Transfer of human T cell lymphotropic virus type I to human term trophoblast cells in vitro

Liu, Xiangdong; Zachar, Vladimír; Hager, Henrik; Koppelhus, Uffe; Ebbesen, Peter

doi:10.1099/0022-1317-77-2-369

Cited by 7 publications

(3 citation statements)

References 19 publications

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“…However, we found that HTLV-1 provirus was detected in the cord blood and placental villous tissues. We also tested sensitivity to HTLV-1 in the cells of the blood-placental barrier and found increased susceptibility to HTLV-1 infection in the VTs in accordance with previous reports (55)(56)(57). In addition, our study showed that HTLV-1 directly infected VTs in pregnant carriers and that HTLV-1 RNA was expressed at a high level in some of these infected cells.…”

Section: Discussionsupporting

confidence: 90%

HTLV-1 targets human placental trophoblasts in seropositive pregnant women

Tezuka¹,

Fuchi²,

Okuma³

et al. 2020

Journal of Clinical Investigation

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Maternal blood during pregnancy, cord blood, and placental villous tissues at the time of delivery were obtained from subjects to measure the HTLV-1 proviral load (PVL) using real-time PCR. As shown in Figure 1A, HTLV-1 provirus was detected in the maternal blood of 248 of 254 subjects (97.6%), in the placental villous tissues of 140 of 254 subjects (55.1%), and in the cord blood samples of 6 of 254 subjects (2.4%). Overall, 248 women had PVL in the maternal blood, of whom 140 also had PVL in the placenta. Of these 140 women, 6 had PVL in the cord blood. Significant differences in the PVL were observed between the maternal blood, cord blood, and placental villous tissues (Figure 1A). The 248 pregnant carriers with PVL in the maternal blood were divided into those with PVL (n = 140) and without PVL (n = 108) in the placental tissue, and their clinical backgrounds were compared. Women with PVL in the placental tissue had a significantly higher peripheral blood PVL, higher antibody titers, and more multiparas compared with women with no PVL in the placental tissue (Table 1 and Figure 1B). These 2 groups did not differ in terms of birth weight and pregnancy complications (Table 1). There was no significant difference in the clinical backgrounds of pregnant women with HTLV-1 in the placenta when divided into those who tested positive versus negative for HTLV-1 in the cord blood (Supplemental Table 1). This was at least in part due to the small number of pregnant women testing positive for HTLV-1 in the cord blood. In addition, there were insufficient numbers of follow-up surveys of cases of MTCT by intrauterine transmission to allow statistical analysis. These issues are subjects for future investigation. A weak positive correlation between the PVLs in the maternal blood and in the placental villous tissues was observed (Figure 1C), whereas PVL in HTLV-1-positive cord blood samples did not correlate with PVL in the maternal blood or placental villous tissues of the same subject (Figure 1, D and E). To test the possibility that HTLV-1 provirus detected in cord blood was derived from maternal blood contamination of cord blood, microsatellite analysis was performed using short tandem repeat (STR) markers (25). Differences in the patterns of representative STR markers were observed between maternal blood-derived DNA and fetal placental villous tissue-and cord blood-derived DNA (Figure 1F). Similar results were obtained for all 6 samples that tested positive for HTLV-1 provirus in the cord blood. Furthermore, STR analysis and HTLV-1 PVL assay were used to examine how much maternal blood in the cord blood was required to detect a positive signal. A mixing rate of 20% (maternal/fetal cell ratio = 20:80) was the detection limit in the STR analysis, and a mixing rate of 5% (maternal/fetal cell ratio = 5:95) was the detection limit in the HTLV-1 PVL assay (Supplemental Figure 1). A previous study reported that the median rates of maternal blood contamination in the cord blood were 0.27% and 0.

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Section: Discussionsupporting

confidence: 90%

HTLV-1 targets human placental trophoblasts in seropositive pregnant women

Tezuka¹,

Fuchi²,

Okuma³

et al. 2020

Journal of Clinical Investigation

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“…Maternal blood immunoglobulins G (IgGs) are carried across the placenta by receptor-mediated transcytosis into fetal blood (24,36). Trophoblastic cells also form the first efficient barrier to protect the fetus from maternal infection, but its efficiency depends on the pathogen (28,38,55,56). Data concerning the permissivity of purified primary trophoblasts or trophoblastic cell lines to cellfree HIV infection remain controversial (18,32,43,47,62,63).…”

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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“…In in vitro experiments, exposure of the cell-free HTLV-1 virus to trophoblasts did not result in infection [71]. Recently, Tezuka et al demonstrated that during pregnancy of HTLV-1 carriers, HTLV-1 was highly expressed in placental villous tissues, and villous trophoblasts showed high HTLV-1 sensitivity compared to that in other component cells (mesenchymal fibroblasts and placental vascular endothelial cells) of the blood-placental barrier.…”

Section: Transplacental Htlv-1 Transmissionmentioning

confidence: 99%

Mother-to-Child Transmission of Human T-Cell Leukemia Virus Type 1: Mechanisms and Nutritional Strategies for Prevention

Itabashi

Miyazawa

2021

Cancers

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Approximately 95% of mother-to-child transmission (MTCT) of human T-cell leukemia virus type-1 (HTLV-1) is derived from prolonged breastfeeding, which is a major cause of adult T-cell leukemia (ATL). Exclusive formula feeding (ExFF) is therefore generally used to prevent MTCT. A recent cohort study revealed that 55% of pregnant carriers chose short-term breastfeeding for ≤ 3 months in Japan. Our meta-analysis showed that there was no significant increase in the risk of MTCT when breastfeeding was carried out for ≤ 3 months compared with ExFF (pooled relative risk (RR), 0.72; 95% confidence interval (CI), 0.30–1.77), but there was an almost threefold increase in risk when breastfeeding was carried out for up to 6 months (pooled RR, 2.91; 95% CI, 1.69–5.03). Thus, short-term breastfeeding for ≤ 3 months may be useful in preventing MTCT. Breastmilk is the best nutritional source for infants, and any approach to minimizing MTCT by avoiding or limiting breastfeeding must be balanced against the impact on the child’s health and mother–child bonding. To minimize the need for nutritional interventions, it is necessary to identify factors that predispose children born to carrier mothers to MTCT and thereby predict MTCT development with a high degree of accuracy.

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Transfer of human T cell lymphotropic virus type I to human term trophoblast cells in vitro

Cited by 7 publications

References 19 publications

HTLV-1 targets human placental trophoblasts in seropositive pregnant women

HTLV-1 targets human placental trophoblasts in seropositive pregnant women

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

Mother-to-Child Transmission of Human T-Cell Leukemia Virus Type 1: Mechanisms and Nutritional Strategies for Prevention

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