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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Winkler</name></author><author><name sortKey="Werner, Lise" sort="Werner, Lise" uniqKey="Werner L" first="Lise" last="Werner">Lise Werner</name></author><author><name sortKey="Mlisana, Koleka" sort="Mlisana, Koleka" uniqKey="Mlisana K" first="Koleka" last="Mlisana">Koleka Mlisana</name></author><author><name sortKey="Abdool Karim, Salim S" sort="Abdool Karim, Salim S" uniqKey="Abdool Karim S" first="Salim S" last="Abdool Karim">Salim S. Abdool Karim</name></author><author><name sortKey="Ndung U, Thumbi" sort="Ndung U, Thumbi" uniqKey="Ndung U T" first="Thumbi" last="Ndung'U">Thumbi Ndung'U</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:19996938</idno><idno type="pmid">19996938</idno><idno type="doi">10.1097/QAD.0b013e3283353bba</idno><idno type="wicri:Area/PubMed/Corpus">000446</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000446</idno><idno type="wicri:Area/PubMed/Curation">000446</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000446</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.</title><author><name sortKey="Reddy, Kavidha" sort="Reddy, Kavidha" uniqKey="Reddy K" first="Kavidha" last="Reddy">Kavidha Reddy</name><affiliation wicri:level="1"><nlm:affiliation>Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa.</nlm:affiliation><country xml:lang="fr">Afrique du Sud</country><wicri:regionArea>Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban</wicri:regionArea></affiliation></author><author><name sortKey="Winkler, Cheryl A" sort="Winkler, Cheryl A" uniqKey="Winkler C" first="Cheryl A" last="Winkler">Cheryl A. Winkler</name></author><author><name sortKey="Werner, Lise" sort="Werner, Lise" uniqKey="Werner L" first="Lise" last="Werner">Lise Werner</name></author><author><name sortKey="Mlisana, Koleka" sort="Mlisana, Koleka" uniqKey="Mlisana K" first="Koleka" last="Mlisana">Koleka Mlisana</name></author><author><name sortKey="Abdool Karim, Salim S" sort="Abdool Karim, Salim S" uniqKey="Abdool Karim S" first="Salim S" last="Abdool Karim">Salim S. Abdool Karim</name></author><author><name sortKey="Ndung U, Thumbi" sort="Ndung U, Thumbi" uniqKey="Ndung U T" first="Thumbi" last="Ndung'U">Thumbi Ndung'U</name></author></analytic><series><title level="j">AIDS (London, England)</title><idno type="eISSN">1473-5571</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><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></keywords><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></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytidine Deaminase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytidine Deaminase</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>APOBEC-3G Deaminase</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>HIV Infections</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Point Mutation</term><term>Virion</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cytidine deaminase</term><term>Mutation ponctuelle</term><term>Virion</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à VIH</term><term>Virion</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>HIV Infections</term><term>Virion</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytidine deaminase</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>ARN messager</term><term>Infections à VIH</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à VIH</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>HIV Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><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></keywords><keywords scheme="MESH" xml:lang="fr"><term>APOBEC-3G Deaminase</term><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><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term><term>Évolution de la maladie</term></keywords></textClass></profileDesc></teiHeader><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></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19996938</PMID><DateCreated><Year>2009</Year><Month>12</Month><Day>23</Day></DateCreated><DateCompleted><Year>2011</Year><Month>01</Month><Day>03</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1473-5571</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>2</Issue><PubDate><Year>2010</Year><Month>Jan</Month><Day>16</Day></PubDate></JournalIssue><Title>AIDS (London, England)</Title><ISOAbbreviation>AIDS</ISOAbbreviation></Journal><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></Pagination><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><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Reddy</LastName><ForeName>Kavidha</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Winkler</LastName><ForeName>Cheryl A</ForeName><Initials>CA</Initials></Author><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><Initials>T</Initials></Author><Author ValidYN="Y"><CollectiveName>CAPRISA Acute Infection Study Team</CollectiveName></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN26120080001E</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>D43TW00231</GrantID><Acronym>TW</Acronym><Agency>FIC NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>D43 TW000231</GrantID><Acronym>TW</Acronym><Agency>FIC NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19 AI051794</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19 AI 51794</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>AIDS</MedlineTA><NlmUniqueID>8710219</NlmUniqueID><ISSNLinking>0269-9370</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><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></Chemical><Chemical><RegistryNumber>EC 3.5.4.5</RegistryNumber><NameOfSubstance UI="D003564">Cytidine Deaminase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CitationSubset>X</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Infect Dis. 2007 Apr 1;195(7):960-4</RefSource><PMID 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UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015658" MajorTopicYN="N">HIV Infections</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015497" MajorTopicYN="Y">HIV-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017354" MajorTopicYN="N">Point Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011110" MajorTopicYN="N">Polymorphism, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014771" MajorTopicYN="N">Virion</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS404546</OtherID><OtherID Source="NLM">PMC3470914</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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|clé= pubmed:19996938
|texte= APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:19996938" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a SidaSubSaharaV1
| This area was generated with Dilib version V0.6.32. |  |