| Project/Area Number |
09670319
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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 | Tokai University |
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Principal Investigator |
KOGA Yasuhiro Tokai University School of Medicine, Professor, 医学部, 教授 (60170221)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cytomegalovirus / graft-versus-host reaction / reactivation / MCMV-DNA / iNOS / NO / latent infection / lung / サイトメガロウイルス / 潜伏感染 / 再活性化 |
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| Research Abstract |
At 5 week after intraperitoneal infection of murine cytomegalovirus in adult (C3H/I-Ie x BALB/c)Fl mice, MCMV-DNA was found in the salivary glands but not in the lungs or hearts. Since graft-versus-host reaction (GVIIR) is well known as a major risk factor for CMV reactivation, parental BALB/c spleen cells were then intravenously transferred to these mice to induce GVHR.A high copy number of MCMV-DNA was observed in the lungs as well as the hearts and livers at 4 to 6 weeks after the cell transfer. It was thus suggested that the amplifcation in the copy number of MCMV-DNA in these organs was caused by GVHR.
The role of nitric oxide (NO) in the increase of NCMV-DNA was then investigated because a marked elevation in the inducible nitric oxide synthase (iNOS) was accompanied in such mice undergoing GVIIR.The administration of L-arginine, a substrate for NO, increased the amount of MCNV-DNA in the lungs and the hearts after the induction of GVHR.On the other hand, an NO antagonist inhibited the appearance of MCMV-DNA.Therefore it was suggested that the NO generated in the tissue especially those of lungs and hearts by GVHR plays a crucial role in the amplification of latently infected MCMV-DNA.
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