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Saudi Journal of Kidney Diseases and Transplantation
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REVIEW ARTICLE Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 5  |  Page : 831-834
Epidemiology and transmission of hepatitis G virus infection in dialysis patients


1 Gastroenterintestinal and Liver Disease Research Center, Iran University of Medical Sciences, Tehran, Iran
2 Baqiyatallah Research Center for Gastroenterology and Liver Disease, Baqiyatallah University of Medical Sciences, Tehran, Iran
3 Infectious Disease Department, Tehran University of Medical Sciences, Tehran, Iran

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Date of Web Publication31-Aug-2010
 

   Abstract 

Hepatitis G virus (HGV) or GB-virus type C (GBV-C) is distributed globally and is present in the volunteer blood donor population. For epidemiological studies, HGV is of interest in hemodialysis patients who are at risk of parenterally transmitted infections. The role of HGV in producing illness and hepatic disease has yet to be determined. A review of literature was performed in 2009 to summarize scientific reports on epidemiology and pathogenesis of the HGV infection and its exposure through hemodialysis.

How to cite this article:
Fallahian F, Alavian SM, Rasoulinejad M. Epidemiology and transmission of hepatitis G virus infection in dialysis patients. Saudi J Kidney Dis Transpl 2010;21:831-4

How to cite this URL:
Fallahian F, Alavian SM, Rasoulinejad M. Epidemiology and transmission of hepatitis G virus infection in dialysis patients. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2019 Aug 21];21:831-4. Available from: http://www.sjkdt.org/text.asp?2010/21/5/831/68875

   Introduction Top


A recently discovered and identified non-A-E hepatitis virus has been designated the name hepatitis G virus (HGV), which is a member of the Flaviviridae family. The genomic sequen­ces of these viruses have been determined by different researchers, which were found to be 1600 nucleotide long. Based on genomic se­quence comparisons, HGV is also named as GB-C. It is highly controversial virus regar­ding pathogenesis, mode of transmission, and site of replication. [1] The GBV-C/HGV virus has clearly established transmission modes, which include mainly blood contamination and occa­sionally sexual transmission. [2],[3],[4] It is frequently found among transfused patients, [5],[6] intravenous drug abusers, [2] and hemodialysis (HD) patients. Blood donors seronegative for HCV and HBV are at low risk for HGV infection. [7] HGV-RNA prevalence is low and observed primarily in males, [8] and increased significantly with age. [9],[10],[11] In addition, seroprevalence against HGV was associated with hospitalizations before 1990. [9]

Chronic carriage of HGV is possible, but does not result in chronic hepatitis. [12],[13],[14],[15],[16],[17],[18] Although GBV-C is detected in many patients with chro­nic hepatitis, [19] it does not appear to cause liver disease. [20] In addition, it does not appear to mo­dulate the course response to treatment of chronic HCV or hepatitis B virus infectios. [7],[21]

A phylogenetic analysis also revealed that GBV-C has five major genotypes: type 1 pre­dominates in West Africa, type 2 in Europe and the United States, type 3 in parts of Asia, type 4 in Southeast Asia, and type 5 in South Africa. [22] None of the South African isolates grouped with group 3 variants described from Southeast Asia. [23] Analysis of 5'NCR sequences from a large number of isolates of HGV, in­cluding newly obtained sequences from Pakis­tan, Zaire and Scotland, were associated with specific polymorphisms in the 5'NCR. [24]

We reviewed the medical literature of HGV infection in the different dialysis populations to determine the prevalence, and routes of trans­mission of HGV infection.


   Epidemiology and Transmission of HGV Infection in Dialysis Patients Top


In a study of the frequency of HGV exposure in 77 subjects on HD and 13 subjects on con­tinuous ambulatory peritoneal dialysis (CAPD) patients in Iran, 3.89% of the HD patients and none of the CAPD patients tested were po­sitive for anti-E2. Co-infection with HCV or HBV was not observed in the anti-E2 positive patients. In addition, no relationship was noted between HGV exposure and age, sex, history of blood transfusion, time on dialysis and HCV or HBV markers. [25] In a follow-up study, the prevalence of HGV exposure was 0% in the 27 dialysis staff, while the prevalence of anti-HCV and anti-HBs was 37.03% and 33.33%, respectively. [26]

In a study of 2796 hemodialysis patients in Germany, antibodies against HGV were detec­ted in 17.5% of patients and viremia in 19.6%. In addition, 3.0% of the patients were positive for both antibodies and HGV-RNA. It was found that more than five blood transfusions increased the risk of HGV infection signifi­cantly. HGV is common in German hemodia­lysis patients, but in contrast to other paren­terally transmitted viruses there is no further risk for new infections during hemodialysis, except for patients who have received several blood transfusions. [27]

High frequency (20%) of GBV-C/HGV vire­mia (GBV-C/HGV RNA) was revealed in a cohort of patients on CAPD from Italy. In most patients (94%), the presence of anti-E2 GBV-C/HGV antibody was associated with clearance of GBV-C/HGV from serum. No relationship was noted between anti-E2 GBV­C/HGV antibody (or GBV-C/ HGV viremia) and age, sex, race, time on dialysis, anti-HCV antibody, HBsAg status, and anti-HIV positi­vity. The frequency of GBV-C/HGV infection in CAPD patients was much higher than that in blood donors. The clinical significance of GBV­C/HGV in CAPD remains unclear. [28]

Serum samples from 160 patients in a chronic HD unit were collected at the time of initiation of chronic HD therapy and annually thereafter. Forty healthy staff members were also enrolled as control subjects. Three of the 40 (7.5%) heal­thy staff members were positive for HGV RNA or HGV E2 antibodies, in contrast to 40 of the 160 (25%) HD patients, including 14 (8.8%) who were positive for HGV RNA only, 25 (15.6%) who were positive for HGV E2 antibody only, and 1 (0.6%) who was positive for both markers. HGV exposure did not cor­relate with gender, age, duration of HD the­rapy, or history of blood transfusions. At least 20 of the 40 (50%) patients with HGV expo­sure had been infected before the start of chronic HD therapy. Nine (22.5%) patients ac­quired new HGV infections after starting chro­nic HD therapy, with an incidence rate of > 2.6% per year. HGV infection was not found to cause significant elevation of alanine ami­notransferase levels in the group exposed to it. Besides transmission through blood transfu­sion, HGV may have been transmitted from patient-to-patient within the HD unit. The com­pliance with standard universal precautions should be carefully re-examined, but it is still not universally recommended to routinely screen for HGV infection among patients on chronic HD. [29]

To determine the seroprevalence of hepatitis G virus (HGV) infection, a study surveyed antibody to HGV (anti-E2) and HGV RNA in 298 residents of a hepatitis C virus (HCV)­endemic area of Japan and in 225 HD patients. The total HGV marker (anti-E2 and/or HGV RNA) prevalences were 12.4% in the residents and 14.2% in the HD patients, which were sig­nificantly lower than the prevalences of the antibodies to HCV (19.8% and 42.7%, respec­tively) and anti-HBc ((29.2% and 44.9%, res­pectively). [30]

Paired sera from 292 patients undergoing chronic HD treatment in four units in the Los Angeles area, USA were tested for HGV RNA before and after they had been on HD. At study entry the HGV prevalence was 17%. HGV positivity was strongly associated with the location of HD patients among the units; some HD individuals with current HGV infec­tion showed biochemical signs of liver disease without other apparent causes. De novo acqui­sition of HGV occurred within HD units in the absence of evident parenteral risk factors for HGV other than their presence in the HD envi­ronment. A large portion of HGV viremic pa­tients showed non-persistently detectable HGV viremia during the study. Furthermore, the acquisition of HGV was not associated with a rise in ALT activity unlike prior experience with de novo HCV in HD patients. [31]

The prevalence of hepatitis B (HBV), hepa­titis C (HCV), GB virus C/hepatitis G (GBV­C/HGV) and TT (TTV) viruses in patients with chronic renal failure who were on conservative management before entering into an HD pro­gram (predialysis) in comparison with HD pa­tients was studied to elucidate whether the high prevalence of these viruses is influenced by that observed in the predialysis stage. No differences regarding age, gender, previous surgery and number of transfusions were found between infected and uninfected patients with­in and between both groups, and the preva­lence of the viruses predialysis may influence their prevalence in dialysis units. [32]

In conclusion, HGV is distinct from hepatitis C virus (HCV) and the newly discovered GBV-A and GBV-B agents, while GBV-C re­presents an isolate of HGV. The structure of the HGV genome resembles that of HCV. HGV replicates in peripheral blood cells, while replication in liver cells has not been ob­served till date. Epidemiological data indicate that the virus is prevalent throughout the world, and is transmitted via blood/blood pro­ ducts, sexually and vertically from infected mothers to children. A phylogenetic analysis also revealed that GBV-C has five major geno­types. HGV infection does not appear to have a major role in liver disease or potentially mo­dulate the course of other chronic viral infec­tions. Further investigations are required to explain the modes of HGV transmission, the clinical significance of HGV infection, and the major risk factors for transmission in special at risk populations.

 
   References Top

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2.Ramezani A, Mohraz M, Vahabpour R, et al. Frequency of hepatitis G virus infection among HIV positive subjects with parenteral and sexual exposure. J Gastrointestin Liver Dis 2008;17(3): 269-72.  Back to cited text no. 2      
3.Kaya S, Cicioglu Aridogan B, Demirci M. The prevalence of hepatitis G virus in patients with hepatitis B and C virus infections. Mikrobiyol Bul 2004;38(4):421-7.  Back to cited text no. 3      
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5.Moatter T, Adil S, Haroon S, Azeemuddin S, Hassan F, Khurshid M. Prevalence of hepatitis G virus in Pakistani children with transfusion de­pendent beta-thalassemia major. Indian J Pathol Microbiol 1999;42(4):475-82.  Back to cited text no. 5      
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10.Handa A, Jubran RF, Dickstein B, et al. GB virus C/Hepatitis G virus infection is frequent in American children and young adults. Clin Infect Dis 2000;30(3):569-71.  Back to cited text no. 10      
11.Anastassopoulou CG, Paraskevis D, Tassopoulos NC, et al. Molecular epidemiology of GB virus C/hepatitis G virus in Athens, Greece. J Med Virol 2000;61(3):319-26.  Back to cited text no. 11      
12.Blanc PL, Boumrazne R, Sarzier JM, Forel C. Extrahepatic symptoms in the course of GBV­C/HGV infection. Med Mal Infect 2009;39(4): 264-6.  Back to cited text no. 12      
13.Jeon MJ, Shin JH, Suh SP, Lim YC, Ryang DW. TT virus and hepatitis G virus infections in Korean blood donors and patients with chronic liver disease. World J Gastroenterol 2003;9(4): 741-4.  Back to cited text no. 13      
14.Handajani R, Soetjipto, Lusida MI, et al. 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(2): 662-8.  Back to cited text no. 14      
15.Par A, Takacs M, Brojnas J, et al. Viral co­infections in hepatitis C: HBV, HBV-C/HGV and TTV studies. Orv Hetil 2004;145(19):987-92.  Back to cited text no. 15      
16.Watanabe MA, Milanezi CM, Silva WA Jr, et al. Molecular investigation of GB virus C RNA in hemodialysis and thalassemics patients from Brazil. Ren Fail 2003;25(1):67-75.  Back to cited text no. 16      
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22.Hattori J, Ibe S, Nagai H, et al. Prevalence of infection and genotypes of GBV-C/HGV among homosexual men. Microbiol Immunol 2003;47 (10):759-63.  Back to cited text no. 22      
23.Sathar MA, Soni PN, Pegoraro R, et al. A new variant of GB virus C/hepatitis G virus (GBV­C/HGV) from South Africa. Virus Res 1999;64 (2):151-60.  Back to cited text no. 23      
24.Smith DB, Cuceanu N, Davidson F, et al. Discrimination of hepatitis G virus/GBV-C geo­graphical variants by analysis of the 5' non­coding region. J Gen Virol 1997;78(Pt 7):1533­-42.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]  
25.Eslamifar A, Hamkar R, Ramezani A, et al. Hepatitis G virus exposure in dialysis patients. Int Urol Nephrol 2007;39(4):1257-63.  Back to cited text no. 25      
26.Eslamifar A, Hamkar R, Ramezani A, et al. Hepatitis G virus exposure in dialysis staff. Ther Apher Dial 2007;11(5):370-4.  Back to cited text no. 26      
27.Hinrichsen H, Leimenstoll G, Stegen G, et al. Prevalence of and risk factors for hepatitis G (HGV) infection in haemodialysis patients: a multicentre study. Nephrol Dial Transplant 2002; 17(2):271-5.  Back to cited text no. 27      
28.Fabrizi F, De Vecchi AF, Lunghi G, Finazzi S, Bisegna S, Ponticelli C. Epidemiology of GB virus c/hepatitis g virus infection in patients on peritoneal dialysis. Perit Dial Int 2002;22(3):405­-10.  Back to cited text no. 28      
29.Huang JJ, Lee WC, Ruaan MK, Wang MC, Chang TT, Young KC. Incidence, transmission, and clinical significance of hepatitis G virus infection in hemodialysis patients. Eur J Clin Microbiol Infect Dis 2001;20(6):374-9.  Back to cited text no. 29      
30.Furusyo N, Hayashi J, Ariyama I, Sawayama Y, Etoh Y, Kashiwagi S. Lower hepatitis G virus infection prevalence compared to hepatitis B and C virus infection prevalences. Dig Dis Sci 2000;45(1):188-95.  Back to cited text no. 30      
31.Martin P, Fabrizi F, Dixit V, et al. Epidemiology and natural history of hepatitis G virus infection in chronic hemodialysis patients. Am J Nephrol 1999;19(5):535-40.  Back to cited text no. 31      
32.Lopez-Alcorocho JM, Barril G, Ortiz-Movilla N, et al. Prevalence of hepatitis B, hepatitis C, GB virus C/hepatitis G and TT viruses in predialysis and hemodialysis patients. J Med Virol 2001;63 (2):103-7.  Back to cited text no. 32      

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Correspondence Address:
Farahnaz Fallahian
Gastroenterintestinal and Liver Disease Research Center, Iran University of Medical Sciences, Firuzgar Hospital, Vali asr Square, Aban St., Tehran
Iran
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    Abstract
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    References
 

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