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Titolo:
POTENT INHIBITION OF RESPIRATORY SYNCYTIAL VIRUS-REPLICATION USING A 2-5A-ANTISENSE CHIMERA TARGETED TO SIGNALS WITHIN THE VIRUS GENOMIC RNA
Autore:
PLAYER MR; BARNARD DL; TORRENCE PF;
Indirizzi:
NIDDKD,SECT BIOMED CHEM,MED CHEM LAB,NIH,BLDG 8,ROOM B2A02 BETHESDA MD 20892 NIDDKD,SECT BIOMED CHEM,MED CHEM LAB,NIH BETHESDA MD 20892 UTAH STATE UNIV,INST ANTIVIRAL RES LOGAN UT 84362
Titolo Testata:
Proceedings of the National Academy of Sciences of the United Statesof America
fascicolo: 15, volume: 95, anno: 1998,
pagine: 8874 - 8879
SICI:
0027-8424(1998)95:15<8874:PIORSV>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTISENSE OLIGODEOXYNUCLEOTIDES; THERAPEUTIC AGENTS; SEQUENCE-ANALYSIS; 2-5A ANTISENSE; GENE; OLIGONUCLEOTIDES; RIBONUCLEASE; SUBGROUP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
M.R. Player et al., "POTENT INHIBITION OF RESPIRATORY SYNCYTIAL VIRUS-REPLICATION USING A 2-5A-ANTISENSE CHIMERA TARGETED TO SIGNALS WITHIN THE VIRUS GENOMIC RNA", Proceedings of the National Academy of Sciences of the United Statesof America, 95(15), 1998, pp. 8874-8879

Abstract

The 2-5A system is a recognized mechanistic component of the antiviral action of interferon. Interferon-induced 2-5A synthetase generates 2-5A, which, in turn, activates the latent constitutive RNase L that degrades viral RNA. Chemical conjugation of 2-5A to an antisense oligonucleotide can target the 2-5A-dependent RNase L to the antisense-specified RNA and effect its selective destruction. Such a 2-5A-antisense chimera (NIH351) has been developed that targets a consensus sequence within the respiratory syncytial virus (RSV) genomic RNA. NIH351 was 50-to 90-fold more potent against RSV strain A2 than was ribavirin, the presently approved drug for clinical management of RSV infection. It was similarly active against a variety of RSV strains of both A and B subgroups and possessed a cell culture selectivity index comparable to ribavirin. In addition, the anti-RSV activity of NIH351 was shown to be virus-specific and a result of a true antisense effect, because a scrambled nucleotide sequence in the antisense domain of NIH351 caused asignificant decrease in antiviral activity. The 2-5A system's RNase Lwas implicated in the mechanism of action of NIH351 because a congener with a disabled 2-5A moiety was of greatly reduced anti-RSV effectiveness. These findings represent an innovative approach to the control of RSV replication.

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Documento generato il 30/09/20 alle ore 09:38:31