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Titolo:
A mutation in human immunodeficiency virus type 1 protease, N88S, that causes in vitro hypersensitivity to amprenavir
Autore:
Ziermann, R; Limoli, K; Das, K; Arnold, E; Petropoulos, CJ; Parkin, NT;
Indirizzi:
ViroLog Inc, S San Francisco, CA 94080 USA ViroLog Inc S San Francisco CAUSA 94080 c, S San Francisco, CA 94080 USA Ctr Adv Biotechnol & Med, Piscataway, NJ 08854 USA Ctr Adv Biotechnol & Med Piscataway NJ USA 08854 Piscataway, NJ 08854 USA Rutgers State Univ, Dept Chem, Piscataway, NJ 08854 USA Rutgers State Univ Piscataway NJ USA 08854 Chem, Piscataway, NJ 08854 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 9, volume: 74, anno: 2000,
pagine: 4414 - 4419
SICI:
0022-538X(200005)74:9<4414:AMIHIV>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VITRO; HIV-INFECTION; INHIBITOR; THERAPY; RESISTANCE; VX-478; COMBINATION; SITE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Parkin, NT 270 E Grand Ave, S San Francisco, CA 94080 USA 270 E Grand AveS San Francisco CA USA 94080 sco, CA 94080 USA
Citazione:
R. Ziermann et al., "A mutation in human immunodeficiency virus type 1 protease, N88S, that causes in vitro hypersensitivity to amprenavir", J VIROLOGY, 74(9), 2000, pp. 4414-4419

Abstract

Amprenavir (Agenerase, 141-W94, VX-478) is a human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PRI) recently approved for the treatmentof HIV-1 infection in the United States, A major cause of treatment failure is the development of resistance to PRIs, One potential use for amprenavir is as salvage therapy for patients for whom treatment that includes one (or more) of the other four currently approved PRIs-saquinavir, indinavir, ritonavir, and nelfinavir-has failed. We evaluated the cross-resistance to amprenavir of viruses that evolved during treatment with the two most commonly prescribed PRIs, nelfinavir and indinavir, Unexpectedly, a dramatic increase in susceptibility (2.5- to 12.5-fold) was observed with 20 of 312 (6.4%) patient viruses analyzed, The most pronounced increases in susceptibility were strongly associated with an N88S mutation in protease, All viruses that carried the N88S mutation were hypersensitive to amprenavir, Site-directed mutagenesis studies confirmed the causal role of N88S in determining amprenavir hypersensitivity. The presence of the N88S mutation and associatedamprenavir hypersensitivity may be useful in predicting an improved clinical response to amprenavir salvage therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/10/20 alle ore 08:58:28