R5 varianty HIV 1 přednostně infikují T buňky typu CD62L- CD4+ a jsou potenciálně rezistentní vůči nukleosidovým inhibitorům reverzní transkriptázy

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F06%3A00048943" target="_blank" >RIV/68378050:_____/06:00048943 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors

Popis výsledku v původním jazyce

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 resultcorrelated 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.

Název v anglickém jazyce

R5 variants of human immunodeficiency virus type 1 preferentially infect CD62L- CD4+ T cells and are potentially resistant to nucleoside reverse transcriptase inhibitors

Popis výsledku anglicky

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 resultcorrelated 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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2006

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Virology

ISSN

0022-538X

e-ISSN

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Svazek periodika

80

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

854-865

Kód UT WoS článku

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EID výsledku v databázi Scopus

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