Frequency of early in utero HIV-1 infection: a blind DNA polymerase chain reaction study on 100 fetal thymuses

Brossard, Y.; Aubin, Jean-Thierry; Mandelbrot, Laurent; Bignozzi, Christiane; Brand, Denys; Chaput, Agnès; Roume, J.; Mulliez, N; Mallet, François; Agut, Henri; Barin, Françis; Bréchot, Christian; Goudeau, Alain; Huraux, Jean‐Marie; Barrat, J; Blot, Philippe; Chavinié, J; Ciraru-Vigneron, N; Engelman, Philippe; Hervé, François; Papiernik, E; Henrion, R

doi:10.1097/00002030-199509040-00007

Cited by 93 publications

(22 citation statements)

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“…Some previous studies have tried to document HIV status of pregnancy losses [34-36]. One study which did so by in situ hybridization showed that 60% of the spontaneous fetal losses (6/10) were associated with HIV transmission to the fetus [35].…”

Section: Discussionmentioning

confidence: 99%

Pregnancy loss and role of infant HIV status on perinatal mortality among HIV-infected women

et al. 2012

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BackgroundHIV-infected women, particularly those with advanced disease, may have higher rates of pregnancy loss (miscarriage and stillbirth) and neonatal mortality than uninfected women. Here we examine risk factors for these adverse pregnancy outcomes in a cohort of HIV-infected women in Zambia considering the impact of infant HIV status.MethodsA total of 1229 HIV-infected pregnant women were enrolled (2001–2004) in Lusaka, Zambia and followed to pregnancy outcome. Live-born infants were tested for HIV by PCR at birth, 1 week and 5 weeks. Obstetric and neonatal data were collected after delivery and the rates of neonatal (<28 days) and early mortality (<70 days) were described using Kaplan-Meier methods.ResultsThe ratio of miscarriage and stillbirth per 100 live-births were 3.1 and 2.6, respectively. Higher maternal plasma viral load (adjusted odds ratio [AOR] for each log10 increase in HIV RNA copies/ml = 1.90; 95% confidence interval [CI] 1.10–3.27) and being symptomatic were associated with an increased risk of stillbirth (AOR = 3.19; 95% CI 1.46–6.97), and decreasing maternal CD4 count by 100 cells/mm3 with an increased risk of miscarriage (OR = 1.25; 95% CI 1.02–1.54). The neonatal mortality rate was 4.3 per 100 increasing to 6.3 by 70 days. Intrauterine HIV infection was not associated with neonatal morality but became associated with mortality through 70 days (adjusted hazard ratio = 2.76; 95% CI 1.25–6.08). Low birth weight and cessation of breastfeeding were significant risk factors for both neonatal and early mortality independent of infant HIV infection.ConclusionsMore advanced maternal HIV disease was associated with adverse pregnancy outcomes. Excess neonatal mortality in HIV-infected women was not primarily explained by infant HIV infection but was strongly associated with low birth weight and prematurity. Intrauterine HIV infection contributed to mortality as early as 70 days of infant age. Interventions to improve pregnancy outcomes for HIV-infected women are needed to complement necessary therapeutic and prophylactic antiretroviral interventions.

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Section: Discussionmentioning

confidence: 99%

Pregnancy loss and role of infant HIV status on perinatal mortality among HIV-infected women

et al. 2012

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“…Hofbauer cells also may facilitate HIV vertical transmission given that an HIV coreceptor, dendritic cell specific intercellular adhesion molecule-3-grabbing non integrin (DC-SIGN), is expressed on these cells, and DC-SIGN polymorphisms are associated with risk of mother-to-child HIV transmission (Boily-Larouche et al, 2012). However, studies of animal and human fetuses indicate that there is almost no HIV transmission during the first and second trimesters of pregnancy (Brossard et al, 1995; Van Dyke et al, 1999), suggesting that this process has a limited biological role.…”

Section: Bypassing the Syncytiotrophoblast Layermentioning

confidence: 99%

Microbial Vertical Transmission during Human Pregnancy

Arora

Sadovsky

Dermody

et al. 2017

Cell Host & Microbe

289

269

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Congenital infections with pathogens such as Zika virus, Toxoplasma gondii, Listeria monocytogenes, Treponema pallidium, parvovirus, HIV, varicella zoster virus, Rubella, Cytomegalovirus, and Herpesviruses are a major cause of morbidity and mortality worldwide. Despite the devastating impact of microbial infections on the developing fetus, relatively little is known about how pathogens associated with congenital disease breach the placental barrier to transit vertically during human pregnancy. In this review, we focus on transplacental transmission of pathogens during human gestation. We introduce the structure of the human placenta and describe the innate mechanisms by which the placenta restricts microbial access to the intrauterine compartment. Based on current knowledge, we also discuss the potential pathways employed by microorganisms to overcome the placental barrier and prospects for the future.

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“…Aside from the descriptions of rare early in utero transmission events [22], the timing of transmission has been mostly estimated using partially indirect dynamic models [2]. Such probabilistic approaches exclusively rely on the virus detection at successive sampling time points after delivery [23].…”

Section: Introductionmentioning

confidence: 99%

Estimating the Timing of Mother-to-Child Transmission of the Human Immunodeficiency Virus Type 1 Using a Viral Molecular Evolution Model

et al. 2014

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BackgroundMother-to-child transmission (MTCT) is responsible for most pediatric HIV-1 infections worldwide. It can occur during pregnancy, labor, or breastfeeding. Numerous studies have used coalescent and molecular clock methods to understand the epidemic history of HIV-1, but the timing of vertical transmission has not been studied using these methods. Taking advantage of the constant accumulation of HIV genetic variation over time and using longitudinally sampled viral sequences, we used a coalescent approach to investigate the timing of MTCT.Materials and MethodsSix-hundred and twenty-two clonal env sequences from the RNA and DNA viral population were longitudinally sampled from nine HIV-1 infected mother-and-child pairs [range: 277–1034 days]. For each transmission pair, timing of MTCT was determined using a coalescent-based model within a Bayesian statistical framework. Results were compared with available estimates of MTCT timing obtained with the classic biomedical approach based on serial HIV DNA detection by PCR assays.ResultsFour children were infected during pregnancy, whereas the remaining five children were infected at time of delivery. For eight out of nine pairs, results were consistent with the transmission periods assessed by standard PCR-based assay. The discordance in the remaining case was likely confused by co-infection, with simultaneous introduction of multiple maternal viral variants at the time of delivery.ConclusionsThe study provided the opportunity to validate the Bayesian coalescent approach that determines the timing of MTCT of HIV-1. It illustrates the power of population genetics approaches to reliably estimate the timing of transmission events and deepens our knowledge about the dynamics of viral evolution in HIV-infected children, accounting for the complexity of multiple transmission events.

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Frequency of early in utero HIV-1 infection: a blind DNA polymerase chain reaction study on 100 fetal thymuses

Cited by 93 publications

References 0 publications

Pregnancy loss and role of infant HIV status on perinatal mortality among HIV-infected women

Pregnancy loss and role of infant HIV status on perinatal mortality among HIV-infected women

Microbial Vertical Transmission during Human Pregnancy

Estimating the Timing of Mother-to-Child Transmission of the Human Immunodeficiency Virus Type 1 Using a Viral Molecular Evolution Model

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