2015 Fiscal Year Final Research Report
H11/HSPB8 confers HIV resistance to Human placental trophoblasts
Project/Area Number |
26860305
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Virology
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Research Institution | Yokohama City University |
Principal Investigator |
KUDOH Ayumi 横浜市立大学, 医学部, 助教 (30616404)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Keywords | HIV-2 / H11 / Vpx / 母子感染 / 胎盤 |
Outline of Final Research Achievements |
HIV infection relies on the dynamic interplay between host and virus factors. Placental trophoblasts cells form the interface between the fetal and maternal environments and serve to limit the maternal-fetal spread of viral infection. Although the primary trophoblast cells are known to express CCR5 and CXCR4, the co-receptors for HIV entry, these cells are highly resistant to infection of HIV-2 encoding an accessory protein Vpx that counteracts a host restriction factor SAMHD1. Using a proteomic approach, we identified H11 as a negative regulator of Vpx in human trophoblasts. We found that H11 interacted with Vpx and enforced the degradation of Vpx by a proteasome-dependent mechanism. Targeted knockdown of H11 in trophoblasts restored the function of Vpx leading to the efficient infection of HIV-2. These finding may support the hypothesis that marked expression of H11 in trophoblasts may contribute to the maternal-infant viral transmission during gestation periods.
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Free Research Field |
ウイルス学
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