ArticlePloS one2009
Functional genetic variants in DC-SIGNR are associated with mother-to-child transmission of HIV-1.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00198718 (Vitamin A Supplementation of Breast Feeding Mothers and Their Neonates at Delivery), which is not on this map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Vitamin A Supplementation of Breast Feeding Mothers and Their Neonates at Delivery: Impact on Mother to Child Transmission of HIV During Lactation, HIV Infection Among Women During the Postpartum Year, and Infant Mortality.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- The VNTR polymorphism of the DC-SIGNR gene and susceptibility to HIV-1 infection: a meta-analysis.PloS one · 2012Pooled it
- Relationship between the Number of Repeats in the Neck Regions of L-SIGN and Augmented Virus Replication and Immune Responses in Dengue Hemorrhagic Fever.International journal of molecular sciences · 2024Article
- COVID-19-associated liver injury: from bedside to bench.Journal of gastroenterology · 2021Review
- Innate Immune Response Against HIV-1.Advances in experimental medicine and biology · 2021Article
- Host Molecular Factors and Viral Genotypes in the Mother-to-Child HIV-1 Transmission in Sub-Saharan Africa.Journal of public health in Africa · 2017Review
- Host factors and early treatments to restrict paediatric HIV infection and early disease progression.Journal of virus eradication · 2015Review
- Solution NMR analyses of the C-type carbohydrate recognition domain of DC-SIGNR protein reveal different binding modes for HIV-derived oligosaccharides and smaller glycan fragments.The Journal of biological chemistry · 2013Article
- HIV-1 pathogenesis: the virus.Cold Spring Harbor perspectives in medicine · 2012Article
- Naturally-occurring genetic variants in human DC-SIGN increase HIV-1 capture, cell-transfer and risk of mother-to-child transmission.PloS one · 2012Article
- Different regions of HIV-1 subtype C env are associated with placental localization and in utero mother-to-child transmission.Journal of virology · 2011Article
- Role of DC-SIGN and L-SIGN receptors in HIV-1 vertical transmission.Human immunology · 2011Review
- HIV-1 co-receptor usage: influence on mother-to-child transmission and pediatric infection.Journal of translational medicine · 2011Review
- Host factors that influence mother-to-child transmission of HIV-1: genetics, coinfections, behavior and nutrition.Future virology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMother-to-child transmission (MTCT) is the main cause of HIV-1 infection in children worldwide. Given that the C-type lectin receptor, dendritic cell-specific ICAM-grabbing non-integrin-related (DC-SIGNR, also known as CD209L or liver/lymph node-specific ICAM-grabbing non-integrin (L-SIGN)), can interact with pathogens including HIV-1 and is expressed at the maternal-fetal interface, we hypothesized that it could influence MTCT of HIV-1. METHODS AND
findingsTo investigate the potential role of DC-SIGNR in MTCT of HIV-1, we carried out a genetic association study of DC-SIGNR in a well-characterized cohort of 197 HIV-infected mothers and their infants recruited in Harare, Zimbabwe. Infants harbouring two copies of DC-SIGNR H1 and/or H3 haplotypes (H1-H1, H1-H3, H3-H3) had a 3.6-fold increased risk of in utero (IU) (P = 0.013) HIV-1 infection and a 5.7-fold increased risk of intrapartum (IP) (P = 0.025) HIV-1 infection after adjusting for a number of maternal factors. The implicated H1 and H3 haplotypes share two single nucleotide polymorphisms (SNPs) in promoter region (p-198A) and intron 2 (int2-180A) that were associated with increased risk of both IU (P = 0.045 and P = 0.003, respectively) and IP (P = 0.025, for int2-180A) HIV-1 infection. The promoter variant reduced transcriptional activity in vitro. In homozygous H1 infants bearing both the p-198A and int2-180A mutations, we observed a 4-fold decrease in the level of placental DC-SIGNR transcripts, disproportionately affecting the expression of membrane-bound isoforms compared to infant noncarriers (P = 0.011).
conclusionThese results suggest that DC-SIGNR plays a crucial role in MTCT of HIV-1 and that impaired placental DC-SIGNR expression increases risk of transmission.
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