| Project/Area Number |
09670827
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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 |
Pediatrics
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| Research Institution | Nagoya City University |
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Principal Investigator |
SUGIYAMA Kohachiro Nagoya City University, Medical, Lecturer, 医学部, 講師 (60117827)
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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 |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | GBV-C / HGV / RT-PCR / Anti-E2 antibody / Gene Analysis / Vertical transmission / Child / 血清肝炎 |
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| Research Abstract |
The transmission route of GBV-C/Hepatitis G virus (HGV) and the pathological role of this virus infection in liver disorder in children were investigated.
(1) The prevalence of HGV in pregnant Japanese women (aged 30.2 +/- 4.4 years) was 0.3% (1/288).
(2) The prevalence of HGV in children with no history of blood transfusion was 0.5% (5/1000). The mothers in all 5 families were positive, and among the 3 families two of the total 4 siblings were positive. Therefore, the prevalence of HGV in children born to HGV RNA-positive mothers was 78% (7/9). The mother in each case was positive for HGV and sequence homology analysis revealed no difference between child and their mothers, suggesting mother-to-infant transmission was the route of infection in these children.
(3) We detected HGV in 33.3% (11/33) and anti-E2 antibody in 3.7% (1/27) children in the malignant and 3 of 56 (5.4%) and 1.9% (1/53) children in the non-malignant groups. Neither HGV nor anti-E2 antibody was detected in the HBV and non A-C hepatitis groups. HGV and anti-E2 antibody were detected in 7 of 23 (30%) and 1 of 18 (5.6%) children in the HCV group. All these cases had a history of blood transfusion. The presence of HGV infection does not seem to be as critical as conventionally thought in association with childhood liver dysfunction.
(4) No anti-E2 antibody (0/330) was detected in children with no history of blood transfusion. This suggests that children infected with HGV became a carrier and the rate of seroconversion to anti-E2 antibody is low in childhood.
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