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Titolo:
Mechanism of selective inhibition of respiratory syncytial virus by a benzodithiin compound (RD3-0028)
Autore:
Sudo, K; Konno, K; Watanabe, W; Shigeta, S; Yokota, T;
Indirizzi:
Rational Drug Design Labs, Fukushima 9601242, Japan Rational Drug Design Labs Fukushima Japan 9601242 kushima 9601242, Japan Fukushima Univ, Sch Med, Dept Microbiol, Fukushima 9601295, Japan Fukushima Univ Fukushima Japan 9601295 crobiol, Fukushima 9601295, Japan
Titolo Testata:
MICROBIOLOGY AND IMMUNOLOGY
fascicolo: 7, volume: 45, anno: 2001,
pagine: 531 - 537
SICI:
0385-5600(2001)45:7<531:MOSIOR>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
FUSION PROTEIN; MONOCLONAL-ANTIBODIES; ANTIVIRAL ACTIVITIES; IN-VITRO; INFECTION; MICE; GLYCOPROTEIN; IMMUNE; DERIVATIVES; RESPONSES;
Keywords:
RD3-0028; respiratory syncytial virus; F1 protein; resistant viruses;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Sudo, K Yamanouchi Pharmaceut Co Ltd, Inst Drug Discovery Res, Pharacol Labs, 21 Miyukigaoka, Tsukuba, Ibaraki 3058585, Japan Yamanouchi Pharmaceut Co Ltd 21 Miyukigaoka Tsukuba Ibaraki Japan 3058585
Citazione:
K. Sudo et al., "Mechanism of selective inhibition of respiratory syncytial virus by a benzodithiin compound (RD3-0028)", MICROB IMMU, 45(7), 2001, pp. 531-537

Abstract

RD3-0028, a compound with a benzodithiin structure, was found to be a potent inhibitor of respiratory syncytial virus (RSV) replication. Its action is specific; no activity is seen against influenza A virus, measles virus, herpes simplex virus type 1 or 2, or human cytomegalovirus, A time-dependentdrug addition experiment indicated that the antiviral activity occurs in the late stage of the RSV replication cycle, since this compound completely inhibited syncytium formation even when added up to 16 hr after the infection of cell monolayers at an MOI of 3, RD3-0028 had no direct virucidal effect on RSV, Western blotting analysis showed that RD3-0028 significantly decreased the amount of RSV proteins released into the cell culture medium. Moreover, five independent isolates of the RSV long strain were selected for growth in RD3-0028 (5-20 mug/ml). These resistant viruses were more than 80-fold less sensitive to RD3-0028 than the long strain. The F gene segment of each of these viruses was sequenced and in each case the mutant RNA segment contained at least one sequence alteration, converting asparagine 276 totyrosine (F1 protein). These results suggest that RD3-0028 inhibits RSV replication by interfering with intracellular processing of the RSV fusion protein, or a step immediately thereafter, leading to loss of infectivity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 19:52:50