Identification of HTLV‐I Sequence in Cord Blood Mononuclear Cells of Neonates Born to HTLV‐I Antigen/Antibody‐positive Mothers by Polymerase Chain Reaction

Saito, Shigeru; Furuki, K.; Ando, Yoshiya; Tanigawa, Takuo; Kakimoto, Kazuhiro; Moriyama, I.; Ichijo, Motohiko

doi:10.1111/j.1349-7006.1990.tb02663.x

Cited by 36 publications

(13 citation statements)

References 15 publications

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“…In line with previous reports (Fujino et al, 1992;Saito et al, 1991;Satow et al, 1991), our data indicate the possibility that human placental trophoblast may become persistently infected with HTLV-I in vivo but that this infection is likely to be of a limited productivity. It remains to be elucidated to what extent local factors, namely a cytokine network typically restricted to the placental micro-environment (Mitchell et al, 1993), may play a part in modulation of virus expression in the infected placental cells and thereby regulate transplacental passage of HTLV-I.…”

Section: Short Communicationsupporting

confidence: 81%

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Cell-mediated transmission of human T cell lymphotropic virus type I to human malignant trophoblastic cells results in long-term persistent infection

Liu

Zachar

Nørskov‐Lauritsen

et al. 1995

Journal of General Virology

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We investigated permissiveness of the malignantly transformed trophoblast (choriocarcinoma) cell lines JAR, BeWo and JEG-3 to the human T cell lymphotropic virus type I (HTLV-I). After co-culture with the productively infected cell line MT-2 the choriocarcinoma cell lines were analysed for infection over a period of three months. The presence of HTLV-I viral DNA was examined by PCR using primers targeting the gag, pol, env and pX specific sequences. All amplified segments were found consistently in the cell cultures throughout the period of study. Further analysis that aimed to characterize the size variation of the integrated proviral DNA by Southern blotting revealed the presence of integrated proviral sequences which consisted, for the most part, of incomplete genomes. The presence of the full-length HTLV-I genome, however, was unequivocally confirmed in clonally expanded cell cultures derived from the originally infected parental cells. In order to analyse virus expression at the transcriptional level, we used reverse transcriptase (RT)-mediated PCR that was targeted at intra-exon regions (gag, pol, env andpX), and the splicing sites of the env and pX-tax/rex mRNAs. When compared with MT-2 cells, substantially lower levels of all transcripts were found in all the cell lines analysed. We were unsuccessful in attempts to detect viral protein expression using polyvalent or Tax-and Gag-specific monoclonal antibodies by Western blot analysis or immunoprecipitation, and we could not detect any RT activity released into the supernatant of the infected cells either. Collectively, these data suggest that the trophoblastic cells may become persistently but essentially non-productively infected with HTLV-I.

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Section: Short Communicationsupporting

confidence: 81%

“…Several previous reports, however, have suggested that HTLV-I may be acquired in utero. In these studies (Saito et al, 1991 ;Satow et al, 1991) virus-specific DNA and antigens were detected in cord-blood lymphocytes from the offsprings of HTLV-I carrier mothers. These data argue that the placenta might play a direct role in the infection of the fetus.…”

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confidence: 99%

Cell-mediated transmission of human T cell lymphotropic virus type I to human malignant trophoblastic cells results in long-term persistent infection

Liu

Zachar

Nørskov‐Lauritsen

et al. 1995

Journal of General Virology

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“…Whether the HTLV-I-positive lymphocytes survive longer and establish HTLV-I infection in the children remains to be re-evaluated by other confirmatory methods, such as polymerase chain reaction (PCR) to detect HTLV-I proviral DNA in lymphocytes of the relevant children (Kwok et aZ., 1988). Indeed, Saito et al (1989Saito et al ( , 1990 reported several cases of HTLV-I-seronegative and PCR-positive children who were born to HTLV-I carrier mothers. On the other hand, Matsumoto et al (1990) reported a correlation between PCR positivity and IF seropositivity in HTLV-I-infected donors.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of maternal antibody on mother‐to‐child transmission of human T‐lymphotropic virus type I

Takahashi

Takezaki

Oki

et al. 1991

Intl Journal of Cancer

134

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In order to evaluate the protective role of the maternal antibody against mother-to-child transmission of HTLV-I, we followed a total of 780 children born to HTLV-I carrier mothers by investigating the level of anti-HTLV-I antibody transferred in utero, decline of the maternal antibody and seroconversion in post-natal life. The anti-HTLV-I antibody was positively detected within the first 3-6 months of life and declined at 6-12 months after birth in all children. After the maternal antibody declined, seroconversion occurred in some of the children following either breast feeding or bottle feeding. The seroconversion rates of short-term (less than or equal to 6 months) and long-term (greater than or equal to 7 months) breast feeders were 4.4% (4/90 cases) and 14.4% (20/139 cases), and the rate of bottle feeders was 5.7% (9/158 cases). Long-term breast feeding yielded more seroconverters than short-term breast feeding; 14.4% (20/139 cases) vs. 4.4% (4/90 cases), RR = 3.68, p = 0.018. The seroconversion rate of short-term breast feeders was nearly equal to that of bottle feeders; 4.4% (4/90 cases) vs. 5.7% (9/158 cases), RR = 0.770, p = 0.471. When neonatal lymphocytes were cultured with breast milk cells of HTLV-I carrier mothers, the in vitro infection of HTLV-I was inhibited by the addition of HTLV-I-seropositive cord-blood plasma. Our results suggest that the maternal antibody may inhibit HTLV-I infection by short-term breast feeding but not by long-term breast feeding after decline of the maternal antibody.

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“…Depending on the study, about 10.5 to 39.6% of breast‐fed children born to HTLV‐I‐seropositive mothers become infected (Hino et al, 1996; Hirata et al, 1992; Nyambi et al, 1996; Takahashi et al, 1991; Tsuji et al, 1990; Wiktor et al, 1993, 1997; Yoshinaga et al, 1995) as compared with only 0 to 12.8% of bottle‐fed children (Hino et al, 1996; Hirata et al, 1992; Takahashi et al, 1991; Tsuji et al, 1990), suggesting that transplacental or other modes of transmission may also operate. An early study advanced this hypothesis, based on detection of HTLV‐I‐proviral DNA in cord‐blood samples, to explain the seroconversion of bottle‐fed children (Saito et al, 1990). But in a follow‐up study on bottle‐fed children, none of 7 children found HTLV‐I‐positive by PCR in their cord blood seroconverted, while 9 children who gave negative PCR results seroconverted (Hino et al, 1997; Kawase et al, 1992).…”

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Mother-to-child transmission of human T-cell-leukemia/lymphoma virus type I: Implication of high antiviral antibody titer and high proviral load in carrier mothers

et al. 1999

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In order to gain new insights into the risk factors influencing human‐T‐cell‐leukemia/lymphoma‐virus‐type‐I (HTLV‐I) mother‐to‐child transmission, a retrospective study of HTLV‐I infection among children born to HTLV‐I‐seropositive women was carried out in a highly HTLV‐I‐endemic population of African origin living in French Guyana. The study covered 81 HTLV‐I‐seropositive mothers and their 216 children aged between 18 months old and 12 years old. All plasma samples were tested for the presence of HTLV‐I antibodies by ELISA, immunofluorescence assay and Western blot. HTLV‐I provirus was detected, in the DNA extracted from peripheral‐blood mononuclear cells, by polymerase chain reaction (PCR) using primers specific for 3 different HTLV‐I genomic regions (LTR, gag and pX) and quantified by a competitive PCR assay. Out of the 216 children, 21 were found to be HTLV‐I‐seropositive, giving a crude HTLV‐I transmission rate of 9.7%, while among the 180 breast‐fed children 10.6% were HTLV‐I‐seropositive. Perfect concordance between serological and PCR results was observed, and none of the 195 HTLV‐I‐negative children was found HTLV‐I‐positive by PCR. In conditional (by family) logistic‐regression models, HTLV‐I seropositivity in children was associated with an elevated maternal anti‐HTLV‐I‐antibody titer (OR 2.2, p = 0.0013), a high maternal HTLV‐I proviral load (OR 2.6, p = 0.033) and child's gender, girls being more frequently HTLV‐I‐infected than boys: OR 3.6, p = 0.0077 in the model including maternal anti‐HTLV‐I‐antibody titer and OR 4.1, p = 0.002 in the model including the maternal HTLV‐I proviral load. Int. J. Cancer 82:832–836, 1999. © 1999 Wiley‐Liss, Inc.

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Identification of HTLV‐I Sequence in Cord Blood Mononuclear Cells of Neonates Born to HTLV‐I Antigen/Antibody‐positive Mothers by Polymerase Chain Reaction

Cited by 36 publications

References 15 publications

Cell-mediated transmission of human T cell lymphotropic virus type I to human malignant trophoblastic cells results in long-term persistent infection

Cell-mediated transmission of human T cell lymphotropic virus type I to human malignant trophoblastic cells results in long-term persistent infection

Inhibitory effect of maternal antibody on mother‐to‐child transmission of human T‐lymphotropic virus type I

Mother-to-child transmission of human T-cell-leukemia/lymphoma virus type I: Implication of high antiviral antibody titer and high proviral load in carrier mothers

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