HIV-1 proviral DNA polymerase chain reaction detection in chorionic villi after exclusion of maternal contamination by variable number of tandem repeats analysis

Andreis, C.; Simoni, Giuseppe; Rossella, F.; Castagna, C.; Pesenti, Elena; Porta, Giovanni; Colucci, Giuseppe; Giuntelli, S.; Pardi, Giorgio; Semprini, A

doi:10.1097/00002030-199606001-00004

Cited by 35 publications

(24 citation statements)

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“…Indeed, HIV-1 has been detected on both the maternal and fetal portions of the placenta, i.e. in decidual macrophages, leukocytes, trophoblasts, Hofbauer cells, in villous endothelial cells, and CD3-expressing placental cells (8,(13)(14)(15)(16)(17)(18). Moreover, some authors have shown that HIV-1 undergoes productive replication in the placenta.…”

mentioning

confidence: 99%

The Low Viral Production in Trophoblastic Cells Is Due to a High Endocytic Internalization of the Human Immunodeficiency Virus Type 1 and Can Be Overcome by the Pro-inflammatory Cytokines Tumor Necrosis Factor-α and Interleukin-1

Vidricaire¹,

Tardif²,

Tremblay

2003

Journal of Biological Chemistry

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mentioning

confidence: 99%

The Low Viral Production in Trophoblastic Cells Is Due to a High Endocytic Internalization of the Human Immunodeficiency Virus Type 1 and Can Be Overcome by the Pro-inflammatory Cytokines Tumor Necrosis Factor-α and Interleukin-1

Vidricaire¹,

Tardif²,

Tremblay

2003

Journal of Biological Chemistry

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“…Comparison of maternal HIV-1 variants and virus populations detected in neonates at birth indicated that only some viruses are transmitted to the fetus and suggested that a selection occurs (1,48,52,61). Although maternal HIV may enter the fetal blood directly through microbreaches of the placenta (9), studies on blood and placenta specimens obtained from a cohort of untreated, HIV-1-positive pregnant women and infants have shown HIV-1 sequences within the placenta of all seropositive pregnant women, irrespective of the virological status of the infants (20,41,64). In addition, only a limited number of maternal viruses were detected in the placenta (41), suggesting that in utero transmission is controlled by subtle regulatory mechanisms related to characteristics (structural and/or functional) of the viral variants and/or related to the development/organization of placenta cell subpopulations.…”

mentioning

confidence: 99%

Cell-to-Cell Contact Results in a Selective Translocation of Maternal Human Immunodeficiency Virus Type 1 Quasispecies across a Trophoblastic Barrier by both Transcytosis and Infection

Lagaye

Derrien

et al. 2001

J Virol

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Mother-to-child transmission can occur in utero, mainly intrapartum and postpartum in case of breastfeeding. In utero transmission is highly restricted and results in selection of viral variant from the mother to the child. We have developed an in vitro system that mimics the interaction between viruses, infected cells present in maternal blood, and the trophoblast, the first barrier protecting the fetus. Trophoblastic BeWo cells were grown as a tight polarized monolayer in a two-chamber system. Cell-free virions applied to the apical pole neither crossed the barrier nor productively infected BeWo cells. In contrast, apical contact with human immunodeficiency virus (HIV)-infected peripheral blood mononuclear cells (PBMCs) resulted in transcytosis of infectious virus across the trophoblastic monolayer and in productive infection correlating with the fusion of HIV-infected PBMCs with trophoblasts. We showed that viral variants are selected during these two steps and that in one case of in utero transmission, the predominant maternal viral variant characterized after transcytosis was phylogenetically indistinguishable from the predominant child's virus. Hence, the first steps of transmission of HIV-1 in utero appear to involve the interaction between HIV type 1-infected cells and the trophoblastic layer, resulting in the passage of infectious HIV by transcytosis and by fusion/infection, both leading to a selection of virus quasispecies.

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“…We and others have shown that trophoblasts, possibly the primary target for viral infection in the placenta, always carry HIV-1 genomes independent of transmission. [56][57][58] The viral population in these cells was a selected variant of those present in the mother's PBMCs. These data, together with our finding that trophoblastic cell lines in vitro preferentially select CXCR4-using viral variants, suggest that in utero transmission may favor passage of such viruses.…”

Section: Discussionmentioning

confidence: 99%

HIV Type 1 Chemokine Receptor Usage in Mother-to-Child Transmission

Salvatori

Scarlatti

2001

AIDS Research and Human Retroviruses

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To investigate the role of the HIV-1 phenotype in mother-to-child HIV-1 transmission, we evaluated coreceptor usage and replication kinetics in chemokine receptor-expressing U87MG.CD4 cells of primary isolates from 32 HIV-1-infected mothers of Italian origin, none under preventive antiretroviral therapy, and from their infected infants. Five of 15 mothers of infected children and 2 of 17 mothers of uninfected children harbored viruses able to use CXCR4 as coreceptor. However, all isolates used CCR5, alone or in association with CXCR4. The replicative capacity in coreceptor-expressing cells of the viral isolates did not differ between the two groups of mothers. All mothers with an R5 virus transmitted a virus with the same coreceptor usage, whereas those four with a multitropic virus transmitted such a virus in one case. Although the presence of a mixed viral population was documented in the mothers, we did not observe transmission solely of X4 viruses. Interestingly, the only child infected with a multitropic virus carried a defective CCR5 allele. Analysis of the env V3 region of the provirus from this child revealed infection with multiple viral variants with a predominance of R5-type over X4-type sequences. These findings show that CCR5 usage of a viral isolate is not a discriminating risk factor for vertical transmission. Furthermore, X4 viruses can be transmitted to the newborn, although less frequently. In particular, we document the transmission of multiple viral variants with different coreceptor usage in a Delta32 CCR5 heterozygous child, and demonstrate that the heterozygous genotype per se does not contribute to the restriction of R5-type virus spread.

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HIV-1 proviral DNA polymerase chain reaction detection in chorionic villi after exclusion of maternal contamination by variable number of tandem repeats analysis

Cited by 35 publications

References 0 publications

The Low Viral Production in Trophoblastic Cells Is Due to a High Endocytic Internalization of the Human Immunodeficiency Virus Type 1 and Can Be Overcome by the Pro-inflammatory Cytokines Tumor Necrosis Factor-α and Interleukin-1

The Low Viral Production in Trophoblastic Cells Is Due to a High Endocytic Internalization of the Human Immunodeficiency Virus Type 1 and Can Be Overcome by the Pro-inflammatory Cytokines Tumor Necrosis Factor-α and Interleukin-1

Cell-to-Cell Contact Results in a Selective Translocation of Maternal Human Immunodeficiency Virus Type 1 Quasispecies across a Trophoblastic Barrier by both Transcytosis and Infection

HIV Type 1 Chemokine Receptor Usage in Mother-to-Child Transmission

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