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Titolo:
Multiple drug resistance genotype causing failure of antiretroviral treatment in an HIV-infected patient heavily exposed to nucleoside analogues
Autore:
Villalba, N; Gomez-Cano, M; Holguin, A; Soriano, V;
Indirizzi:
Hosp Carlos 3, Inst Salud Carlos III, Dept Infect Dis, Madrid, Spain Hosp Carlos 3 Madrid Spain d Carlos III, Dept Infect Dis, Madrid, Spain
Titolo Testata:
EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
fascicolo: 5, volume: 18, anno: 1999,
pagine: 372 - 375
SICI:
0934-9723(199905)18:5<372:MDRGCF>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
VIRUS TYPE-1 RESISTANT; REVERSE-TRANSCRIPTASE; COMBINATION THERAPY; INVITRO SELECTION; ZIDOVUDINE; MUTATIONS; 2',3'-DIDEOXYINOSINE; INHIBITORS; VARIANTS; STRAINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
14
Recensione:
Indirizzi per estratti:
Indirizzo: Soriano, V Hosp Carlos 3, Inst Salud Carlos III, Dept Infect Dis, Madrid, Spain Hosp Carlos 3 Madrid Spain I, Dept Infect Dis, Madrid, Spain
Citazione:
N. Villalba et al., "Multiple drug resistance genotype causing failure of antiretroviral treatment in an HIV-infected patient heavily exposed to nucleoside analogues", EUR J CL M, 18(5), 1999, pp. 372-375

Abstract

A 37-year-old homosexual man began antiretroviral combination therapy withdidanosine (ddI), lamivudine (3TC) and indinavir (IDV) after being exposedpreviously to zidovudine (ZDV), ddI and 3TC in different sequential regimens. The patient's viral load did not fall below a detectable level despite his adherence to drug therapy, which was considered optimal. Stavudine (d4T) was prescribed in the third month of treatment instead of ddI without anyevident improvement in the treatment response. A point mutation nested PCRassay showed that the patient carried a virus with a codon Q151M mutation,which confers multiple drug resistance to nucleoside analogues. Genetic sequence analysis showed that, despite none of the classically associated mutations to Q151M being present at the beginning of treatment, continuous genetic evolution under selective drug pressure allowed the virus to accumulate mutations at codons 62, 74 and 116 over time. As expected, the CD4+ cell count declined during the study period, and the viral load remained detectable.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 11:44:46