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Apoptosis in Placentas From Human T-Lymphotropic Virus Type I–Seropositive Pregnant Women: A Possible Defense Mechanism Against Transmission From Mother to Fetus

From the School of Health Sciences and the Department of Obstetrics and Gynecology, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.

Address reprint requests to: Toshinori Fujino, MD School of Health Sciences Kagoshima University 8-35-1 Sakuragaoka Kagoshima, 890-8506 Japan E-mail: toshinet{at}health.nop.kagoshima-u-ac-jp

Objective: The mechanism by which the placenta serves as the barrier against mother-to-fetus transmission of microorganisms remains to be elucidated. Programmed cell death, apoptosis, is considered a cellular defense mechanism against infection. The hypothesis of this study is that apoptosis of human T-lymphotropic virus type I (HTLV-I)–infected placental villous cells is involved in the defense mechanism against mother-to-fetus transmission of HTLV-I.

Methods: Apoptosis was compared in term placentas from eight HTLV-I–seropositive pregnant women and eight HTLV-I–seronegative pregnant women by the terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end-labeling method. In addition, an in vitro cocultivation with an HTLV-I–infected lymphocyte cell line (MT-2 cells) was performed to examine whether placental villous cells were infected with HTLV-I and apoptosis was induced.

Results: The incidence of apoptosis-positive cells (nuclei) in placentas from the HTLV-I–seropositive pregnant women was higher than in the HTLV-I–seronegative pregnant women (P < .02). Cocultivation with MT-2 cells showed that trophoblast cells were able to be infected with HTLV-I and that apoptosis was induced in the placental villous cells.

Conclusion: HTLV-I infection induces apoptosis in the placenta. We speculate that apoptosis may be involved in the defense mechanism of the placenta against mother-to-fetus transmission of HTLV-I.