Analysis of placental barrier functions for intra uterine viral infections

2015 Fiscal Year Final Research Report

• Project/Area Number: 24390382
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Nihon University
• Principal Investigator: HAYAKAWA Satoshi 日本大学, 医学部, 教授 (30238084)
• Co-Investigator(Kenkyū-buntansha): USHIJIMA Hiroshi 日本大学, 医学部, 客員教授 (10091068) ; HONDA Mitsuo 日本大学, 医学部, 客員教授 (20117378) ; AIZAWA Shihoko 日本大学, 医学部, 准教授 (30513858)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 母子感染 / 胎盤関門 / 風疹 / インフルエンザ / HIV / 上皮間葉移行

Outline of Final Research Achievements

In　order to analyze the mechanisms of intrauterine viral transmission, viral susceptibility of trophoblastic cells, yolk sac cells, immortalized trophoblasts and endothelial cells in various differentiation stages were examined. Trophoblasts and endothelial cells were highly resistant to rubella viruses cloned from both clinical isolates and vaccine strains while endothelial cells were easily and persistently infected. Influenza A viruses replicates in immortalized human early trophoblasts and induce apoptosis but their release was highly restricted. HIV replicated in syncytial trophoblasts but do not replicates in cellular and invasive trophoblasts.
Interestingly, TLR signals induces endothelial mesenchymal transition (EMT)of trophoblastic layers and enable viral entry into villous mesenchyma and subsequently fetal circulations.

Free Research Field

産婦人科学