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M9480855.TXT
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1994-09-05
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Document 0855
DOCN M9480855
TI Cellular mechanisms account for decreased anti-HIV-1 activity of
nucleoside analogs.
DT 9410
AU Doerr HW; Cinatl J Jr; Weber B; Cinatl J; Department of Medical
Virology, J.W. Goethe University,; Frankfurt/M, Federal Republic of
Germany.
SO Abstr Gen Meet Am Soc Microbiol. 1994;94:484 (abstract no. T-14). Unique
Identifier : AIDSLINE ASM94/94313090
AB We tested whether cellular mechanisms (cell resistance) may account for
decreased anti-HIV-1 activity of nucleoside analogs. For this aim
several MOLT-4 cell sublines were established which exerted resistance
against toxic effects of nucleoside analogs including AZT, ddI or ddC
and MOLT-4 subline resistant to different cytotoxic agents (e.g.
vincristine, daunomycin) so-called multidrug resistance. The results
showed that anti-HIV-1 activities of AZT, ddI and ddC were significantly
decreased in MOLT-4 sublines resistant to the respective nucleoside
kinases. In the multidrug resistant MOLT-4 subline which expressed high
levels of P-glycoprotein significantly decreased anti-HIV-1 activities
of AZT and ddI were demonstrated. This effect was associated with
decreased accumulation of the nucleoside analogs in the multidrug
resistant cells. Our in vitro results showed that different cellular
mechanisms (other than virus itself) may account for failure of
nucleoside analogs to inhibit efficiently HIV replication.
DE Carrier Proteins/BIOSYNTHESIS Cell Line Didanosine/*TOXICITY Drug
Resistance Human HIV-1/*DRUG EFFECTS/PHYSIOLOGY Membrane
Glycoproteins/BIOSYNTHESIS Tumor Cells, Cultured Virus
Replication/*DRUG EFFECTS Zalcitabine/*TOXICITY Zidovudine/*TOXICITY
MEETING ABSTRACT
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).