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| rdf:type
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| Description
| - V ex-vivo infikované lidské lymfoidní tkáni a v PBMC jsme sledovali vliv aktivace CD4+ T buněk na převažující výskyt R5 nebo X4 variant HIV-1 v různých subpopulacích CD4+ T buněk. V těchto systémech jsme dále sledovali citlivost replikace HIV k inhibitorům reverzní transkriptázy. Prokázali jsme, že R5 varianty HIV-1 přednostně vyvolávají produktivní infekci v pomalu se dělících HLA-DR- CD62L- CD4+ T buňkách. Naproti tomu X4 varianty HIV-1 vyvolávají produktivní infekci přednostně v aktivovaných HLA-DR+ CD62L+ CD4+ T buňkách. Schopnost nukleozidových inhibitorů reverzní transkriptázy inhibovat HIV-1 replikaci byla 20krát vyšší v aktivovaných T buňkách než v pomalu se dělících HLA-DR- CD62L- CD4+ T buňkách. Hladina thymidin kinázové mRNA korelovala s intenzitou buněčného růstu a byla vyšší v buňkách citlivých na nukleozidové inhibitory reverzní transkriptázy. Nenukleozidový inhibitor reverzní transkriptázy byl stejně účinný v obou typech buněk. (cs)
- We investigated the effect of the activation status of CD4+ T cells on the predominance of R5 and X4 HIV-1 variants in different subsets of CD4+ T cells in ex vivo-infected human lymphoid tissues and PBMCs. In these cell systems, we examined the sensitivity of HIV replication to reverse transcriptase inhibitors. We demonstrate that R5 HIV-1 variants preferentially produced productive infection in slowly dividing HLA-DR- CD62L- CD4+ T cells. In contrast, X4 HIV-1 variants preferentially produced productive infection in activated HLA-DR+ CD62L+ CD4+ T cells. The abilities of the nucleoside reverse transcriptase inhibitors to stop HIV-1 replication were 20 times greater in activated T cells than in slowly dividing HLA-DR- CD62L- CD4+ T cells. Thes result correlated with higher levels of thymidine kinase mRNA in activated than in slowly dividing HLA-DR- CD62L- CD4+ T cells. The non-nucleoside reverse transcriptase inhibitor was equally efficient in both cell substets.
- We investigated the effect of the activation status of CD4+ T cells on the predominance of R5 and X4 HIV-1 variants in different subsets of CD4+ T cells in ex vivo-infected human lymphoid tissues and PBMCs. In these cell systems, we examined the sensitivity of HIV replication to reverse transcriptase inhibitors. We demonstrate that R5 HIV-1 variants preferentially produced productive infection in slowly dividing HLA-DR- CD62L- CD4+ T cells. In contrast, X4 HIV-1 variants preferentially produced productive infection in activated HLA-DR+ CD62L+ CD4+ T cells. The abilities of the nucleoside reverse transcriptase inhibitors to stop HIV-1 replication were 20 times greater in activated T cells than in slowly dividing HLA-DR- CD62L- CD4+ T cells. Thes result correlated with higher levels of thymidine kinase mRNA in activated than in slowly dividing HLA-DR- CD62L- CD4+ T cells. The non-nucleoside reverse transcriptase inhibitor was equally efficient in both cell substets. (en)
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| Title
| - R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors
- R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors (en)
- R5 varianty HIV 1 přednostně infikují T buňky typu CD62L- CD4+ a jsou potenciálně rezistentní vůči nukleosidovým inhibitorům reverzní transkriptázy (cs)
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| skos:prefLabel
| - R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors
- R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors (en)
- R5 varianty HIV 1 přednostně infikují T buňky typu CD62L- CD4+ a jsou potenciálně rezistentní vůči nukleosidovým inhibitorům reverzní transkriptázy (cs)
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| skos:notation
| - RIV/68378050:_____/06:00048943!RIV07-AV0-68378050
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| http://linked.open.../vavai/riv/strany
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/68378050:_____/06:00048943
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - HIV 1; inhibitors of reverse transcriptase (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...odStatuVydavatele
| - US - Spojené státy americké
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...i/riv/nazevZdroje
| |
| http://linked.open...in/vavai/riv/obor
| |
| http://linked.open...ichTvurcuVysledku
| |
| http://linked.open...cetTvurcuVysledku
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| http://linked.open...UplatneniVysledku
| |
| http://linked.open...v/svazekPeriodika
| |
| http://linked.open...iv/tvurceVysledku
| - Blažková, Jana
- Hirsch, I.
- Trejbalová, Kateřina
- Pion, M.
- Gondois-Rey, F.
- Biancotto, A.
- Bettendroffer, L.
- Fernandez, M. A.
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| http://linked.open...n/vavai/riv/zamer
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| issn
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| number of pages
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| is http://linked.open...avai/riv/vysledek
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