1999 Fiscal Year Final Research Report Summary
Analysis of trans-placental HIV infection
| Project/Area Number |
10671572
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nihon University |
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Principal Investigator |
HAYAKAWA Satoshi Nihon Univ. School of Medicine Department of Obstetrics and Gynecology, Assistant Professor, 医学部, 講師 (30238084)
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| Co-Investigator(Kenkyū-buntansha) |
NISHINARITA Susumu Nihon Univ. School of Medicine Department of Internal Medicine, Assistant Professor, 医学部, 講師 (70110963)
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| Project Period (FY) |
1998 – 1999
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| Keywords | HIV / chemokine / vertical transmission / IL-16 |
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| Research Abstract |
Recent advances in perinatal care for HIV infected mothers decreased vertical transmission rates as low as 2% in Japan. However the mechanism of transplacental infection of HIV is still enigmatic and uncontrollable. In this study, we described placental pathology in HIV infected mothers in order to examine patho-physiology of congenital HIV infection and morphological basis of possible placental barriers.
Subjects and methods Twelve placental samples were obtained from HIV infected mothers by AIDS working group of Japan. All cases were delivered by elective caesarean section before onset of labour. Eleven of 12 patients received oral AZT administration. No neonates delivered showed evidence of congenital infection. We examined placentae by HE stain, TUNEL and immunohistochemiistry. Various components of placental cells were separated by MACS coated with anti EGF-R, erb-B2 and CD11b which recognize villous trophoblasts (VT), extravillos trophoblasts (EVT) and Hofbauer cells (Hob) respectively. Presence of HIVgp120 RNA was examined by RT-PCR.
Results By routine histological study, we observed increased frequency of intervillitis and apoptosis in placentae delivered from HIV infected patients. By quantitative analysis using TUNEL stain, we observed increased numbers of apoptotic scores. Immunohistochemical stain revealed presence of HIV p24 antigen in 2 of 12 placentae. P24 was localized both in VT and Hob. Using antigenically separated placental cells, we detected HIV gp120 RNA both in VT, EVT and Hob.
Conclusion Previous reports suggest possible placental barrier to explain low transmission rates of HIV from infected mothers However we suggest, possible postplacental barriers which protect vertical transmission of HIV from infected placentae to fetuses.
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