Natural History of GBV-C/Hepatitis G Virus Infection Through the Follow-Up of GBV-C/Hepatitis G Virus–Infected Blood Donors and Recipients Studied by RNA Polymerase Chain Reaction and Anti-E2 Serology

Lefrère, Jean‐Jacques; Loiseau, Pascale; Maury, Jacqueline; Lasserre, Jacqueline; Mariotti, Martine; Ravera, N; Lerable, Joëlle; Lefèvre, Guillaume; Morand‐Joubert, Laurence; Girot, Robert

doi:10.1182/blood.v90.9.3776

Cited by 53 publications

(44 citation statements)

References 24 publications

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“…In a study with healthy individuals aged 16-67 years in Uzbekistan, it has also been shown that GBV-C/HGV infection was distributed among younger people [Kato et al, 1997]. The high value (18%) encountered in age group of 21-30 years was likely due to the persistence of GBV-C/HGV infection, commonly for 5-10 years, as previously reported [Lefrère et al, 1997]. Indeed, such a long period of infection increases the probability of viral RNA detection in a cross-sectional study.…”

Section: Discussionsupporting

confidence: 68%

Age-specific prevalence and genetic diversity of GBV-C/hepatitis G virus in Brazil

Lampe

Saback

Viazov³

et al. 1998

J. Med. Virol.

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The recently discovered GBV-C/hepatitis G virus (GBV-C/HGV) has been shown to be parenterally transmitted. The occurrence of community-acquired GBV-C/HGV infections has also been reported. In order to study the variations with age of the GBV-C/HGV prevalence, sera from 268 individuals without liver disease, aged 0-80 years, and living in the city of Rio de Janeiro, Brazil, were tested by reverse transcription-nested polymerase chain reaction for the presence of GBV-C/HGV RNA. Age-specific seroprevalence was low (2.3%) among children under the age of 10, reached a maximum of 18% in young adults (21-30 years), and declined in older age groups. Among 170 blood donors aged 18-60, the rate of individuals with antibodies against the viral envelope E2 protein increased with age, from about 6% between the ages of 18 and 24 to about 35% for individuals from the age of 43 to 60. The results suggest that sexual transmission of GBV-C/HGV might occur and that the virus could be eliminated after a long period of infection. The nucleotide sequences of GBV-C/HGV genome fragments, 422 base pairs (bp) in the E2 region and 354 bp in the nonstructural 5 region, were determined for 11 and 31 isolates, respectively. Phylogenetic tree based on concatenated E2 + NS5 sequences showed that Brazilian strains belonged to three clusters, two of which were previously characterized as genotypes 1 and 2.

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Section: Discussionsupporting

confidence: 68%

Age-specific prevalence and genetic diversity of GBV-C/hepatitis G virus in Brazil

Lampe

Saback

Viazov³

et al. 1998

J. Med. Virol.

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“…The clinical relevance of HGV infection is still being debated, because most viremic subjects have normal ALT levels (3)(4)(5)(12)(13)(14). HGV RNA has been detected in some patients with non-A-E fulminant hepatitis (12) or with acute and chronic forms of hepatitis (3,4).…”

Section: Discussionmentioning

confidence: 99%

“…Seroconversion to viral proteins is almost always associated with the disappearance of detectable viremia (9)(10)(11), which implies that the humoral immune response usually leads to viral clearance. Although HGV RNA status can cause acute and chronic hepatitis, most viremic subjects tend to have normal levels of alanine aminotransferase (ALT) (3)(4)(5)(12)(13)(14); thus, the real pathogenetic potential of HGV remains uncertain.…”

mentioning

confidence: 99%

High rate of maternal‐infant transmission of hepatitis G virus in HIV‐1 and hepatitis C virus‐infected women

1999

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Palomba E, Bairo A, Tovo P-A. High rate of maternal-infant transmission of hepatitis G virus in HIV-1 and hepatitis C virus-infected women. Acta Paediatr 1999; 88: 1392-5. Stockholm. ISSN 0803-5253 The prevalence of hepatitis G virus (HGV) infection was investigated in 56 mothers with both human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection. Thirty-three (58.8%) women had markers of HGV infection, including 7/15 (46.6%) with no history of parenteral exposure to blood. Sixteen (48%) had HGV RNA in serum by a polymerase chain reaction assay, and 17 (52%) had antibody to E2 viral protein. No woman was positive for both markers. Of 20 infants born to the 16 mothers with HGV viremia, 9 (45%, 95% CI 34-56%) acquired the infection. No infected child seroconverted to HGV during the first year of life. At the latest visit (mean: 37.1 mo, range: 9-89 mo) 7 children were still seronegative HGV RNA carriers, 1 was both RNA-and antibody-negative, while 1 RNA-negative child had developed the E2 antibody. Of the 20 HGV-exposed infants, 2 contracted HCV and 1 HIV-1 (all 3 with HGV coinfection). No abnormalities in clinical findings and ALT levels were observed throughout the follow-up period in the six children with HGV infection alone. Our findings show that HGV infection is widespread among HIV-1-and HCV-infected women. Maternal-infant transmission of HGV is common and occurs independently from that of HIV-1 and HCV in women with triple infection. Most perinatally HGV-infected children develop persistent infection with no clinical or biological signs of liver damage, at least in the first years of life. & Children, hepatitis G virus infection, natural history, prevalence P-A Tovo,

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“…Like hepatitis C virus (HCV), GBV-C infection is found worldwide and is capable of persistent human infection [8,9]. GBV-C infection is common, and between 1 and 5% of healthy blood donors in developed countries are viraemic at the time of donation.…”

Section: Epidemiology and Disease Associationmentioning

confidence: 99%

GB virus type C interactions with HIV: the role of envelope glycoproteins

Mohr

Stapleton

2009

Journal of Viral Hepatitis

110

180

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SUMMARY GB virus C/hepatitis G virus (GBV-C/HGV) is the most closely related human virus to hepatitis C virus (HCV). GBV-C is lymphotropic and not associated with any known disease, although it is associated with improved survival in HIV-infected individuals. In peripheral blood mononuclear cells, GBV-C induces the release of soluble ligands for HIV entry receptors (RANTES, MIP-1a, MIP-1b and SDF-1), suggesting that GBV-C may interact with lymphocytes to induce a chemokine and/or cytokine milieu that is inhibitory to HIV infection. Expression of GBV-C envelope glycoprotein E2 in CD4+ T cells or addition of recombinant E2 to CD4 cells recapitulates the HIV inhibition seen with GBV-C infection. Like HCV E2, GBV-C E2 is predicted to be post-translationally processed in the endoplasmic reticulum and is involved with cell binding. The C-termini of GBV-C E1 and E2 proteins contain predicted transmembrane domains sharing features with HCV TM domains. To date, cellular receptor(s) for GBV-C E2 have not been identified. GBV-C E2-mediated HIV inhibition is dose-dependent and HIV replication is blocked at the binding and/or entry step. In addition, a putative GBV-C E2 fusion peptide interferes with HIV gp41 peptide oligomerization required for HIV-1 fusion, further suggesting that GBV-C E2 may inhibit HIV entry. Additional work is needed to identify the GBV-C E2 cellular receptor, characterize GBV-C E2 domains responsible for HIV inhibition, and to examine GBV-C E2-mediated fusion in the context of the entire envelope protein or viral-particles. Understanding the mechanisms of action may identify novel approaches to HIV therapy.

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Natural History of GBV-C/Hepatitis G Virus Infection Through the Follow-Up of GBV-C/Hepatitis G Virus–Infected Blood Donors and Recipients Studied by RNA Polymerase Chain Reaction and Anti-E2 Serology

Cited by 53 publications

References 24 publications

Age-specific prevalence and genetic diversity of GBV-C/hepatitis G virus in Brazil

Age-specific prevalence and genetic diversity of GBV-C/hepatitis G virus in Brazil

High rate of maternal‐infant transmission of hepatitis G virus in HIV‐1 and hepatitis C virus‐infected women

GB virus type C interactions with HIV: the role of envelope glycoproteins

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