Hepatitis G virus in long-term survivors of haematological malignancy

Neilson, Jeff; Harrison, Paul M.; Milligan, Donald; Skidmore, Susan J.; Collingham, Kathryn E.

doi:10.1016/s0140-6736(96)91122-8

Cited by 55 publications

(22 citation statements)

References 3 publications

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“…Thus, severe impairment of the immune function could have facilitated the persistence of an HGV infection, while patients with no or mild immunosuppressive regimens were able to clear the virus, possibly by forming neutralizing antibodies. This assumption is substantiated by two recent reports showing higher rates of HGV infections in polytransfused immunosuppressed renal or bone marrow transplant recipients than in polytransfused immunocompetent patients [19, 20]. Whether the HGV-RNA-negative patients had already formed protective antibodies prior to the transfusion of HGV-positive blood cannot be answered but seems unlikely.…”

Section: Discussionmentioning

confidence: 98%

Epidemiological and Clinical Aspects of Hepatitis G Virus Infection in Blood Donors and Immunocompromised Recipients of HGV-Contaminated Blood

et al. 1998

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Background and objectives: The infectiousness and clinical relevance of the newly discovered blood-borne Flaviviridae-like agent, termed hepatitis G virus (HGV), are not well understood. Materials and methods: Twenty-three transfusion recipients of two HGV-affected long-term blood donors were studied for HGV genome and antibodies to the putative envelope 2 glycoprotein (anti-E2) of HGV. Nine recipients had nonhematological disorders and 14 suffered from severe hematological diseases and 7 of them received allogeneic bone marrow or blood stem cell transplantation. The molecular epidemiology of the observed HGV infection was studied by direct sequencing of parts of the 5′-noncoding region, NS3, and NS5 region of HGV in the 2 long-term donors and in their 6 recipients who became HGV RNA positive. Additionally, 549 individuals – homologous (n = 254) and autologous blood donors (n = 202), and medical staff (n = 89) – were investigated for the presence of HGV RNA. Results: HGV RNA in serum was found in 15 of the 23 (65%) transfusion recipients with known exposure of HGV-contaminated blood. Seven of the remaining 8 recipients showed only an anti-E2 response, indicating previous HGV infection with spontaneous clearance of the virus. In one recipient neither HGV RNA nor anti-E2 could be detected. Molecular evidence for HGV transmission by the 2 donors was found in 3 of the 6 recipients studied. The alanine aminotransferase levels were not significantly different in the HGV RNA positive and negative recipients, and none of the 23 recipients developed posttransfusion hepatitis. Persistent HGV infection was observed especially in recipients with severe hematological disorders or in those in whom intensive immunosuppressive treatment was necessary. Of the 549 individuals studied, 10 (1.8%) were healthy carriers of HGV RNA. Conclusion: The persistence of transfusion-acquired HGV infection is not associated with acute or chronic hepatitis, but may be influenced by the recipient’s underlying disease.

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Section: Discussionmentioning

confidence: 98%

Epidemiological and Clinical Aspects of Hepatitis G Virus Infection in Blood Donors and Immunocompromised Recipients of HGV-Contaminated Blood

et al. 1998

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“…Subsequent analysis of patients infected with HGV alone showed that just over half of them had abnonnal ALT levels, but in almost half of these patients ALT levels were only minimally above the upper limit of normal [24], Subsequent studies indicate that up to 3/4 of hepatitis G viraemic patients have normal transaminase levels. This has been shown to be the case in liver transplant patients [30,31], patients with haematological malignancies [37], lep rous patients [38] and thalassaemics [39]. The absence of ALT abnormalities does not necessarily mean that histolog ical changes in liver biopsy material are absent.…”

Section: Routes Of Hgv (Gbv-c) Transmissionmentioning

confidence: 99%

Current Status of Hepatitis G Virus (GBV-C) in Transfusion: Is It Relevant?

Karayiannis¹,

Thomas²

1997

Vox Sanguinis

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A new flavivirus, provisionally designated hepatitis G virus or GBV-C has recently been described. The virus is parenterally transmitted by exposure to blood through transfusion, intravenous drug use and haemodialysis. Heat- or chemically- treated blood products are associated with reduced risk of infection. The virus may also be transmitted from mother to infant and by the sexual route. Although hepatitis G virus has been detected in patients with acute and chronic hepatitis, a causative role of the virus in such cases has not been established. The majority of long term carriers of the virus appear to have no liver, biochemical or histological abnormalities.

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“…1 ' 11 - [13][14][15][16][17][18][19][20][21][22][23] The most frequent virus that coinfects patients with HGV is HCV. Whether HGV alters the course of hepatitis C in patients who are coinfected with both viruses is unknown.…”

Section: O M P a R A T I V E H I S T O L O G I C F E A T U R E S O mentioning

confidence: 99%

“…32 Not surprisingly, the rate of coinfection is high (7%-49%) among patients also infected with the other parenterally spread hepatitis B, C, or D viruses. 1,n ' [13][14][15][16][17][18][19][20][21][22][23] We found that biopsy specimens from patients who were coinfected with HGV and HCV had similar histologic features to biopsy specimens of patients infected with HCV alone. The histologic features that we observed most commonly were portal lymphoplasmacytic inflammation, mild to moderate piecemeal necrosis, mild spotty parenchymal inflammation with hepatocyte dropout or necrosis, mild macrovesicular steatosis, variable amounts of fibrosis, and occasional The lack of biopsy specimens from HCV control patients, matched closely for these important clinical features, may have precluded these investigators from discerning a difference between the patient and control groups.…”

Section: Ajcp • December 1997mentioning

confidence: 99%

“…15 ' 38,42,[51][52][53] Hepatitis G virus has been identified in 1% to 3% of voluntary blood donors despite these patients having normal results of liver function tests, 23,42,48 and elevated transaminase levels have been d o c u m e n t e d in 25% to 50% of HGV-positive patients. 13,32,37,42 The virus can cause chronic infection and has been detected in some patients up to 8 years after transfusion. 54 However, it did not cause clinical hepatitis in the majority of infected patients.…”

Section: Ajcp • December 1997mentioning

confidence: 99%

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