Long-term persistence of hepatitis G virus in immunocompetent patients

Jj, Lefrére; Mariotti, Martine; Lerable, Joëlle; Thauvin, M; Girot, Robert

doi:10.1016/s0140-6736(05)65313-5

Cited by 19 publications

(12 citation statements)

References 4 publications

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“…Hepatitis G viraemia appears to persist for at least 12 months after transmission, but there are some reports that viraemia may last for as long as 5-10 years [18,19]. A chronic carrier state has been suggested by the findings of clinical and biochemical recovery in patients with chronic and persistent viraemia [20].…”

Section: Discussionmentioning

confidence: 99%

Hepatitis G virus in clotting factor concentrates

Alonso-Rubiano¹,

Gerber²,

Friedman

et al. 2003

Haemophilia

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Blood-borne hepatitis is a well-known complication in patients with bleeding disorders. A recently discovered parentally transmitted virus, hepatitis G [GB virus C (GBV-C)] has an increased prevalence in patients with haemophilia. Clotting factor concentrates derived from pools of human plasma currently undergo viral inactivation techniques known to be effective against hepatitis B, C and HIV; however, the effectiveness of current purification and viral inactivation techniques against newly discovered viruses such as GBV-C is unknown. A total of 37 vials of clotting factor concentrates manufactured in the USA from 1981 to 1995 were tested for the presence of GBV-C virus. All samples that did not undergo a specific viral inactivation step were positive for GBV-C. Viral inactivation techniques that did not uniformly remove GBV-C included vapour heat treatment and dry heat treatments for less than 144 h. All samples treated by pasteurization, solvent detergent or dry heat for 144 h, were negative for the presence of GBV-C.

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Section: Discussionmentioning

confidence: 99%

Hepatitis G virus in clotting factor concentrates

Alonso-Rubiano¹,

Gerber²,

Friedman

et al. 2003

Haemophilia

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“…Cases of acute or chronic hepatitis [Muerhoff et al, 1995;Simons et al, 1995a,b;Hering-lake et al, 1996;Leary et al, 1996;Linne et al, 1996;Alter et al, 1997] have been linked to this infection, but the role of the GBV-C/HGV in these conditions has been rebutted subsequently [Alter et al, 1996;Lefrère et al, 1997;Loiseau et al, 1997]. The most recent studies confirm that the GBV-C/HGV infection appears totally symptomless in all carriers whatever their immune status [Alter et al, 1996;Kudo et al, 1996;Lefrère et al, 1996Lefrère et al, , 1997Loiseau et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

GBV-C/hepatitis G virus (HGV) RNA load in immunodeficient individuals and in immunocompetent individuals

et al. 1999

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The aim of this study was to establish the mean plasma GBV-C/hepatitis G virus (HGV) RNA load in groups of GBV-C/HGV-infected individuals with varied immune status and to determine the most frequent patterns of evolution of the plasma GBV-C/HGV RNA load over time during the natural history of infection. The mean plasma GBV-C/HGV RNA load observed was, from the lowest to the highest: 5.21 log in immunodepressed multiply-transfused patients, 6.45 log in HIV-positive individuals, 6.66 log in immunocompetent multiply-transfused patients, and 6.71 log in blood donors. The difference was significant between the four groups (P < 0.0001). The most frequent pattern of evolution of the plasma GBV-C/HGV RNA load was as follows: after the primary GBV-C/HGV infection, the viral load was elevated from the onset; then, a high, persistent and relatively steady viral RNA level was the rule; and when it occurred, the loss of viremia was not preceded by a decrease before recovery from GBV-C/HGV infection.

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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%

“…Retrospective studies have shown that HGV-RNA can persist for many years in immunocompetent individuals and blood donors, in the absence of ALT abnormalities [6,21,24,39,46]. This questions the suggestion that immunosup pression may increase the risk of HGV infection after trans fusion-related exposure.…”

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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Long-term persistence of hepatitis G virus in immunocompetent patients

Cited by 19 publications

References 4 publications

Hepatitis G virus in clotting factor concentrates

Hepatitis G virus in clotting factor concentrates

GBV-C/hepatitis G virus (HGV) RNA load in immunodeficient individuals and in immunocompetent individuals

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

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