2005 Fiscal Year Final Research Report Summary
Analyses on the mechanisms by which differentiated pericytes are resistant to HIV-1 infection.
| Project/Area Number |
15590412
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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 |
Virology
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| Research Institution | Gunma University |
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Principal Investigator |
OUE Atsushi GUNMA UNIVERSITY, LECTURER, 大学院・医学系研究科, 講師 (80260107)
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| Project Period (FY) |
2003 – 2005
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| Keywords | HIV-1 / Endothelial cells / Pericytes / Differentiation / Reverse transcrivtase / Brain microvessels |
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| Research Abstract |
HIV-1 is a causative agent for AIDS. Not only immunological changes, HIV-1 also causes neurological disorders. We have previously isolated HIV-1 variant, which is infectious to brain-derived pericytes. Pericytes are located at the abluminal side of the microvessels and cover the surface of the endothelial cells. In the brain, pericytes are important constituent for the blood-brain barrier (BBB). It is known that BBB plays an important role for neuronal damages induced by HIV-1 infection. To mimic in vivo situation and to better understand the biological features of the brain pericytes, we isolated human brain pericytes (HBPs) and cocultured them with the human brain microvascular endothelial cells (HBMECs). We observed the dramatic morphological changes in HBPs with extended and multibranched cytoplasmic processes. Interestingly, this differentiated pericytes were highly resistant to HIV-1 infection. Results of HIV-1-cell binding assay indicated that the level of attached viruses were significantly lower in cocultured pericytes as compared to monocultured pericytes, suggesting that the cell surface molecule involved in HIV-1 attachment, such as heparan sulfate proteoglycan might be changed after differentiation of pericytes.
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