| Project/Area Number |
16K19141
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Virology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Toyoda Mako 熊本大学, エイズ学研究センター, 研究員 (70771129)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | ウイルス / HIV-1 / SERINC3/5 / Nef / HLA / ウィルス / 感染症 |
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| Outline of Final Research Achievements |
The host proteins SERINC 3 and 5 have been revealed as inhibitors of HIV-1 infectivity that are counteracted by Nef. However, it remains unclear whether this ability affects viral replication in vivo. Here, we examined the effects of patient-derived sequences on Nef’s ability to counteract SERINC3/5 and its association with patients’ viral load. We collected plasma viral RNA from HLA-typed, treatment-naive, chronically HIV-1 subtype B-infected subjects and determined Nef-encoding region sequences. Correlation between the Nef polymorphisms and plasma viral load was analyzed. We identified two Nef mutations that are correlated inversely with viral load. The Nef’s ability to counteract SERINC3/5 was assessed by using JTAg wild-type cells and the JTAg variant engineered to lack expression of both SERINC3/5. Viruses produced by JTAg, but not SERINC3/5-deleted JTAg, demonstrated that the two Nef mutations markedly impaired SERINC3/5 counteraction function.
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