Saudi Journal of Kidney Diseases and Transplantation

: 2010  |  Volume : 21  |  Issue : 5  |  Page : 831--834

Epidemiology and transmission of hepatitis G virus infection in dialysis patients

Farahnaz Fallahian1, Seyed-Moayed Alavian2, Mehrnaz Rasoulinejad3,  
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

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


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;21:831-834

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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 2021 Apr 20 ];21:831-834
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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

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.


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