SEARCH

SEARCH BY CITATION

28 February 2002

Dear Editor

Hepatitis G virus/GB virus C (HGV/GBV-C) is a blood-borne flavivirus of humans that was first characterized in 1995. While up to 80% of acutely infected individuals spontaneously clear the virus, chronic viraemia is common and can persist for up to 16 years.1 The production of antibodies to the HGV/GBV-C envelope protein E2 has been associated with the clearance of the virus and is believed to protect against reinfection.2 In communities in developed countries, HGV/GBV-C has a high prevalence in recipients of multiple transfusions and injecting drug users (IDU), but among African populations, the age-stratified prevalence of HGV/GBV-C viraemia in children is between 8% and 20%.3 Perinatal transmission with a high rate of viral persistence may explain the high frequency of viraemia observed in these children.4

A single Australian study has demonstrated that HGV/GBV-C viraemia is present in 11.1% of patients with haemophilia, 48.6% of IDU and 5.4% of children presenting for acute hospital care.5 We report the results of a prospective study to determine the prevalence of HGV markers in relatively healthy Australian children.

Hepatitis G virus/GBV-C viral RNA and anti-E2 were assayed in the serum of otherwise-healthy children presenting for elective day surgery at the Royal Children's Hospital, Melbourne, between October 1997 and January 1998. Children with a history of major illness, previous transfusion, or invasive obstetric or surgical procedures were excluded. After informed consent was obtained, blood was drawn at anaesthetic induction, and three 200 µL aliquots of serum were stored at −70°C until analysis.

Hepatitis G virus/GBV-C RNA in serum was detected with reverse transcription-polymerase chain reaction (RT-PCR) using virus-specific primers from the NS5b region, as previously des­cribed.6 Anti-E2 antibodies were assayed using a microplate EIA (Roche Diagnostics, Branchberg, NJ, USA). In addition, hepatitis B surface antigen (HBsAg) and anti-hepatitis C (anti-HCV) were determined using commercial screening assays (Abbott Diagnostics, Illinois, USA) as a measure of the risk of chronic hepatitis within the group.

Out of the 153 children (aged 2 months to 15 years; 109 boys) tested, two were positive for HGV/GBV-C RNA (prevalence 1.3%; 95% CI 0.1−4.6%). Both patients were boys, one was 11 months of age and the other was 7 years old. Each was positive for HGV/GBV-C using both sets of primers and there were no discordant RT-PCR results. None of the participants were positive for anti-E2, HBsAg or anti-HCV. Clearly, the prevalence of HGV/GBV-C infection in healthy Australian children is low. Unlike the previous Australian study, which found a viraemia rate of 5.4% in 95 children presenting to a hospital accident and emergency department,5 we have examined 153 otherwise-well children presenting for minor elective surgery. Our study excluded those children with a history of transfusion and major illness. None of the children were infected with HBV or HCV. In the absence of other risk factors, perinatal transmission is the most likely source of transmission in the two viraemic patients in this study.

Several studies have examined the prevalence of HGV in healthy children from Europe and Asia. HGV viraemia varies from 0−9.1%,7,8 compared to 18−60%,4,9 in those with paren­teral or perinatal exposure. HGV/GBV-C appears to be more prevalent in adolescents in Africa and South America with evidence of ongoing acquisition via a further, possibly sexual, route of transmission.10

In conclusion, we have demonstrated a very low level of HGV/GBV-C viraemia in otherwise-healthy Australian children from an urban population, confirming the findings of other studies from developed countries.

References

  1. Top of page
  2. References
  • 1
    Masuko K, Mitsui T, Iwano K et al. Infection with Hepatitis GB virus C in patients on maintainence haemodialysis. N. Engl. J. Med.1996; 334: 148590.
  • 2
    Thomas DL, Vlahov D, Alter H et al. Association of antibody to GB Virus C (Hepatitis G virus) with viral clearance and protection from reinfection. J. Infect. Dis. 1998; 177: 53942.
  • 3
    Simons JN, Desai SM, Mushahwar IK. The GB viruses: isolation, characterization, diagnosis and epidemiology. Viral Hepatitis Rev. 1996; 2: 22946.
  • 4
    Chen HL, Chang MH, Lin HH et al. Antibodies to E2 protein of Hepatitis G in children: Different responses according to age at infection. J. Paediatr. 1998; 133: 3825.
  • 5
    Hyland CA, Mison L, Solomon N et al. Exposure to GB virus type C or Hepatitis G in selected Australian adult and children populations. Transfusion1998; 38: 8217.
  • 6
    Hardikar W, Moaven LD, Bowden DS, Locarnini SA, Smith AL. Hepatitis G. Viroprevalence and seroconversion in a high risk group of children. J. Viral Hepatitis1999; 6: 33741.
  • 7
    Hayashi J, Furusyo N, Sawayama Y et al. Hepatitis G virus in the general population and in patients on hemodialysis. Dig. Dis. Sci.1998; 43: 21438.
  • 8
    Lampe E, Saback F, Viasov S, Roggendorf M, Niel C. Age-­specific prevalence and genetic diversity of GBV-C/Hepatitis G virus in Brazil. J. Med. Virol. 1998; 56: 3943.DOI: 10.1002/(sici)1096-9071(199809)56:1<39::aid-jmv7>3.0.co;2-o
  • 9
    Szabo A, Sallay P, Kribben A et al. Hepatitis G virus infection in children on dialysis and after renal transplantation. Pediatr. ­Nephrol.1998; 12: 925.
  • 10
    Mphahlele MJ, Aspinall S, Spooner R, Carman WF. Age related prevalence of Hepatitis G virus in South Africans. J. Clin. Pathol. 1999; 52: 7527.