst Virol, D-3550 Marburg, Germany Univ Giessen, Inst Virol, D-6300 Giessen, Germany Univ Giessen Giessen Germany D-6300 Inst Virol, D-6300 Giessen, Germany
Titolo Testata:
ARCHIVES OF VIROLOGY
fascicolo: 12, volume: 143, anno: 1998,
pagine: 2343 - 2352
SICI:
0304-8608(1998)143:12<2343:DOPOTF>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
M-PROTEIN BINDS; FUSION GLYCOPROTEIN; EPITHELIAL-CELLS; BUDDING SITE; MDCK CELLS; ACTIVATION; POLARITY; CLARA; LUNGS; HN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Tashiro, M NatliInst Infect Dis, Dept Viral Dis & Vaccine Control, Gakuen 4-7-1 Musash Natl Inst Infect Dis Gakuen 4-7-1 Musashi Murayama Tokyo Japan 2080011
Citazione:
H. Okada et al., "Determinants of pantropism of the F1-R mutant of Sendai virus: specific mutations involved are in the F and M genes", ARCH VIROL, 143(12), 1998, pp. 2343-2352

Abstract

Mutations in the fusion, F, protein of Sendai virus resulting in increasedcleavability by ubiquitous host protease(s), and mutations in the matrix, M, protein resulting in bipolar budding, are both important determinants for the systemic infection in mice caused by the protease activating pantropic mutant, F1-R. Several mutants of Sendai virus (BY, BF, and KD-M) with phenotypes of bipolar budding and/or increased cleavability off protein were isolated. Genomic RNA sequence analysis of the F and M genes of the mutants revealed that several deduced amino acids in the F and M proteins were different from those of F1-R, T-5 (a revertant of F1-R), and wild-type viruses. The BF and KD-M mutants that budded bipolarly and were also activated by ubiquitous proteases were examined for replication in tissue culture cells and in mice. All of the mutants exhibited multiple-step replication in MDCK,MDBK, and LLC-MK2 cells without trypsin, but formed plaques only in MDCK cells. One of the mutants, designated KD-52M, was similar to F1-R in that itformed plaques in all three cell lines without addition of exogenous protease. However, none of the mutant viruses, including KD-52M, caused a systemic infection in mice. The mutated M protein of F1-R enhances the disruptionof microtubles. However, none of the mutants with a bipolar budding phenotype (BY, BF, and KD-M), disrupted the microtubules to the same extent as F1-R. All of these mutants had mutations in the M protein that were differentfrom those found in F1-R. Taken together, these results suggest that mutations at Ser115 to Pro in the F protein and at Asp 128 to Gly and Ile210 to Thr in the M protein of F1-R are the mutations specifically required for the systemic infection caused by F1-R.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 10:31:58