Le SIDA en Afrique subsaharienne (serveur d'exploration)

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APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.

Identifieur interne : 000942 ( Ncbi/Curation ); précédent : 000941; suivant : 000943

APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.

Auteurs : Kavidha Reddy [Afrique du Sud] ; Cheryl A. Winkler ; Lise Werner ; Koleka Mlisana ; Salim S. Abdool Karim ; Thumbi Ndung'U

Source :

RBID : pubmed:19996938

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English descriptors

Abstract

In the absence of HIV-1 virion infectivity factor (Vif), cellular cytosine deaminases such as apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G) inhibit the virus by inducing hypermutations on viral DNA, among other mechanisms of action. We investigated the association of APOBEC3G mRNA levels and genetic variants on HIV-1 susceptibility, and early disease pathogenesis using viral load and CD4 T-cell counts as outcomes.

DOI: 10.1097/QAD.0b013e3283353bba
PubMed: 19996938

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pubmed:19996938

Le document en format XML

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<term>APOBEC-3G Deaminase</term>
<term>Adult</term>
<term>CD4 Lymphocyte Count</term>
<term>Cytidine Deaminase (genetics)</term>
<term>Cytidine Deaminase (metabolism)</term>
<term>Disease Progression</term>
<term>Female</term>
<term>Genotype</term>
<term>HIV Infections (blood)</term>
<term>HIV Infections (immunology)</term>
<term>HIV Infections (virology)</term>
<term>HIV-1</term>
<term>Humans</term>
<term>Point Mutation (genetics)</term>
<term>Polymorphism, Genetic</term>
<term>RNA, Messenger (blood)</term>
<term>Viral Load</term>
<term>Virion (genetics)</term>
<term>Virion (immunology)</term>
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<term>APOBEC-3G Deaminase</term>
<term>ARN messager (sang)</term>
<term>Adulte</term>
<term>Charge virale</term>
<term>Cytidine deaminase (génétique)</term>
<term>Cytidine deaminase (métabolisme)</term>
<term>Femelle</term>
<term>Génotype</term>
<term>Humains</term>
<term>Infections à VIH (immunologie)</term>
<term>Infections à VIH (sang)</term>
<term>Infections à VIH (virologie)</term>
<term>Mutation ponctuelle (génétique)</term>
<term>Numération des lymphocytes CD4</term>
<term>Polymorphisme génétique</term>
<term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term>
<term>Virion (génétique)</term>
<term>Virion (immunologie)</term>
<term>Évolution de la maladie</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Cytidine Deaminase</term>
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<keywords scheme="MESH" type="chemical" xml:lang="en">
<term>APOBEC-3G Deaminase</term>
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<term>Cytidine deaminase</term>
<term>Mutation ponctuelle</term>
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<term>Infections à VIH</term>
<term>Virion</term>
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<term>HIV Infections</term>
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<term>ARN messager</term>
<term>Infections à VIH</term>
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<term>Génotype</term>
<term>Humains</term>
<term>Numération des lymphocytes CD4</term>
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<div type="abstract" xml:lang="en">In the absence of HIV-1 virion infectivity factor (Vif), cellular cytosine deaminases such as apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G) inhibit the virus by inducing hypermutations on viral DNA, among other mechanisms of action. We investigated the association of APOBEC3G mRNA levels and genetic variants on HIV-1 susceptibility, and early disease pathogenesis using viral load and CD4 T-cell counts as outcomes.</div>
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