Analysis of HBV replication mechanism and development of new anti-HBV treatment
| Project/Area Number |
11670535
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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 |
Gastroenterology
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| Research Institution | Showa University |
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Principal Investigator |
YOSHIBA Shinsho Showa University, School of Medicine, Associate Professor (20010457)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Kazuaki Showa University, School of Medicine, Assistant Professor (90232529)
MICHINORI Kohara The Tokyo Metropolitan Institute of Medical Science, Dept. Microbiology and Cell Biology, Researcher (10250218)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | HCV / real-time PCR / HBV DNA / HCV core / HCV NS3 / 4A / IFN / RTD-PCR |
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| Research Abstract |
Regulation of HBV replication remains unclear. HBV replication is suppressed in patients with HBV and HCV co-infection. HBV-DNA and HCV-RNA were therefore quantitatively analyzed in livers and sera from co-infected patients. HBV-DNA and HCV-RNA were quantitated using real-timePCR. Quantities of HBV-DNA in sera from co-infected patients were very low (8-19000 copies/mL). HBV-DNA was detected in liver from co-infected patients at 2-20 copies per 100 hepatocytes, accounting for 1/1000 to 1/10,000 of HBsAg positive patients. In livers of patients with HCC and HCV or HBV mono-infection, the viruses existed predominantly in non-cancerous tissue, with levels 10- to 1000-fold and 1- to 100-fold higher than in cancerous tissue, respectively. In contrast, patients co-infected with HCV and HBV displayed decreased HBV levels in non-cancerous tissue, but no change in cancerous tissue. In experimental study, HCV core protein suppressed HBV replication, however, HCV NS3/4A protein accelerates HBV replication. It might be mediated by the impairment of IFN induction.
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Report
(2 results)
Research Products
(9 results)
