APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.
Identifieur interne : 000446 ( PubMed/Curation ); précédent : 000445; suivant : 000447APOBEC3G 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 (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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<keywords scheme="KwdFr" xml:lang="fr"><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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<term>Virion</term>
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<term>Virion</term>
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<term>Infections à VIH</term>
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</keywords>
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</keywords>
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<term>CD4 Lymphocyte Count</term>
<term>Disease Progression</term>
<term>Female</term>
<term>Genotype</term>
<term>HIV-1</term>
<term>Humans</term>
<term>Polymorphism, Genetic</term>
<term>Viral Load</term>
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<term>Adulte</term>
<term>Charge virale</term>
<term>Femelle</term>
<term>Génotype</term>
<term>Humains</term>
<term>Numération des lymphocytes CD4</term>
<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>
</front>
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<DateCreated><Year>2009</Year>
<Month>12</Month>
<Day>23</Day>
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<Day>03</Day>
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<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>25</Day>
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<Issue>2</Issue>
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<Month>Jan</Month>
<Day>16</Day>
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<Title>AIDS (London, England)</Title>
<ISOAbbreviation>AIDS</ISOAbbreviation>
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<ArticleTitle>APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.</ArticleTitle>
<Pagination><MedlinePgn>195-204</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1097/QAD.0b013e3283353bba</ELocationID>
<Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">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.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Study participants were 250 South African women at high risk for HIV-1 subtype C infection. We used real-time PCR to measure the expression of APOBEC3G in HIV-negative and HIV-positive primary infection samples. APOBEC3G variants were identified by DNA re-sequencing and TaqMan genotyping.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">We found no correlation between APOBEC3G expression levels and plasma viral loads (r = 0.053, P = 0.596) or CD4 T-cell counts (r = 0.030, P = 0.762) in 32 seroconverters. APOBEC3G expression levels were higher in HIV-negative individuals as compared with HIV-positive individuals (P < 0.0001), including matched pre and postinfection samples from the same individuals (n = 13, P < 0.0001). Twenty-four single nucleotide polymorphisms, including eight novel, were identified within APOBEC3G by re-sequencing and genotyping. The H186R mutation, a codon-changing variant in exon 4, and a 3' extragenic mutation (rs35228531) were associated with high viral loads (P = 0.0097 and P < 0.0001) and decreased CD4 T-cell levels (P = 0.0081 and P < 0.0001), respectively.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">These data suggest that APOBEC3G transcription is rapidly downregulated upon HIV-1 infection. During primary infection, APOBEC3G expression levels in peripheral blood mononuclear cells do not correlate with viral loads or CD4 T-cell counts. Genetic variation of APOBEC3G may significantly affect early HIV-1 pathogenesis, although the mechanism remains unclear and warrants further investigation.</AbstractText>
</Abstract>
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<ForeName>Cheryl A</ForeName>
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<Author ValidYN="Y"><LastName>Werner</LastName>
<ForeName>Lise</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mlisana</LastName>
<ForeName>Koleka</ForeName>
<Initials>K</Initials>
</Author>
<Author ValidYN="Y"><LastName>Abdool Karim</LastName>
<ForeName>Salim S</ForeName>
<Initials>SS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ndung'u</LastName>
<ForeName>Thumbi</ForeName>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
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<Chemical><RegistryNumber>EC 3.5.4.5</RegistryNumber>
<NameOfSubstance UI="D000071480">APOBEC-3G Deaminase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.5.4.5</RegistryNumber>
<NameOfSubstance UI="C464924">APOBEC3G protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>EC 3.5.4.5</RegistryNumber>
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