GB Virus C (GBV‐C) Infection in Hepatitis C Virus (HCV)/HIV–Coinfected Patients Receiving HCV Treatment: Importance of the GBV‐C Genotype

Schwarze‐Zander, Carolynne; Blackard, Jason T.; Zheng, Hui; Addo, Marylyn M.; Lin, Wenyu; Robbins, Gregory; Sherman, Kenneth E.; Zdunek, Dietmar; Heß, Georg; Chung, Raymond T.

doi:10.1086/505713

Cited by 58 publications

(70 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We observed a significant difference in CD4 cell counts in HIV-positive persons co-infected with GBV-C genotype 2 compared to GBV-C genotype 1 even after controlling for race, HIV viral load and ART use (Schwarze-Zander et al, 2006). GBV-C genotype 2 was also marginally more sensitive to interferonbased HCV therapy than genotype 1.…”

Section: Consensusmentioning

confidence: 71%

“…However, some other studies have not shown such a survival advantage (Birk et al, 2002;Björkman et al, 2004). While it has been suggested that GBV-C genotype may play a role in modulating HIV disease progression (Alcalde et al, 2010;Muerhoff et al, 2003;Schwarze-Zander et al, 2006), which could explain the divergent findings among these studies, additional investigation is required to evaluate this hypothesis adequately. As a necessary first step, we characterized complete ORF sequences from individuals with GBV-C infection in the United States.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Recombination among GB virus C (GBV-C) isolates in the United States

Blackard

Polen

et al. 2016

Journal of General Virology

View full text Add to dashboard Cite

Section: Consensusmentioning

confidence: 71%

mentioning

confidence: 99%

Recombination among GB virus C (GBV-C) isolates in the United States

Blackard

Polen

et al. 2016

Journal of General Virology

View full text Add to dashboard Cite

“…However, anti-E2 antibodies are occasionally found during active viraemia and some of these individuals may be in the act of clearing viraemia (Schwarze-Zander et al, 2006;Tan et al, 1999;Williams et al, 2004). Some recent reports describe the detection of anti-HPgV peptide antibodies (Fernández et al, 2013;Gó mara et al, 2011); however, no clear relationship between peptide-reactive antibodies in actively HPgV-infected or convalescent subjects has been reported.…”

Section: B-cell Function and Antibody Productionmentioning

confidence: 99%

Tropism of human pegivirus (formerly known as GB virus C/hepatitis G virus) and host immunomodulation: insights into a highly successful viral infection

Chivero

Stapleton

2015

Journal of General Virology

View full text Add to dashboard Cite

Human pegivirus (HPgV; originally called GB virus C/hepatitis G virus) is an RNA virus within the genus Pegivirus of the family Flaviviridae that commonly causes persistent infection. Worldwide, 750 million people are actively infected (viraemic) and an estimated 0.75-1.5 billion people have evidence of prior HPgV infection. No causal association between HPgV and disease has been identified; however, several studies described a beneficial relationship between persistent HPgV infection and survival in individuals infected with human immunodeficiency virus. The beneficial effect appeared to be related to a reduction in host immune activation. HPgV replicates well in vivo (mean plasma viral loads typically .1¾10 7 genome copies ml -1 ); however, the virus grows poorly in vitro and systems to study this virus are limited. Consequently, mechanisms of viral persistence and host immune modulation remain poorly characterized, and the primary permissive cell type (s) has not yet been identified. HPgV RNA is found in liver, spleen, bone marrow and PBMCs, including Tand B-lymphocytes, NK-cells, and monocytes, although the mechanism of cell-to-cell transmission is unclear. HPgV RNA is also present in serum microvesicles with properties of exosomes. These microvesicles are able to transmit viral RNA to PBMCs in vitro, resulting in productive infection. This review summarizes existing data on HPgV cellular tropism and the effect of HPgV on immune activation in various PBMCs, and discusses how this may influence viral persistence. We conclude that an increased understanding of HPgV replication and immune modulation may provide insights into persistent RNA viral infection of humans. IntroductionHuman pegivirus (HPgV) is an RNA virus within the Pegivirus A species and family Flaviviridae (Adams et al., 2013;Stapleton et al., 2012a). The virus was originally called hepatitis G virus (HGV)/GB virus type C (GBV-C). The letters 'GB' represented the initials of a surgeon with acute hepatitis whose sera caused hepatitis in marmosets (Deinhardt et al., 1967). Subsequent studies found that this virus did not cause hepatitis and there was no direct evidence that the surgeon ('G. B.') was infected with HPgV. Thus, the virus (HGV/GBV-C), along with several related primate and bat viruses (GBV-A, GBV-C czp , GBV-D), was assigned to a new genus (Pegivirus) and renamed as HPgV (Adams et al., 2013;Stapleton et al., 2012a). HPgV has a 9.4 kb positive-sense ssRNA genome that is organized similarly to hepatitis C virus (HCV) (Fig. 1). HPgV and HCV are unusual amongst RNA viruses in that they commonly cause persistent infection in immune-competent humans.Although HPgV is not as efficient at establishing persistent infection as HCV, an estimated 25 % of infections persist and the other 75 % clear viraemia within 2 years of infection (Gutierrez et al., 1997;Tanaka et al., 1998a). The prevalence of HPgV viraemia in cross-sectional serum surveys of healthy blood donors in developed countries is between 1 and 5 %, whilst up to 20 % of blood donors in ...

show abstract

“…Several lines of evidence suggest a possible inhibition of HIV-1 by GBV-C through increase in soluble ligands for HIV-1 correceptor and activation of innate immunity (Lalle, 2008;Mohr & Stapleton, 2009). In addition, the beneficial effect of GBV-C on survival of HIV-1 infected patients might be genotype specific (Schwarze-Zander et al, 2006). Two GBV-C proteins, E2 and NS5A, have been shown to modulate CD4+ T-lymphocyte chemokine receptor expression and chemokine release in vitro, then inhbiting HIV replication.…”

Section: Hiv Co-infectionmentioning

confidence: 99%