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 : 000943APOBEC3G 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'USource :
- AIDS (London, England) [ 1473-5571 ] ; 2010.
Descripteurs français
- KwdFr :
- APOBEC-3G Deaminase, ARN messager (sang), Adulte, Charge virale, Cytidine deaminase (génétique), Cytidine deaminase (métabolisme), Femelle, Génotype, Humains, Infections à VIH (immunologie), Infections à VIH (sang), Infections à VIH (virologie), Mutation ponctuelle (génétique), Numération des lymphocytes CD4, Polymorphisme génétique, VIH-1 (Virus de l'Immunodéficience Humaine de type 1), Virion (génétique), Virion (immunologie), Évolution de la maladie.
- MESH :
- génétique : Cytidine deaminase, Mutation ponctuelle, Virion.
- immunologie : Infections à VIH, Virion.
- métabolisme : Cytidine deaminase.
- sang : ARN messager, Infections à VIH.
- virologie : Infections à VIH.
- APOBEC-3G Deaminase, Adulte, Charge virale, Femelle, Génotype, Humains, Numération des lymphocytes CD4, Polymorphisme génétique, VIH-1 (Virus de l'Immunodéficience Humaine de type 1), Évolution de la maladie.
English descriptors
- KwdEn :
- APOBEC-3G Deaminase, Adult, CD4 Lymphocyte Count, Cytidine Deaminase (genetics), Cytidine Deaminase (metabolism), Disease Progression, Female, Genotype, HIV Infections (blood), HIV Infections (immunology), HIV Infections (virology), HIV-1, Humans, Point Mutation (genetics), Polymorphism, Genetic, RNA, Messenger (blood), Viral Load, Virion (genetics), Virion (immunology).
- MESH :
- chemical , blood : RNA, Messenger.
- chemical , genetics : Cytidine Deaminase.
- chemical , metabolism : Cytidine Deaminase.
- chemical : APOBEC-3G Deaminase.
- blood : HIV Infections.
- genetics : Point Mutation, Virion.
- immunology : HIV Infections, Virion.
- virology : HIV Infections.
- Adult, CD4 Lymphocyte Count, Disease Progression, Female, Genotype, HIV-1, Humans, Polymorphism, Genetic, Viral Load.
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:19996938Le document en format XML
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<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>
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<term>Viral Load</term>
<term>Virion (genetics)</term>
<term>Virion (immunology)</term>
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<term>Charge virale</term>
<term>Cytidine deaminase (génétique)</term>
<term>Cytidine deaminase (métabolisme)</term>
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<term>Infections à VIH (immunologie)</term>
<term>Infections à VIH (sang)</term>
<term>Infections à VIH (virologie)</term>
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<term>Virion (génétique)</term>
<term>Virion (immunologie)</term>
<term>Évolution de la maladie</term>
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<term>Virion</term>
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<term>Infections à VIH</term>
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<term>Disease Progression</term>
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<term>Genotype</term>
<term>HIV-1</term>
<term>Humans</term>
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<term>Génotype</term>
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<term>Polymorphisme génétique</term>
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<front><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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