Project/Area Number |
21790450
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Virology
|
Research Institution | Kinki University |
Principal Investigator |
HAKATA Yoshiyuki Kinki University, 医学部, 助教 (30344500)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | HIV-1感染抵抗性遺伝子 / HIV-1 / Rac2 / 感染抵抗性遺伝子 / CCR5 / CCL5 / CCL3/4 / TNF / IL6 / CCL3 / CCL4 / SNPs |
Research Abstract |
Several genetic variations have been identified as factors which affect HIV-1 infection in human. We have recently discovered that human rac2 gene is one of the restriction genes for HIV-1 infection and individuals who possess high-expression type rac2 allele in their genome tend to be more resistant to HIV-1 infection as compared to people with low-expression type rac2 gene allele. During the term of this grant, we identified a single nucleotide polymorphism controlling Rac2 expression in an intron region of the rac2 gene. We found that Rac2 decreases CCR5 expression, a critical co-receptor for HIV-1 infection, at transcriptional level but increases CCL5 which binds to CCR5 and inhibits HIV-1 infection. These results suggest that higher Rac2 expression affects the HIV-1-cell interaction, leading to more resistant against HIV-1 infection.
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