ArticlePloS one2011
Expression of APOBEC3G/3F and G-to-A hypermutation levels in HIV-1-infected children with different profiles of disease progression.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanism of Viral Suppression among HIV Elite Controllers and Long-Term Nonprogressors in Nigeria and South Africa.Viruses · 2022Review
- Impact of Suboptimal APOBEC3G Neutralization on the Emergence of HIV Drug Resistance in Humanized Mice.Journal of virology · 2020Article
- USP49 potently stabilizes APOBEC3G protein by removing ubiquitin and inhibits HIV-1 replication.eLife · 2019Article
- Role of APOBEC3H in the Viral Control of HIV Elite Controller Patients.International journal of medical sciences · 2018Article
- Increased expression with differential subcellular location of cytidine deaminase APOBEC3G in human CD4(+) T-cell activation and dendritic cell maturation.Immunology and cell biology · 2016Article
- Natural Single-Nucleotide Variations in the HIV-1 Genomic SA1prox Region Can Alter Viral Replication Ability by Regulating Vif Expression Levels.Journal of virology · 2016Article
- Extremely High Mutation Rate of HIV-1 In Vivo.PLoS biology · 2015Article
- Multiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them all.Journal of molecular biology · 2014Review
- AID and APOBECs span the gap between innate and adaptive immunity.Frontiers in microbiology · 2014Review
- Human APOBEC3G-mediated hypermutation is associated with antiretroviral therapy failure in HIV-1 subtype C-infected individuals.Journal of the International AIDS Society · 2013Article
- Upregulation of innate antiviral restricting factor expression in the cord blood and decidual tissue of HIV-infected mothers.PloS one · 2013Article
- The role of cytidine deaminases on innate immune responses against human viral infections.BioMed research international · 2013Review
- APOBEC3G-Augmented Stem Cell Therapy to Modulate HIV Replication: A Computational Study.PloS one · 2013Article
- Association of APOBEC3G genotypes and CD4 decline in Thai and Cambodian HIV-infected children with moderate immune deficiency.AIDS research and therapy · 2012Article
- Running loose or getting lost: how HIV-1 counters and capitalizes on APOBEC3-induced mutagenesis through its Vif protein.Viruses · 2012Review
- APOBEC3G expression and hypermutation are inversely associated with human immunodeficiency virus type 1 (HIV-1) burden in vivo.Virology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIncreasing evidence has accumulated showing the role of APOBEC3G (A3G) and 3F (A3F) in the control of HIV-1 replication and disease progression in humans. However, very few studies have been conducted in HIV-infected children. Here, we analyzed the levels of A3G and A3F expression and induced G-to-A hypermutation in a group of children with distinct profiles of disease progression. METHODOLOGY/PRINCIPAL
findingsPerinatally HIV-infected children were classified as progressors or long-term non-progressors according to criteria based on HIV viral load and CD4 T-cell counts over time. A group of uninfected control children were also enrolled in the study. PBMC proviral DNA was assessed for G-to-A hypermutation, whereas A3G and A3F mRNA were isolated and quantified through TaqMan® real-time PCR. No correlation was observed between disease progression and A3G/A3F expression or hypermutation levels. Although all children analyzed showed higher expression levels of A3G compared to A3F (an average fold of 5 times), a surprisingly high A3F-related hypermutation rate was evidenced in the cohort, irrespective of the child's disease progression profile.
conclusionOur results contribute to the current controversy as to whether HIV disease progression is related to A3G/A3F enzymatic activity. To our knowledge, this is the first study analyzing A3G/F expression in HIV-infected children, and it may pave the way to a better understanding of the host factors governing HIV disease in the pediatric setting.
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