MJA: Wong et al., Should we be screening blood donors for hepatitis G virus?

Should we be screening blood donors for hepatitis G virus?

The case against screening

Given the absence of a disease association, screening is not justified

Ping-Yee Wong, Patrick J Coghlan and Peter W Angus

MJA 1998; 169: 375-377
For the case against, see Moaven

Introduction - Is HGV pathogenic? - How common is the infection among blood donors? - What is the sensitivity and specificity of current tests for HGV? - What are the costs of testing? - What are the risks of not screening? - What is the prevailing expert opinion? - Conclusion - Acknowledgement - References - Authors' details
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Introduction
The availability of a reliable source of safe blood and blood products is essential for medical practice. Currently, blood donors in Australia are screened for syphilis, hepatitis B surface antigen (HBsAg), and antibodies for HIV types 1 and 2, hepatitis C virus (HCV) and human T cell lymphotropic virus (HTLV) types I and II. This screening of blood donors and modern blood product manufacturing techniques have greatly reduced the risk of transmission of serious disease by transfusion.¹ In the future, advances in genomic amplification technology may allow routine screening of donor blood for HCV, HBV and HIV genomes, and thus further reduce risks by allowing detection of viraemia during the so-called "window period" of acute infection (the phase of infection before seroconversion).
Advances in molecular biological techniques will also enable the development of tests for new potentially pathogenic agents transmitted through blood transfusion, of which the recently discovered hepatitis G virus (HGV) is likely to be but one. These developments will inevitably result in pressure on blood service administrations to expand their screening repertoire. However, the introduction of a new test can be costly "in diminished donor resources, injured donor relationships, and reduced blood supply",² and financially. Furthermore, experience has shown that blood donor screening tests are difficult to withdraw once introduced,³ even if it can later be shown that the test does not improve outcomes. The decision of Australian blood transfusion services to screen all blood donations for HTLV-I in 1992-1993 is one such example.⁴
Although there is no consensus regarding the pathogenicity of HGV, there have been calls for the introduction of screening for this newly discovered flavivirus. For this issue the key questions are:ATsubA:Is there evidence that HGV is transmitted through blood transfusion? HGV transmission by blood transfusion has been clearly demonstrated in several studies.^5-7 For example, in a retrospective study, Heuft et al traced the donations from two HGV RNA positive blood donors over the previous 18 months.⁶ Of 23 recipients who received a transfusion from either of the two donors, 15 (65%) tested positive for HGV RNA after six to 11 months. The authors were able to demonstrate by molecular sequencing that three of six (50%) recipients tested were infected by either of the donors, by sequence homology between donor and recipient of more than 99%.
Is HGV pathogenic?
Transfusion-associated HGV infection is usually not associated with any detectable illness or abnormality of liver function tests.⁸ A few instances of mild alanine aminotransferase elevation have been documented in recipients of HGV-infected blood, but a cause-and-effect relationship has not been proven.⁸ Following acute infection HGV RNA may persist in plasma for a decade or more.⁸ In one study, most individuals were found to have cleared their infection after a period of viraemia of 2-6 months,⁹ but persistence of HGV RNA is much more likely in immunocompromised subjects.⁶
HGV has been linked with fulminant hepatic failure;¹⁰ however, the Australian experience has been that, in patients with fulminant liver failure referred for liver transplantation who were found to be HGV positive, the virus appeared to have been transmitted to the patients after the onset of their illness, as the result of transfusion with HGV-infected blood products.¹¹ There is also no convincing evidence that chronic HGV infection causes liver injury or exacerbates other chronic liver diseases.¹² Thus, there is considerable doubt that HGV even qualifies as a "hepatitis virus".¹³
To date, HGV infection has not been linked with disease of any other organ system. However, vertical transmission of HGV has been demonstrated^7,14 and sexual transmission is suspected.¹⁵
How common is the infection among blood donors?
The prevalence of HGV RNA in various volunteer blood donor populations is summarised in the Box. HGV has been found in all countries where testing has been performed. Its prevalence varies from 1% to 9%; in Australia it is reported to be between 1% and 4%.^17,22 Thus, HGV appears to be ubiquitous, and screening for the virus would lead to exclusion of a significant proportion of healthy blood donors.
Box

What is the sensitivity and specificity of current tests for HGV?
At this time, no serological test has the potential to be used for screening; the recently described anti-E2 antibody to HGV seems to indicate past rather than current infection.²³ Most studies use the reverse transcription polymerase chain reaction (RT-PCR) test to detect viraemia. Although this test appears reasonably specific, the actual specificity depends on the primers used.²⁴ As the infected individual may not always be viraemic, the false-negative rate may be unacceptably high.⁸ Furthermore, none of the PCR approaches that have been used have been subjected to detailed analysis of their sensitivity and specificity. As there is no confirmatory test available, there would be considerable difficulty in dealing with discordant results and in donor counselling.
What are the costs of testing?
The RT-PCR test is expensive and cumbersome to employ on a large scale. A major investment in equipment and staff training programs is required. The logistical difficulties involved in the transport of PCR-quality samples over long distances and the delay in obtaining results will add to the overall cost.
Additionally, Australian blood services can ill-afford the deferral of up to 4% of blood donors as a result of positive test results, because this will occur on top of the steady decline in whole blood donations of 27% since 1981.²⁵ There are likely to be false positive and discordant results, and these will add significantly to the number of deferrals.
The test may reduce the rate of transfusion-transmitted HGV infection, but may lead to anxiety and ill-will among HGV-positive donors who will probably have no clinically apparent disease.²⁶
What are the risks of not screening?
As outlined above, HGV has not been linked to significant disease. Thus, even if blood is not screened for HGV and the recipient does develop a positive test for the virus, the risk to the patient is minimal.
The legal issues which arise concerning screening for HGV are complicated. An NHMRC expert committee, when it considered the legal ramifications related to HTLV-I screening,²⁷ reflected that, whereas it is not easy for people transfused with contaminated blood to claim successfully for compensation, the spectre of large damages does significantly influence a blood transfusion service's decision on whether to screen. Blood services can deal with the perceived risk from adverse public opinion by putting an evidence-based view about the pros and cons of the new screening test on record and encouraging public debate and discussion.
What is the prevailing expert opinion?
Recent reviews^2,28-31 do not support routine screening of donated blood for HGV. The American Association of Blood Banks, in its most recent examination of the issue, concluded that screening was not warranted, but called for ongoing studies to look for "a detectable disease marker for HGV", and "additional searches for hepatic and extrahepatic disease associations" of HGV infection before making a final decision.³² As far as we are aware, no blood service has introduced routine HGV RNA testing of blood donors.
Conclusion
The development of successful tests for viruses such as HIV and HCV has been a major breakthrough that has greatly reduced the risks associated with blood transfusion. HGV is likely to be the first of a number of new viruses that will be detected in people by studies using the new molecular biological techniques. However, in the absence of evidence of a major ongoing disease risk associated with blood transfusion, blood services need to respond with caution to calls for the introduction of new test strategies. In these situations a rational and transparent process should lead to a reasonable outcome for stakeholders.
In the absence of a clear disease association with HGV and with the knowledge that testing would be costly and cause a further diminution in the availability of blood products for no apparent reason, we do not believe that HGV screening can be justified at this time.
Acknowledgement
The authors would like to thank Dr Anthony Keller, Chairman of the National Donor and Product Safety Committee, Australian Red Cross Blood Service, for his critical comments on a final draft of the manuscript.
References

Schreiber GB, Busch MP, Kleinman SH, Korelitz JJ. The risk of transfusion- transmitted viral infections. N Engl J Med 1996; 334: 1685-1690.
Alter HJ. G-pers, creepers, where'd you get those papers? A reassessment of the literature on the hepatitis G virus [editorial]. Transfusion 1997; 37: 569-572.
Holland PV. Viral infections and the blood supply [editorial]. N Engl J Med 1996; 334: 1734-1735.
Whyte GS. Is screening of Australian blood donors for HTLV-I necessary? Med J Aust 1997; 166: 478-481.
Shimizu M, Osada K, Okamoto H. Transmission of GB virus C by blood transfusions during heart surgery. Vox Sang 1997; 72: 76-78.
Heuft HG, Berg T, Schreier E, et al. Epidemiological and clinical aspects of hepatitis G virus infection in blood donors and immunocompromised recipients of HGV-contaminated blood. Vox Sang 1998; 74: 161-167.
Roth WK, Waschk D, Marx S, et al. Prevalence of hepatitis G virus and its strain variant, the GB agent, in blood donations and their transmission to recipients. Transfusion 1997; 37: 651-656.
Alter HJ, Nakatsuji Y, Melpolder J, et al. The incidence of transfusion-associated hepatitis G virus infection and its relation to liver disease. N Engl J Med 1997; 336: 747-754.
Simons JN, Desai SM, Mushahwar IK. The GB viruses: isolation, characterization, diagnosis, and epidemiology. Viral Hepatitis Reviews 1996; 2: 229-246.
Yoshiba M, Okamoto H, Mishiro S. Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology. Lancet 1995; 346: 1131-1132.
Moaven LD, Locarnini SA, Bowden DS, et al. Hepatitis G virus and fulminant hepatic failure: evidence for transfusion related infection. J Hepatol 1997; 27: 613-619.
Goldstein NS, Underhill J, Gordon SC, et al. Comparative histologic features of liver biopsy specimens from patients coinfected with hepatitis G and C viruses with chronic hepatitic C virus alone. An age-, sex-, disease duration-, and transmission-matched controlled study of chronic hepatitis. Am J Clin Pathol 1997; 108: 625-632.
Batts KP. Hepatitis G. A virus in search of a disease [editorial]. Am J Clin Pathol 1997; 108: 616-618.
Viazov S, Riffelmann M, Sarr S, et al. Transmission of GBV-C/HGV from drug-addicted mothers to their babies. J Hepatol 1997; 27: 85-90.
Kao JH, Chen W, Chen PJ, et al. GB virus-C/hepatitis G virus infections in prostitutes: possible role of sexual transmission. J Med Virol 1997; 52: 381-384.
Yoshikawa A, Fukuda S, Itoh K, et al. Infection with hepatitis G virus and its strain variant, the GB agent (GBV-C), among blood donors in Japan. Transfusion 1997; 37: 657-663.
Coghlan PJ, Wong P-Y, Katsoris J, et al. Hepatitis G -- issues for the blood bank [abstract]. Presentation at the Fourth National Symposium on Hepatitis C and Related Viruses Including Hepatitis G. 23 November 1996, St Vincent's Hospital, Melbourne, Australia.
Loiseau P, Mariotti M, Corbi C, et al. Prevalence of hepatitis G virus RNA in French blood donors and recipients. Transfusion 1997; 37: 645-650.
Wang Y, Chen H-S, Fan M-H, et al. Infection with GB virus C and hepatitis C virus in hemodialysis patients and blood donors in Beijing. J Med Virol 1997; 52: 26-30.
Bassit L, Kleter B, Ribeiro-dos-Santos G, et al. Hepatitis G virus: prevalence and sequence analysis in blood donors of Sao Paulo, Brazil. Vox Sang 1997; 74: 83-87.
Jarvis LM, Davidson F, Hanley JP, et al. Infection with hepatitis G virus among recipients of plasma products. Lancet 1996; 348: 1352-1355.
Moaven LD, Hyland CA, Young IF, et al. Prevalence of hepatitis G virus in Queensland blood donors. Med J Aust 1996; 165: 369-371.
Dille BJ, Surowy TK, Gutierrez RA, et al. An ELISA for detection of antibodies to the E2 protein of GB virus C. J Infect Dis 1997; 175: 458-461.
Kao JH, Chen PJ, Chen W, et al. Amplification of GB virus-C/hepatitis G virus RNA with primers from different regions of the viral genome. J Med Virol 1997; 51: 284-289.
Whyte G. Quantitating donor behaviour to model the effect of changes in donor management on sufficiency in the blood service. Vox Sang. In press.
Busch MP. To thy (reactive) donors be true! Transfusion 1997; 37: 117-120.
National Health and Medical Research Council. Case study of screening blood donations for human T-cell lymphotropic virus type I (HTLV-I). Canberra: AGPS, 1993.
Di Bisceglie AM. Hepatitis G virus infection: a work in progress. Ann Intern Med 1996; 125: 772-773.
Allain J-P. Screening blood donors for markers of new viruses [commentary]. Lancet 1997; 349: 584-585.
Karayiannis P, Thomas HC. Current status of hepatitis G virus (GBV-C) in transfusion: is it relevant? Vox Sang 1997; 73: 63-69.
Barbara JA. Does GB virus C ('hepatitis G virus') threaten the safety of our blood supply? [editorial]. Transf Med 1997; 7: 75-76.
Snyder EL, Lipton KS. Hepatitis G virus: status report and assessment of clinical relevance. AABB Association Bulletin 1998; Bulletin No 98-4, 18 July 1998.

(Received 20 May, accepted 12 August, 1998)

Authors' details

Australian Red Cross Blood Service -- Victoria, South Melbourne, VIC.
Ping-Yee Wong, MB BS, MRCP, Senior Medical Officer.

Australian Red Cross Blood Service -- National Office, Fitzroy, VIC.
Patrick J Coghlan, FRCPA, FRCPath, Director of Intellectual Capital.

Gastroenterology and Liver Transplant Units, Austin and Repatriation Hospital, VIC.
Peter W Angus, MD, FRACP, Hepatologist.

Reprints will not be available from the authors.
Correspondence: Dr P-Y Wong, Australian Red Cross Blood Service -- Victoria, PO Box 354, South Melbourne, VIC 3205.
E-mail: pwongATrcbbv.org.au

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Introduction	The availability of a reliable source of safe blood and blood products is essential for medical practice. Currently, blood donors in Australia are screened for syphilis, hepatitis B surface antigen (HBsAg), and antibodies for HIV types 1 and 2, hepatitis C virus (HCV) and human T cell lymphotropic virus (HTLV) types I and II. This screening of blood donors and modern blood product manufacturing techniques have greatly reduced the risk of transmission of serious disease by transfusion.¹ In the future, advances in genomic amplification technology may allow routine screening of donor blood for HCV, HBV and HIV genomes, and thus further reduce risks by allowing detection of viraemia during the so-called "window period" of acute infection (the phase of infection before seroconversion). Advances in molecular biological techniques will also enable the development of tests for new potentially pathogenic agents transmitted through blood transfusion, of which the recently discovered hepatitis G virus (HGV) is likely to be but one. These developments will inevitably result in pressure on blood service administrations to expand their screening repertoire. However, the introduction of a new test can be costly "in diminished donor resources, injured donor relationships, and reduced blood supply",² and financially. Furthermore, experience has shown that blood donor screening tests are difficult to withdraw once introduced,³ even if it can later be shown that the test does not improve outcomes. The decision of Australian blood transfusion services to screen all blood donations for HTLV-I in 1992-1993 is one such example.⁴ Although there is no consensus regarding the pathogenicity of HGV, there have been calls for the introduction of screening for this newly discovered flavivirus. For this issue the key questions are:ATsubA:Is there evidence that HGV is transmitted through blood transfusion? HGV transmission by blood transfusion has been clearly demonstrated in several studies.^5-7 For example, in a retrospective study, Heuft et al traced the donations from two HGV RNA positive blood donors over the previous 18 months.⁶ Of 23 recipients who received a transfusion from either of the two donors, 15 (65%) tested positive for HGV RNA after six to 11 months. The authors were able to demonstrate by molecular sequencing that three of six (50%) recipients tested were infected by either of the donors, by sequence homology between donor and recipient of more than 99%.
Is HGV pathogenic?	Transfusion-associated HGV infection is usually not associated with any detectable illness or abnormality of liver function tests.⁸ A few instances of mild alanine aminotransferase elevation have been documented in recipients of HGV-infected blood, but a cause-and-effect relationship has not been proven.⁸ Following acute infection HGV RNA may persist in plasma for a decade or more.⁸ In one study, most individuals were found to have cleared their infection after a period of viraemia of 2-6 months,⁹ but persistence of HGV RNA is much more likely in immunocompromised subjects.⁶ HGV has been linked with fulminant hepatic failure;¹⁰ however, the Australian experience has been that, in patients with fulminant liver failure referred for liver transplantation who were found to be HGV positive, the virus appeared to have been transmitted to the patients after the onset of their illness, as the result of transfusion with HGV-infected blood products.¹¹ There is also no convincing evidence that chronic HGV infection causes liver injury or exacerbates other chronic liver diseases.¹² Thus, there is considerable doubt that HGV even qualifies as a "hepatitis virus".¹³ To date, HGV infection has not been linked with disease of any other organ system. However, vertical transmission of HGV has been demonstrated^7,14 and sexual transmission is suspected.¹⁵
How common is the infection among blood donors?	The prevalence of HGV RNA in various volunteer blood donor populations is summarised in the Box. HGV has been found in all countries where testing has been performed. Its prevalence varies from 1% to 9%; in Australia it is reported to be between 1% and 4%.^17,22 Thus, HGV appears to be ubiquitous, and screening for the virus would lead to exclusion of a significant proportion of healthy blood donors.
What is the sensitivity and specificity of current tests for HGV?	At this time, no serological test has the potential to be used for screening; the recently described anti-E2 antibody to HGV seems to indicate past rather than current infection.²³ Most studies use the reverse transcription polymerase chain reaction (RT-PCR) test to detect viraemia. Although this test appears reasonably specific, the actual specificity depends on the primers used.²⁴ As the infected individual may not always be viraemic, the false-negative rate may be unacceptably high.⁸ Furthermore, none of the PCR approaches that have been used have been subjected to detailed analysis of their sensitivity and specificity. As there is no confirmatory test available, there would be considerable difficulty in dealing with discordant results and in donor counselling.
What are the costs of testing?	The RT-PCR test is expensive and cumbersome to employ on a large scale. A major investment in equipment and staff training programs is required. The logistical difficulties involved in the transport of PCR-quality samples over long distances and the delay in obtaining results will add to the overall cost. Additionally, Australian blood services can ill-afford the deferral of up to 4% of blood donors as a result of positive test results, because this will occur on top of the steady decline in whole blood donations of 27% since 1981.²⁵ There are likely to be false positive and discordant results, and these will add significantly to the number of deferrals. The test may reduce the rate of transfusion-transmitted HGV infection, but may lead to anxiety and ill-will among HGV-positive donors who will probably have no clinically apparent disease.²⁶
What are the risks of not screening?	As outlined above, HGV has not been linked to significant disease. Thus, even if blood is not screened for HGV and the recipient does develop a positive test for the virus, the risk to the patient is minimal. The legal issues which arise concerning screening for HGV are complicated. An NHMRC expert committee, when it considered the legal ramifications related to HTLV-I screening,²⁷ reflected that, whereas it is not easy for people transfused with contaminated blood to claim successfully for compensation, the spectre of large damages does significantly influence a blood transfusion service's decision on whether to screen. Blood services can deal with the perceived risk from adverse public opinion by putting an evidence-based view about the pros and cons of the new screening test on record and encouraging public debate and discussion.
What is the prevailing expert opinion?	Recent reviews^2,28-31 do not support routine screening of donated blood for HGV. The American Association of Blood Banks, in its most recent examination of the issue, concluded that screening was not warranted, but called for ongoing studies to look for "a detectable disease marker for HGV", and "additional searches for hepatic and extrahepatic disease associations" of HGV infection before making a final decision.³² As far as we are aware, no blood service has introduced routine HGV RNA testing of blood donors.
Conclusion	The development of successful tests for viruses such as HIV and HCV has been a major breakthrough that has greatly reduced the risks associated with blood transfusion. HGV is likely to be the first of a number of new viruses that will be detected in people by studies using the new molecular biological techniques. However, in the absence of evidence of a major ongoing disease risk associated with blood transfusion, blood services need to respond with caution to calls for the introduction of new test strategies. In these situations a rational and transparent process should lead to a reasonable outcome for stakeholders. In the absence of a clear disease association with HGV and with the knowledge that testing would be costly and cause a further diminution in the availability of blood products for no apparent reason, we do not believe that HGV screening can be justified at this time.
Acknowledgement	The authors would like to thank Dr Anthony Keller, Chairman of the National Donor and Product Safety Committee, Australian Red Cross Blood Service, for his critical comments on a final draft of the manuscript.
References	Schreiber GB, Busch MP, Kleinman SH, Korelitz JJ. The risk of transfusion- transmitted viral infections. N Engl J Med 1996; 334: 1685-1690. Alter HJ. G-pers, creepers, where'd you get those papers? A reassessment of the literature on the hepatitis G virus [editorial]. Transfusion 1997; 37: 569-572. Holland PV. Viral infections and the blood supply [editorial]. N Engl J Med 1996; 334: 1734-1735. Whyte GS. Is screening of Australian blood donors for HTLV-I necessary? Med J Aust 1997; 166: 478-481. Shimizu M, Osada K, Okamoto H. Transmission of GB virus C by blood transfusions during heart surgery. Vox Sang 1997; 72: 76-78. Heuft HG, Berg T, Schreier E, et al. Epidemiological and clinical aspects of hepatitis G virus infection in blood donors and immunocompromised recipients of HGV-contaminated blood. Vox Sang 1998; 74: 161-167. Roth WK, Waschk D, Marx S, et al. Prevalence of hepatitis G virus and its strain variant, the GB agent, in blood donations and their transmission to recipients. Transfusion 1997; 37: 651-656. Alter HJ, Nakatsuji Y, Melpolder J, et al. The incidence of transfusion-associated hepatitis G virus infection and its relation to liver disease. N Engl J Med 1997; 336: 747-754. Simons JN, Desai SM, Mushahwar IK. The GB viruses: isolation, characterization, diagnosis, and epidemiology. Viral Hepatitis Reviews 1996; 2: 229-246. Yoshiba M, Okamoto H, Mishiro S. Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology. Lancet 1995; 346: 1131-1132. Moaven LD, Locarnini SA, Bowden DS, et al. Hepatitis G virus and fulminant hepatic failure: evidence for transfusion related infection. J Hepatol 1997; 27: 613-619. Goldstein NS, Underhill J, Gordon SC, et al. Comparative histologic features of liver biopsy specimens from patients coinfected with hepatitis G and C viruses with chronic hepatitic C virus alone. An age-, sex-, disease duration-, and transmission-matched controlled study of chronic hepatitis. Am J Clin Pathol 1997; 108: 625-632. Batts KP. Hepatitis G. A virus in search of a disease [editorial]. Am J Clin Pathol 1997; 108: 616-618. Viazov S, Riffelmann M, Sarr S, et al. Transmission of GBV-C/HGV from drug-addicted mothers to their babies. J Hepatol 1997; 27: 85-90. Kao JH, Chen W, Chen PJ, et al. GB virus-C/hepatitis G virus infections in prostitutes: possible role of sexual transmission. J Med Virol 1997; 52: 381-384. Yoshikawa A, Fukuda S, Itoh K, et al. Infection with hepatitis G virus and its strain variant, the GB agent (GBV-C), among blood donors in Japan. Transfusion 1997; 37: 657-663. Coghlan PJ, Wong P-Y, Katsoris J, et al. Hepatitis G -- issues for the blood bank [abstract]. Presentation at the Fourth National Symposium on Hepatitis C and Related Viruses Including Hepatitis G. 23 November 1996, St Vincent's Hospital, Melbourne, Australia. Loiseau P, Mariotti M, Corbi C, et al. Prevalence of hepatitis G virus RNA in French blood donors and recipients. Transfusion 1997; 37: 645-650. Wang Y, Chen H-S, Fan M-H, et al. Infection with GB virus C and hepatitis C virus in hemodialysis patients and blood donors in Beijing. J Med Virol 1997; 52: 26-30. Bassit L, Kleter B, Ribeiro-dos-Santos G, et al. Hepatitis G virus: prevalence and sequence analysis in blood donors of Sao Paulo, Brazil. Vox Sang 1997; 74: 83-87. Jarvis LM, Davidson F, Hanley JP, et al. Infection with hepatitis G virus among recipients of plasma products. Lancet 1996; 348: 1352-1355. Moaven LD, Hyland CA, Young IF, et al. Prevalence of hepatitis G virus in Queensland blood donors. Med J Aust 1996; 165: 369-371. Dille BJ, Surowy TK, Gutierrez RA, et al. An ELISA for detection of antibodies to the E2 protein of GB virus C. J Infect Dis 1997; 175: 458-461. Kao JH, Chen PJ, Chen W, et al. Amplification of GB virus-C/hepatitis G virus RNA with primers from different regions of the viral genome. J Med Virol 1997; 51: 284-289. Whyte G. Quantitating donor behaviour to model the effect of changes in donor management on sufficiency in the blood service. Vox Sang. In press. Busch MP. To thy (reactive) donors be true! Transfusion 1997; 37: 117-120. National Health and Medical Research Council. Case study of screening blood donations for human T-cell lymphotropic virus type I (HTLV-I). Canberra: AGPS, 1993. Di Bisceglie AM. Hepatitis G virus infection: a work in progress. Ann Intern Med 1996; 125: 772-773. Allain J-P. Screening blood donors for markers of new viruses [commentary]. Lancet 1997; 349: 584-585. Karayiannis P, Thomas HC. Current status of hepatitis G virus (GBV-C) in transfusion: is it relevant? Vox Sang 1997; 73: 63-69. Barbara JA. Does GB virus C ('hepatitis G virus') threaten the safety of our blood supply? [editorial]. Transf Med 1997; 7: 75-76. Snyder EL, Lipton KS. Hepatitis G virus: status report and assessment of clinical relevance. AABB Association Bulletin 1998; Bulletin No 98-4, 18 July 1998. (Received 20 May, accepted 12 August, 1998)