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World Journal of Gastroenterology logoLink to World Journal of Gastroenterology
. 2000 Aug 15;6(4):585–587. doi: 10.3748/wjg.v6.i4.585

Serological prevalence and risk factor analysis of hepatitis G virus infection in Hubei Province of China

De-Ying Tian 1,2,3, Dao-Feng Yang 1,2,3, Ning-Shao Xia 1,2,3, Zheng-Gang Zhang 1,2,3, Hong-Bo Lei 1,2,3, Yuan-Cheng Huang 1,2,3
PMCID: PMC4723563  PMID: 11819653

INTRODUCTION

Hepatitis G virus (HGV),also known as GB virus C, is a recently cloned virus which may be associated with human non A-E hepatitis[1,2]. It is parenterally transmitted and usually coinfected or superinfected with hepatitis B or hepat itis C virus[3-5]. Some investigations have been reported on the serop revalence and molecular prevalence of HGV infection in different areas and diffe rent population[6-15]. Current infection of HGV is diagnosed by detectio n of HGV RNA, and past infection with HGV is detectable by testing anti-HGV env elope protein (E2)[16-17]. To investigate the prevalence of HGV in Hubei Province, a central area of the People’s Republic of China, ELISA and RT-PCR were employed to detect serum anti-HGV and HGV RNA in 1516 patients who were divided into 16 groups.

MATERIALS AND METHODS

Samples

One thousand five hundred and sixteen serum samples were obtained from 16 groups in Hubei Province, including 299 drug users (19.72%), 98 prostitutes (6.46%), 504 blood donors (33.25%), 61 hemodialysis patients (4.02%), 351 cases with viral hepatitis (23.15%), 41 with primary hepatocellular carcinoma (PHC, 2.70%), 51 with hemopathy (3.36%), 53 renal transplant recipients (3.49%) and 3 liver trans plant recipients (0.20%). 55 freshmen, nurses and doctors (3.63%) were employed as healthy controls.

Reagents and detecting methods

Serum HBV markers, HAV IgM, HEV IgM, and anti-HCV were detected by enzyme linked immunoabsorbent assay (ELISA). Anti-HGV was also detected by ELISA and the tes t kits were procured from Wantai Biological Preparation Co Ltd, Beijing. HGV RNA was assayed by reverse transcript polymerase chain reaction (RT-PCR) with the primers of 5’-UTR, and the kits were purchased from the Center of Hepatitis R ea gents, Beijing. Both anti-HGV and HGV RNA were simultaneously measured in the drug users, prostitutes, and healthy subjects. For other groups, HGV RNA was dete cted only when their anti-HGV was positive due to insufficient outlay.

Data statistics

All data were analyzed by means of the Chi-square test.

RESULTS

HGV infections in drug users and prostitutes

The positive rates of anti-HGV and HGV-RNA in drug users were 9.06% (34/375) and 27.20% (102/375); those in prostitutes were 38.77% (38/98) and 20.41% (20/98). The analysis of risk factors of HGV infections in drug users and prostitutes is listed in Tables 1 and 2.

Table 1.

Positive rates of anti-HGV and HGV RNA in drug users and prostitutes

n Anti-HGV HGV RNA
Drug users*
po 211 6.63 (14) 27.96 (49)
iv 164 12.20 (20) 32.92 (54)
Prostitutes
Non-addict 22 9.09 (2) 13.36 (3)
Addict 76 14.43 (36) 22.36 (17)
Healthy group 55 1.82 (1) 0 (0)

*Seventy-six prostitutes who were addicted to drugs were added to this group.

Table 2.

Risk factors of HGV infections in drug users

Sex
Addiction duration
HBV infection
Male Female < 2 years ≥ 2 years HBsAg (+) HBsAg (-)
Anti-HGV 8.65 9.23 6.48 12.58 13.33 9.37
HGV RNA 3.46 32.84 9.72 52.56 16.67 22.78

The positive rate of HGV RNA in intravenous drug users (IVDU) was higher than in oral users (χ2 = 4.36, P < 0.05). The positive rates of anti-HG V in the p rostitutes who were addicted to drugs were higher than those who were not (χ2 = 12.19, P < 0.01).

The statistical difference of anti-HGV positive rate was tested between users a ddicted for more than 2 years and users for less than 2 years (χ2 = 4.29, P < 0.05). The positive rate of HGV-RNA in female users was higher th an that in mal e users(χ2 = 11.55, P < 0. 01), that in the patients who were addicted for more t han 2 years was also higher than those addicted for less than 2 years (χ2 = 79.06, P < 0.01).

HGV infections in blood donors

Seven percent (29/417) of blood donors were found to be anti-HGV positive and 27.5% anti-HGV positive donors were detected to be HGV RNA positive.

HGV infections in the cases of PHC, hemodialysis, liver or kidney transplanta tion (Table 3)

Table 3.

HGV infections in the cases of PHC, hemodialysis, liver or kidney tran splantation

n Anti-HGV HGV RNA in anti-HGV (+) cases
Hemodialysis 61 13.11 (8/61) 37.50 (3/8)
PHC 41 4.80 (2/41) 100.00 (2/2)
Liver transplantation 3 33.30 (1/3) 100.00 (1/1)
Kidney transplantation 53 1.82 (1/53) 0
Total 158 7.5 (12/158) 50.00 (6/12)

HGV infections in the patients with hemopathy

Anti-HGV was detected in 6 (11.7%) out of 51 cases with hemopathy, among them, 4 cases with acute or chronic leukemia, one with aplasia anaemia and one with leukopenia. No HGV RNA was assayed in six anti-HGV positive cases.

HGV infections in the patients with viral hepatitis (Table 4)

Table 4.

Positive rates of anti-HGV and HGV RNA in patients with viral hepatitis

n Anti-HGV HGV RNA in anti-HGV (+) cases
Hepatitis A 35 14.29 (5/35) 20.00 (1/5)
Hepatitis B 214 17.29 (37/214) 35.14 (13/37)
Hepatitis C 62 14.52 (9/62) 55.56 (5/9)
Hepatitis E 25 4.00 (1/25) 0
Hepatitis NA-E 15 26.67 (4/15) 50.00 (2/4)
Total 351 15.05 (56/351) 37.50 (21/56)

The positive rates of anti-HGV and HGV RNA did not correlate with the sex, age, duration, and severity of diseases. The mean levels of ALT and T-Bil in patients with hepatitis B whose anti-HGV was positive were higher than those whose anti-HGV was negative.

DISCUSSION

HGV is a new pathogenic agent which was discovered in 1995, its genome structur e resembles other flaviviruses containing a positive, single plus-strand RNA[1,2]. It has been demonstrated that the distribution of HGV is global[1,2,6-14]. The transmission route of HGV is similar to that of HBV and HCV[1,3,4,11,12]. The investigation on HGV infection rates in Hubei Province of China showed that the infection rates of HGV in cases with viral hepatitis , hemodialysis, hemopathy, transplantation, intravenous drug users (IVDU) and prostitutes were 15.05%, 13. 11%, 16.7%, 9.1% and 14.43%, higher than that in healthy controls (1.82%). The result indicate that HGV infection is common in China .

The infection rate of HGV in drug users varies widely on different documents with a range from 23.8% to 77.4%[7,18-20]. However, there is no contr ov ersy regarding the fact that drug addiction is a high risk factor for HGV infect ion. We found that the positive rate of HGV RNA in IVDU was higher than that in oral drug users (12.82% vs 2.97%, P < 0.05). This suggests that the un sterilized injections contribute to HGV transmission among IVDU.

It is known that sexual contact is a common route for horizontal transmission of HBV, HCV and HDV. Recently, sexual transmission of HGV has been demonstrated[18,21-25]. Our survey found that most of the prostitutes were also addicted to drugs, this may be one of reasons that they had a high HGV infection rate. HGV infection was found in 15.05% of patients with viral hepatitis. This is much higher among the blood donors in the same geographic area. However, there may be bias in this statistical inference, since blood donors who are found to be positive for HBsAg or for anti-HCV through screening programs are told not to donate blood. Thus, the low prevalence of HGV infection may represent a selection bias. This viewpoint was demonstrated by Handajani et al[14].

No agreement has been reached on the pathogenicity of HGV. Most of the recent in vestigations show that HGV infection in patients with hepatitis B and hepatitis C is not associated with any changes in indices of liver diseases, including serum ALT level, Knodell score or histology activity index (HAI)[25-28], and the consequences of hepatitis[27,29]. However, some reports inclu ding this paper found that HGV infection was associated with liver damage, even fulminant hepatitis[31,32]. So further prospective studies are needed to demonstrate its relative significance in causing hepatitis and other diseases.

High infection rates of HGV were also discovered in patients with hemodialysis, PHC, and transplantation. This result may be associated with the more transfusions received by these cases than healthy persons.

A conclusion which can thus be drawn from this study is that HGV infection is common in this area, and the drug users, prostitutes, transplant recipients, blood donors, patients with hemopathy, hemodialysis, and liver diseases are high risk groups for HGV infection.

Footnotes

Supported by a grant from the National 863 Plans, No 102-07-02-07

Edited by Lu J proofread by Mittra S

References

  • 1.Linnen J, Wages J, Zhang-Keck ZY, Fry KE, Krawczynski KZ, Alter H, Koonin E, Gallagher M, Alter M, Hadziyannis S, et al. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science. 1996;271:505–508. doi: 10.1126/science.271.5248.505. [DOI] [PubMed] [Google Scholar]
  • 2.Leary TP, Muerhoff AS, Simons JN, Pilot-Matias TJ, Erker JC, Chalmers ML, Schlauder GG, Dawson GJ, Desai SM, Mushahwar IK. Sequence and genomic organization of GBV-C: a novel member of the flaviviridae associated with human non-A-E hepatitis. J Med Virol. 1996;48:60–67. doi: 10.1002/(SICI)1096-9071(199601)48:1<60::AID-JMV10>3.0.CO;2-A. [DOI] [PubMed] [Google Scholar]
  • 3.Komatsu H, Fujisawa T, Inui A, Sogo T, Morinishi Y, Miyagawa Y, Inui M. GBV-C/HGV infection in children with chronic hepatitis C. J Med Virol. 1999;59:154–159. doi: 10.1002/(sici)1096-9071(199910)59:2<154::aid-jmv5>3.0.co;2-q. [DOI] [PubMed] [Google Scholar]
  • 4.Sauleda S, Reesink HJ, Esteban JI, Hess G, Esteban R, Guardia J. Profiles of GBV-C/hepatitis G virus markers in patients coinfected with hepatitis C virus. J Med Virol. 1999;59:45–51. [PubMed] [Google Scholar]
  • 5.Yu JG, Hou XR, Pan W, Zhang GS, Zhou XM. PCR detection of hepatitis G virus RNA in sera and liver tissuees from patients with chronic hepatitis C. Shijie Huaren Xiaohua Zazhi. 1998;6:580. [Google Scholar]
  • 6.Wu RR, Mizokami M, Cao K, Nakano T, Ge XM, Wang SS, Orito E, Ohba K, Mukaide M, Hikiji K, et al. GB virus C/hepatitis G virus infection in southern China. J Infect Dis. 1997;175:168–171. doi: 10.1093/infdis/175.1.168. [DOI] [PubMed] [Google Scholar]
  • 7.Löve A, Stanzeit B, Gudmundsson S, Widell A. Hepatitis G virus infections in Iceland. J Viral Hepat. 1999;6:255–260. doi: 10.1046/j.1365-2893.1999.00143.x. [DOI] [PubMed] [Google Scholar]
  • 8.Desassis JF, Laperche S, Girault A, Kolko A, Bouchardeau F, Zins B, Poignet JL, Couroucé AM. Prevalence of present and past hepatitis G virus infection in a French haemodialysis centre. Nephrol Dial Transplant. 1999;14:2692–2697. doi: 10.1093/ndt/14.11.2692. [DOI] [PubMed] [Google Scholar]
  • 9.Liu HF, Muyembe-Tamfum JJ, Dahan K, Desmyter J, Goubau P. High prevalence of GB virus C/hepatitis G virus in Kinshasa, Democratic Republic of Congo: a phylogenetic analysis. J Med Virol. 2000;60:159–165. [PubMed] [Google Scholar]
  • 10.Sathar MA, Soni PN, Naicker S, Conradie J, Lockhat F, Gouws E. GB virus C/hepatitis G virus infection in KwaZulu Natal, South Africa. J Med Virol. 1999;59:38–44. [PubMed] [Google Scholar]
  • 11.Elkayam O, Hassoba HM, Ferrell LD, Garcia-Kennedy R, Gish RG, Wright TL, Laffler T, Traylor D, Hunt G, Rosenthal P. GB virus C (GBV-C/HGV) and E2 antibodies in children preliver and postliver transplant. Pediatr Res. 1999;45:795–798. doi: 10.1203/00006450-199906000-00002. [DOI] [PubMed] [Google Scholar]
  • 12.Shimizu M, Osada K, Okamoto H. Transfusion-transmitted hepatitis G virus following open heart surgery. Transfusion. 1996;36:937. doi: 10.1046/j.1537-2995.1996.361097017183.x. [DOI] [PubMed] [Google Scholar]
  • 13.Wong SB, Chan SH, Ren EC. Diversity of GB virus C/hepatitis G virus isolates in Singapore: predominance of group 2a and the Asian group 3 variant. J Med Virol. 1999;58:145–153. doi: 10.1002/(sici)1096-9071(199906)58:2<145::aid-jmv8>3.0.co;2-f. [DOI] [PubMed] [Google Scholar]
  • 14.Handajani R, Soetjipto MI, Suryohudoyo P, Adi P, Setiawan PB, Nidom CA, Soemarto R, Katayama Y, Fujii M, Hotta H. Prevalence of GB virus C/Hepatitis G virus infection among various populations in Surabaya, Indonesia, and identification of novel groups of sequence variants. J Clin Microbiol. 2000;38:662–668. doi: 10.1128/jcm.38.2.662-668.2000. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Isaacson AH, Bhardwaj B, Qian K, Davis GL, Kato T, Mizokami M, Lau JY. Hepatitis G virus infection in renal transplant recipients. J Viral Hepat. 1999;6:151–160. doi: 10.1046/j.1365-2893.1999.00149.x. [DOI] [PubMed] [Google Scholar]
  • 16.Pilot-Matias TJ, Carrick RJ, Coleman PF, Leary TP, Surowy TK, Simons JN, Muerhoff AS, Buijk SL, Chalmers ML, Dawson GJ, et al. Expression of the GB virus C E2 glycoprotein using the Semliki Forest virus vector system and its utility as a serologic marker. Virology. 1996;225:282–292. doi: 10.1006/viro.1996.0602. [DOI] [PubMed] [Google Scholar]
  • 17.Tacke M, Kiyosawa K, Stark K, Schlueter V, Ofenloch-Haehnle B, Hess G, Engel AM. Detection of antibodies to a putative hepatitis G virus envelope protein. Lancet. 1997;349:318–320. doi: 10.1016/S0140-6736(96)06461-6. [DOI] [PubMed] [Google Scholar]
  • 18.Wu JC, Sheng WY, Huang YH, Hwang SJ, Lee SD. Prevalence and risk factor analysis of GBV-C/HGV infection in prostitutes. J Med Virol. 1997;52:83–85. [PubMed] [Google Scholar]
  • 19.Trisler Z, Seme K, Poljak M, Celan-Lucu B, Sakoman S. Prevalence of hepatitis C and G virus infections among intravenous drug users in Slovenia and Croatia. Scand J Infect Dis. 1999;31:33–35. doi: 10.1080/00365549950161853. [DOI] [PubMed] [Google Scholar]
  • 20.Anastassopoulou CG, Paraskevis D, Sypsa V, Psichogiou M, Katsoulidou A, Tassopoulos N, Skoutelis A, Malliori M, Hatzakis A. Prevalence patterns and genotypes of GB virus C/hepatitis G virus among imprisoned intravenous drug users. J Med Virol. 1998;56:246–252. [PubMed] [Google Scholar]
  • 21.Sawayama Y, Hayashi J, Etoh Y, Urabe H, Minami K, Kashiwagi S. Heterosexual transmission of GB virus C/hepatitis G virus infection to non-intravenous drug-using female prostitutes in Fukuoka, Japan. Dig Dis Sci. 1999;44:1937–1943. doi: 10.1023/a:1026664428194. [DOI] [PubMed] [Google Scholar]
  • 22.Yeo AE, Matsumoto A, Shih JW, Alter HJ, Goedert JJ. Prevalence of hepatitis G virus in patients with hemophilia and their steady female sexual partners. Sex Transm Dis. 2000;27:178–182. doi: 10.1097/00007435-200003000-00012. [DOI] [PubMed] [Google Scholar]
  • 23.Stark K, Doering CD, Bienzle U, Pauli G, Hamouda O, Engel AM, Schreier E. Risk and clearance of GB virus C/hepatitis G virus infection in homosexual men: A longitudinal study. J Med Virol. 1999;59:303–306. doi: 10.1002/(sici)1096-9071(199911)59:3<303::aid-jmv7>3.0.co;2-i. [DOI] [PubMed] [Google Scholar]
  • 24.Rey D, Fraize S, Vidinic J, Meyer P, Fritsch S, Labouret N, Schmitt C, Lang JM, Stoll-Keller F. High prevalence of GB virus C/hepatitis G virus RNA in patients infected with human immunodeficiency virus. J Med Virol. 1999;57:75–79. doi: 10.1002/(sici)1096-9071(199901)57:1<75::aid-jmv11>3.0.co;2-b. [DOI] [PubMed] [Google Scholar]
  • 25.Nerurkar VR, Chua PK, Hoffmann PR, Dashwood WM, Shikuma CM, Yanagihara R. High prevalence of GB virus C/hepatitis G virus infection among homosexual men infected with human immunodeficiency virus type 1: evidence for sexual transmission. J Med Virol. 1998;56:123–127. [PubMed] [Google Scholar]
  • 26.Slimane SB, Albrecht JK, Fang JW, Goodman Z, Mizokami M, Qian K, Lau JY. Clinical, virological and histological implications of GB virus-C/hepatitis G virus infection in patients with chronic hepatitis C virus infection: a multicentre study based on 671 patients. J Viral Hepat. 2000;7:51–55. doi: 10.1046/j.1365-2893.2000.00188.x. [DOI] [PubMed] [Google Scholar]
  • 27.Césaire R, Martial J, Maier H, Kerob-Bauchet B, Bera O, Duchaud E, Brebion A, Pierre-Louis S. Infection with GB virus C/hepatitis G virus among blood donors and hemophiliacs in Martinique, a Caribbean island. J Med Virol. 1999;59:160–163. [PubMed] [Google Scholar]
  • 28.Zhao XP, Yang DL, Wang BJ, Yang Y, Shen HX, Peng ZH, Hao LJ. Immunohis tochemical study of HGV expression in liver of patients with hepatitis G. Shijie Huaren Xiaohua Zazhi. 1998;6:586. [Google Scholar]
  • 29.Bizollon T, Guichard S, Ahmed SN, Chevallier P, Ducerf C, Sepetjan M, Baulieux J, Trepo C. Impact of hepatitis G virus co-infection on the course of hepatitis C virus infection before and after liver transplantation. J Hepatol. 1998;29:893–900. doi: 10.1016/s0168-8278(98)80116-5. [DOI] [PubMed] [Google Scholar]
  • 30.Tran A, Hastier P, Longo F, Yang G, Ouzan D, Durant J, Follana R, Buckley M, Saint-Paul MC, Doglio A, et al. Lack of influence of hepatitis G virus infection on alcohol-related hepatic lesions. Scand J Gastroenterol. 1998;33:1209–1212. doi: 10.1080/00365529850172584. [DOI] [PubMed] [Google Scholar]
  • 31.Shu B, Dou XG, Li Y, Wang ZQ. Detection of HGVRNA in sera from patients with fulminant hepatitis in Shenyang. Zhonghua Liuxingbing Zazhi. 1998;19:168–169. [PubMed] [Google Scholar]
  • 32.Chen XR, Xuan MX, Wu DW, Rong YM, Zhou YX, Wan BM, Wei YN, Fu CS. Study on hepatitis G virus infection. Zhonghua Liuxingbing Zazhi. 1999;20:85–87. [PubMed] [Google Scholar]

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