| Project/Area Number |
17380171
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Kyoto University (2006-2007)
Obihiro University of Agriculture and Veterinary Medicine (2005) |
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Principal Investigator |
MIYAZAWA Takayuki Kyoto University, Institute for Virus Research, Associate Professor (80282705)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,980,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2007: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2006: ¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 2005: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | Carnivore / lentiviruses / host range / feline immunodeficiency virus / retroviruses / receptor / AIDS / CD134 / ネコ / FIV / グリア / リンパ球 / ネコ科動物 / 種間伝播 / ワクチン / 後天性免疫不全症 / エイズ / レセプター / 大型ネコ科動物 / ライオン |
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| Research Abstract |
Human immunodeficiency virus (HIV) belongs to the genus lentivirus and induces immunodeficiency in humans. Animals also have own lentiviruses and cause a variety of diseases. Cats also have a pathogenic lentivirus called feline immunodeficiency virus (FIV) and FIV induces immunodeficiency in rats similar to the HIV infection in humans. Large felids such as lions also have lentiviruses, however the viruses are non-pathogenic in natural hosts. To elucidate the mechanisms on the determination of the host range of the feline lentiviruses is important to cope with the emergence of the novel lentiviral infections in felids. We analyzed the mechanisms of FIV infection in a feline glial cell line termed G355-5 cells. FIV strain Petaluma (subtype A) infected the G355-5 cells irrespective of the expression of feline CD134 (fCD134), primary receptor for T-lymphotropic FIV. On the other hand, strain TM2 (subtype B) required the ectopic expression of fCD134 to infect the G355-5 cells. Intriguingly, the strong expression of offCD134 suppressed the infection by strain Petaluma in the G355-5 cells. In addition, the expression of fCD134 suppressed the efficient viral release of strain TM2 from the infected G855-5 cells. The strain TM2-infected G355-5 cells transduced with fCD134 (G355-5/fOX40 cells) became a state of persistent infection. At 50 days post-infection, the infected cells released the infectious FIV particles into the culture medium and the virus was designated as strain TM2PI. TM2PI infected naive G355-5 cells in the absence of fCD134, indicating that strain TM2 mutated in the G355-5 cells to be an fCD134-independent strain. Furthermore, the cells also became a state of persistent infection and can be maintained without coculturing with uninfected G355-5 cells. Because both virus and producer cells were not modified by the genetic engineering techniques, the producer cells may be suitable for antigen preparation of the virus for vaccines.
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