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Jack T Stapleton - One of the best experts on this subject based on the ideXlab platform.

  • Tropism of human peGiVirus (formerly known as GB Virus C/Hepatitis G Virus) and host immunomodulation: insiGhts into a hiGhly successful viral infection.
    Journal of General Virology, 2015
    Co-Authors: Ernest T. Chivero, Jack T Stapleton
    Abstract:

    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 >1×107 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 T- and 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.

  • human peGiVirus rna is found in multiple blood mononuclear cells in vivo and serum derived viral rna containinG particles are infectious in vitro
    Journal of General Virology, 2014
    Co-Authors: Ernest T. Chivero, Nirjal Bhattarai, Robert T Rydze, Mark A Winters, Mark Holodniy, Jack T Stapleton
    Abstract:

    Human peGiVirus (HPGV; previously called GB Virus C/Hepatitis G Virus) has limited pathoGenicity, despite causinG persistent infection, and is associated with prolonGed survival in human immunodeficiency Virus-infected individuals. AlthouGh HPGV RNA is found in and produced by T- and B-lymphocytes, the primary permissive cell type(s) are unknown. We quantified HPGV RNA in hiGhly purified CD4+ and CD8+ T-cells, includinG naive, central memory and effector memory populations, and in B-cells (CD19+), NK cells (CD56+) and monocytes (CD14+) usinG real-time reverse transcription-PCR. SinGle-Genome sequencinG was performed on Viruses within individual cell types to estimate Genetic diversity amonG cell populations. HPGV RNA was present in CD4+ and CD8+ T-lymphocytes (nine of nine subjects), B-lymphocytes (seven of ten subjects), NK cells and monocytes (both four of five). HPGV RNA levels were hiGher in naive (CD45RA+) CD4+ cells than in central memory and effector memory cells (P<0.01). HPGV sequences were hiGhly conserved amonG subjects (0.117±0.02 substitutions per site; ranGe 0.58–0.14) and within subjects (0.006±0.003 substitutions per site; ranGe 0.006–0.010). The non-synonymous/synonymous substitution ratio was 0.07, suGGestinG a low selective pressure. Carboxyfluorescein succinimidyl ester (CFSE)-labelled HPGV RNA-containinG particles precipitated by a commercial exosome isolation reaGent delivered CSFE to uninfected monocytes, NK cells and T- and B-lymphocytes, and HPGV RNA was transferred to PBMCs with evidence of subsequent Virus replication. Thus, HPGV RNA-containinG serum particles includinG microvesicles may contribute to delivery of HPGV to PBMCs in vivo, explaininG the apparent broad tropism of this persistent human RNA Virus.

  • Gb Virus type c interactions with hiv the role of envelope Glycoproteins
    Journal of Viral Hepatitis, 2009
    Co-Authors: Emma L Mohr, Jack T Stapleton
    Abstract:

    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.

  • clinical isolates of Gb Virus type c vary in their ability to persist and replicate in peripheral blood mononuclear cell cultures
    Virology, 2003
    Co-Authors: Sarah L George, Jinhua Xiang, Jack T Stapleton
    Abstract:

    GB Virus C/Hepatitis G Virus (GBV-C) replication in vitro is inefficient and inconsistent. In this study, clinical isolates of GBV-C were evaluated usinG peripheral blood mononuclear cell (PBMC) based culture methods. Isolates varied consistently in their ability to persistently replicate, and yield increased in cells Grown without PHA/IL-2 stimulation. The deduced polyprotein sequence of an isolate that replicated well was determined (GenBank AY196904) and compared to 20 full-lenGth GBV-C sequences. Fourteen of the 16 unique amino acid polymorphisms identified were in the codinG reGions for nonstructural proteins associated with interferon resistance and RNA replication. These data indicate that clinical GBV-C isolates vary in their ability to persist in culture, do not require PHA/IL-2 stimulation, and that sequence variability in key reGulatory reGions may affect Growth in PBMC cultures. Since GBV-C appears to inhibit HIV replication in a coinfection model, these studies should facilitate determination of the mechanism of this interaction.

  • Gb Virus type c Hepatitis G Virus a non pathoGenic flaviVirus associated with prolonGed survival in hiv infected individuals
    Microbes and Infection, 2003
    Co-Authors: Philip M Polgreen, Jinhua Xiang, Qing Chang, Jack T Stapleton
    Abstract:

    GB Virus C (GBV-C) is a common Virus that does not appear to cause disease. GBV-C persists in up to 50% of exposed individuals, and Virus replication appears to be in lymphocytes includinG CD4+ T cells. GBV-C infection is common amonG HIV-positive people, and several studies have found that HIV-positive individuals co-infected with GBV-C survive for statistically siGnificantly lonGer periods of time than people without GBV-C. In vitro studies suGGest that GBV-C inhibits HIV replication and alters cytokine, chemokine and chemokine receptor expression. Thus, GBV-C may be a major factor influencinG the natural history of HIV disease.

Hans L. Tillmann - One of the best experts on this subject based on the ideXlab platform.

  • Gb Virus c infection is there a clinical relevance for patients infected with the human immunodeficiency Virus
    Aids Reviews, 2005
    Co-Authors: Thorsten Kaiser, Hans L. Tillmann
    Abstract:

    In a search for new Hepatitis Viruses, two independent Groups identified Viruses named GB Virus C and Hepatitis G Virus, which turned out to be different strains of the same aGent. Despite its initial ascription to Hepatitis Viruses, this new Virus does not cause any Hepatitis. Thus, the term GB Virus C is preferred. Soon after its discovery, a siGnificantly better clinical course of HIV infection was demonstrated for patients coinfected with the GB Virus C in 1998. These results were confirmed in other further studies, but not in all of them. Importantly, studies not confirminG a positive influence usually found a neutral effect. The data for most of the studies had been mainly collected in the time prior to the availability of hiGhly effective antiretroviral therapy (HAART). Since HAART has become available, some authors have reported a beneficial effect while others have shown only a neutral influence of GB Virus C on HIV, considerinG either survival or the deGree of response to HAART. An explanation for these discrepancies may be that different GB Virus C strains exhibit different replication capacities. UnderstandinG the mechanisms by how GB Virus C and HIV interact may help find new strateGies to fiGht HIV infection. Some recent in vitro findinGs have added evidence on how GB Virus C miGht interact with and inhibit HIV replication. In this review, we update the current knowledGe on GB Virus C, its role in HIV infection in the HAART era, and discuss the potential mechanisms of its beneficial effect.

  • Gb Virus c infection in patients infected with the human immunodeficiency Virus
    Antiviral Research, 2001
    Co-Authors: Hans L. Tillmann, Michael P Manns
    Abstract:

    Hepatitis Virus infections are frequent in patients sufferinG from HIV infection due to similar transmission routes of these Viruses. In addition, Hepatitis Virus infections lead to impaired survival in HIV positive patients. The recently discovered flaviVirus GB Virus C (alias Hepatitis G Virus) was initially believed to be another Hepatitis Virus. While there is still some minor discussion whether GB Virus C (GBV-C) plays a role in fulminant hepatic failure, there is no evidence that this Virus is responsible for chronic liver disease. Thus this 'orphan Virus' still seeks its disease. In this review we concentrate on the published data concerninG the co-infection of GBV-C and HIV. By summarizinG the studies available, we show evidence for a beneficial influence of GBV-C on HIV infection. Many studies demonstrated a hiGh prevalence of GBV-C infection in HIV positive patients due to its parenteral and sexual transmission. However, in contrast to the expectations, GBV-C does not aGGravate the course of patients sufferinG from HIV infection. Even thouGh not uniformly found, one often sees hiGher CD4 counts in patients with onGoinG GBV-C viral replication. Likewise, a lower viral load appears to be accompanied by the presence of GBV-C RNA in the serum. In addition, lonGitudinal studies indicate that GBV-C infection slows down the proGression to AIDS and eventually to death. GBV-C probably influences HIV infection associated disease by either directly inhibitinG HIV replication or enhancinG the immune competence to cope with HIV. Still the definitive mechanism how GBV-C could inhibit the proGression to AIDS and eventually death needs to be identified.

  • infection with Gb Virus c and reduced mortality amonG hiv infected patients
    The New England Journal of Medicine, 2001
    Co-Authors: Hans L. Tillmann, Stefan Heringlake, Hans Heiken, Adriana Knapikbotor, J Ockenga, Judith C Wilber, Bernd Goergen, Jill Detmer, Martin Mcmorrow, Matthias Stoll
    Abstract:

    BackGround The flaviVirus GB Virus C (GBV-C, also desiGnated Hepatitis G Virus) was identified in a search for Hepatitis Viruses, but no disease is currently known to be associated with it. We investiGated the relation between coinfection with GBV-C and the lonG-term outcome in patients infected with the human immunodeficiency Virus (HIV). Methods A total of 197 HIV-positive patients were followed prospectively beGinninG in 1993 or 1994. Of these patients, 33 (16.8 percent) tested positive for GBV-C RNA, 112 (56.9 percent) had detectable antibodies aGainst the GBV-C envelope protein E2, and 52 (26.4 percent) had no marker of GBV-C infection and were considered unexposed. We assessed the relation between GBV-C infection and the proGression of HIV disease. We also tested 169 GBV-C–positive plasma samples with a quantitative branched-chain DNA (bDNA) assay in order to investiGate possible correlations between GBV-C viral load and both the CD4+ cell count and the HIV load. Results AmonG the patients who teste...

  • Gb Virus c Hepatitis G Virus infection a favorable proGnostic factor in human immunodeficiency Virus infected patients
    The Journal of Infectious Diseases, 1998
    Co-Authors: Stefan Heringlake, Hans L. Tillmann, J Ockenga, Matthias Stoll, C Trautwein, Dorte Meissner, Jeffrey Hunt, Cynthia Jou, Natalie Solomon, Reinhold E Schmidt
    Abstract:

    To investiGate a possible influence of GB Virus C (GBV-C) in immunocompromised patients, the prevalences of GBV-C RNA and anti-E2 antibody in 197 human immunodeficiency Virus (HIV)-infected patients and in 120 control blood donors were studied. GBV-C RNA was detected in 33 of 197 HIV-infected patients (16.8%) compared with 1 in 120 blood donors (0.8%) (P < .001). Previous exposure to GBV-C (anti-E2 antibody-positive) was shown in 56.8% of HIV patients and in 9% of blood donors. GBV-C viremia was not associated with Hepatitis. Despite approximately equal duration of HIV infection in all subGroups, the CD4 cell counts were siGnificantly hiGher in GBV-C-viremic patients (344 cells/microL) compared with exposed (259 cells/microL) and unexposed (170 cells/microL) patients (P = .017 and P < .001). Furthermore, Kaplan-Meier analysis demonstrated siGnificantly better cumulative survival in GBV-C RNA-positive HIV-infected patients, suGGestinG that GBV-C miGht be a favorable proGnostic factor in HIV disease.

  • association between fulminant hepatic failure and a strain of Gbv Virus c
    The Lancet, 1996
    Co-Authors: Stefan Heringlake, Sabine Osterkamp, Scott Muerhoff, K Boker, Gerhard Hunsmann, Hans L. Tillmann, Isa K Mushahwar, Christian Trautwein, Michael P Manns
    Abstract:

    BACKGROUND: The GB Virus C (GBV-C) and the Hepatitis G Virus (HGV) have been detected in patients with acute indeterminant Hepatitis and post-transfusion Hepatitis. However, the role of the new Hepatitis Viruses in the aetioloGy of fulminant Hepatitis is little understood. We investiGated the presence of GBV-C/HGV in patients with fulminant hepatic failure. METHODS: Serum samples from 22 German patients with fulminant hepatic failure and 106 symptom-free blood donors (controls) were studied for presence of GBV-C RNA by seminested reverse transcriptase PCR. Primer sequences were derived from the published Gene sequences of the conserved NS3 reGion of the GBV-C prototype and the published isolates. Nucleotide and amino acid sequences of GBV-C-positive isolates, the control RNA, and the published HGV and GBV-C prototype sequences were compared by multiple sequence aliGnment. We also compared the GBV-C sequences of Virus-positive patients who had fulminant hepatic failure with those of 19 patients with chronic Hepatitis from our centre. In addition, we searched databases and published papers for further GBV-C helicase sequences in patients with non-fulminant Hepatitis. FINDINGS: GBV-C RNA was detected in 11 (50%) of the 22 patients with fulminant hepatic failure and in five (4.7%) of 106 control-Group blood donors. AmonG the patients with fulminant hepatic failure, six of seven with fulminant Hepatitis B and five of ten with fulminant non-A-E Hepatitis were positive for GBV-C RNA. Analysis of nucleic acid sequences showed six mutations at defined positions in all 11 patients with fulminant hepatic failure who were positive for GBV-C. None of these mutations were found in the five GBV-C-positive control-Group blood donors. Of the six nucleotide chanGes, four caused no amino acid chanGes, whereas two mutations at position 100 (G to T) and 102 (T to C) led to an alanine to serine chanGe in the predicted translation product. However, comparison with GBV-C sequences of patients with non-fulminant Hepatitis showed that this amino acid mutation was not specific for fulminant hepatic failure. The sequence-motif containinG the six nucleotide mutations detected in all patients with fulminant hepatic failure was found in only two of 19 German patients with chronic Hepatitis from our centre, and in only one of 88 GBV-C sequences from non-fulminant patients reported by others. INTERPRETATION: The frequency of GBV-C RNA is hiGher in fulminant hepatic failure than in any other Group of patients with Hepatitis, particularly in patients with fulminant Hepatitis B or fulminant non-A-E Hepatitis. A specific strain of GBV-C may occur in serum of German patients with fulminant hepatic failure.

Peter Simmonds - One of the best experts on this subject based on the ideXlab platform.

  • Virome Analysis of Transfusion Recipients Reveals a Novel Human Virus That Shares Genomic Features with HepaciViruses and PeGiViruses
    mBio, 2015
    Co-Authors: Amit Kapoor, Peter Simmonds, Arvind Kumar, Nishit Bhuva, Lokendra V. Chauhan, Bohyun Lee, Amadou A. Sall, Zhezhen Jin, Stephen S. Morse, Beth H. Shaz
    Abstract:

    To investiGate the transmission of novel infectious aGents by blood transfusion, we studied chanGes in the virome composition of blood transfusion recipients pre- and posttransfusion. UsinG this approach, we detected and Genetically charac- terized a novel human Virus, human hepeGiVirus 1 (HHpGV-1), that shares features with Hepatitis C Virus (HCV) and human peGiVirus (HPGV; formerly called GB Virus C or Hepatitis G Virus). HCV and HPGV belonG to the Genera HepaciVirus andPeGivi- rusof the familyFlaviviridae. HHpGV-1 was found in serum samples from two blood transfusion recipients and two hemophilia patients who had received plasma-derived clottinG factor concentrates. In the former, the Virus was detected only in the post- transfusion samples, indicatinG blood-borne transmission. Both hemophiliacs were persistently viremic over periods of at least 201 and 1,981 days. The 5=untranslated reGion (UTR) of HHpGV-1 contained a type IV internal ribosome entry site (IRES), structurally similar to althouGh hiGhly diverGent in sequence from that of HCV and other hepaciViruses. However, phyloGenetic analysis of nonstructural Genes (NS3 and NS5B) showed that HHpGV-1 forms a branch within the peGiVirus clade distinct from HPGV and homoloGs infectinG other mammalian species. In common with some peGiVirus variants infectinG rodents and bats, the HHpGV-1 Genome encodes a short, hiGhly basic protein upstream of E1, potentially possessinG a core-like function in packaG- inG RNA durinG assembly. Identification of this new human Virus, HHpGV-1, expands our knowledGe of the ranGe of Genome confiGurations of these Viruses and may lead to a reevaluation of the oriGinal criteria by which the Genera HepaciVirus andPeGivi- rusare defined. IMPORTANCE More than 30 million blood components are transfused annually in the United States alone. Surveillance for infec- tious aGents in the blood supply is key to ensurinG the safety of this critical resource for medicine and public health. Here, we report the identification of a new and hiGhly diverse HCV/GB Virus (GBV)-like Virus from human serum samples. This new vi- rus, human hepeGiVirus 1 (HHpGV-1), was found in serum samples from blood transfusion recipients, indicatinG its potential for transmission via transfusion products. We also found persistent lonG-term HHpGV-1 viremia in two hemophilia patients. HHpGV-1 is unique because it shares Genetic similarity with both hiGhly pathoGenic HCV and the apparently nonpathoGenic HPGV (GBV-C). Our results add to the list of human Viruses and provide data to develop reaGents to study Virus transmission and disease association and for interruptinG Virus transmission and new human infections.

  • The GB Viruses: a review and proposed classification of GBV-A, GBV-C (HGV), and GBV-D in Genus PeGiVirus within the family Flaviviridae
    Journal of General Virology, 2010
    Co-Authors: Steven K. H. Foung, Jens Bukh, A. S. Muerhoff, Peter Simmonds
    Abstract:

    In 1967, it was reported that experimental inoculation of serum from a surGeon (G.B.) with acute Hepatitis into tamarins resulted in Hepatitis. In 1995, two new members of the family Flaviviridae, named GBV-A and GBV-B, were identified in tamarins that developed Hepatitis followinG inoculation with the 11th GB passaGe. Neither Virus infects humans, and a number of GBV-A variants were identified in wild New World monkeys that were captured. Subsequently, a related human Virus was identified [named GBV-C or Hepatitis G Virus (HGV)], and recently a more distantly related Virus (named GBV-D) was discovered in bats. Only GBV-B, a second species within the Genus HepaciVirus (type species Hepatitis C Virus), has been shown to cause Hepatitis; it causes acute Hepatitis in experimentally infected tamarins. The other GB Viruses have however not been assiGned to a Genus within the family Flaviviridae. Based on phyloGenetic relationships, Genome orGanization and pathoGenic features of the GB Viruses, we propose to classify GBV-A-like Viruses, GBV-C and GBV-D as members of a fourth Genus in the family Flaviviridae, named PeGiVirus (pe, persistent; G, GB or G). We also propose renaminG ‘GB’ Viruses within the tentative Genus PeGiVirus to reflect their host oriGin.

  • new dna Viruses identified in patients with acute viral infection syndrome
    Journal of Virology, 2005
    Co-Authors: Peter Simmonds, Amit Kapoor, Morris S Jones, Vladimir V Lukashov, Frederick Hecht, Eric Delwart
    Abstract:

    A sequence-independent PCR amplification method was used to identify viral nucleic acids in the plasma samples of 25 individuals presentinG with symptoms of acute viral infection followinG hiGh-risk behavior for human immunodeficiency Virus type 1 transmission. GB Virus C/Hepatitis G Virus was identified in three individuals and Hepatitis B Virus in one individual. Three previously undescribed DNA Viruses were also detected, a parvoVirus and two Viruses related to TT Virus (TTV). Nucleic acids in human plasma that were distantly related to bacterial sequences or with no detectable similarities to known sequences were also found. Nearly complete viral Genome sequencinG and phyloGenetic analysis confirmed the presence of a new parvoVirus distinct from known human and animal parvoViruses and of two related TTV-like Viruses hiGhly diverGent from both the TTV and TTV-like miniVirus Groups. The detection of two previously undescribed viral species in a small Group of individuals presentinG acute viral syndrome with unknown etioloGy indicates that a rich yield of new human Viruses may be readily identifiable usinG simple methods of sequence-independent nucleic acid amplification and limited sequencinG.

  • detection in chimpanzees of a novel flaviVirus related to Gb Virus c Hepatitis G Virus
    Journal of General Virology, 1998
    Co-Authors: N J Adams, L M Jarvis, L E Prescott, J C M Lewis, Myra O Mcclure, D B Smith, Peter Simmonds
    Abstract:

    Infection with Hepatitis G Virus (HGV) or GB Virus-C (GBV-C) is widely distributed in human populations. Viruses related to GBV-C/HGV have been recovered from several New World primate species, includinG tamarins, owl monkeys and marmosets. To understand more about the relationship between GB Viruses and their hosts, we used primers from the 5' non-codinG (5'NC), non-structural 3 (NS3) and NS5 reGions in nested polymerase chain reactions to screen for related Viruses infectinG non-captive chimpanzees (Pan troGlodytes, troGlodytes and verus subspecies). Sequences from the 5'NCR and NS5 reGions were amplified from samples taken from 3 of 39 chimpanzees, and from one chimpanzee in the NS3 reGion. Sequence comparisons of each reGion revealed that the GB Virus infectinG chimpanzees was distinct from both GBV-C/HGV and from any of the known GBV-A sequences, but was more closely related to human Viruses. GB Viruses recovered from different chimpanzees were more diverse than variants of GBV-C/HGV found in humans, with 25% sequence diverGence in the 5'NCR and 20% (9.5% amino acid) sequence diverGence in NS5 between variants recovered from the troGlodytes and verus subspecies, compared with 7.4% and 10.4% (1.9% amino acid) diverGence amonGst GBV-C/HGV variants infectinG humans. FindinG GBV-C/HGV-related Viruses in an Old World monkey species suGGests that GB-like Viruses may be widely distributed in simians, and suGGests a close evolutionary relationship with their natural hosts.

  • sexual transmission of Gb Virus c Hepatitis G Virus
    Journal of Medical Virology, 1998
    Co-Authors: Martina F Scallan, Dan Clutterbuck, L M Jarvis, Gordon Scott, Peter Simmonds
    Abstract:

    AlthouGh it is established that infection with GB Virus C (GBV-C) or Hepatitis G Virus (HGV) can be transmitted parenterally, the prevalence of GBV-C/HGV viremia in the General population (2-5%) is relatively hiGh compared with other parenterally borne Viruses such as Hepatitis C Virus. To investiGate the possibility of sexual transmission of GBV-C/HGV, we determined the frequency of viremia by the polymerase chain reaction and seroloGical reactivity to the E2 protein by ELISA in samples collected from individuals at risk for sexually transmitted diseases attendinG a city Genitourinary medicine clinic. GBV-C/HGV viremia was detected in 27 of 87 male homosexuals (31%) and 9 of 50 prostitutes (18%), frequencies siGnificantly Greater than those in matched controls (2/63) and local blood donors (2.3%). AmonG nonviremic individuals, a hiGh frequency of seroloGical reactivity to the E2 protein of GBV-C/HGV was also observed in the risk Groups (male homosexuals: 14/60; prostitutes: 11/41), althouGh these fiGures are likely to be underestimates of the frequency of past infection as detectable anti-E2 reactivity may attenuate rapidly over time followinG resolution of infection. Infection with GBV-C/HGV was more frequent amonG those coinfected with human immunodeficiency Virus type 1. AmonG male homosexuals from whom retrospective samples were available, evidence for de novo infection was found in 9 of 22 individuals over a mean samplinG time of 2.9 years, predictinG an annualized incidence of GBV-C/HGV infection of approximately 11% in this Group. The hiGh prevalence and incidence of GBV-C/HGV infection in these individuals and prostitutes provides stronG evidence for its spread by sexual contact. Further studies are required to investiGate the mechanism of its transmission and the clinical siGnificance of acute and persistent infection in these risk Groups.

Dingshinn Chen - One of the best experts on this subject based on the ideXlab platform.

  • mother to infant transmission of Gb Virus c Hepatitis G Virus the role of hiGh titered maternal viremia and mode of delivery
    The Journal of Infectious Diseases, 1998
    Co-Authors: Hohsiung Lin, Jiahorng Kao, Peijer Chen, Meihwei Chang, Kuoyi Yeh, Dingping Liu, Dingshinn Chen
    Abstract:

    To study mother-to-infant transmission of GB Virus ClHepatitis G Virus (GBV-C/HGV), blood samples of infants born to carrier mothers were collected beGinninG 3 months after birth and were tested for GBV-C/HGV RNA until 1 year of aGe. Of 2046 mothers, 2.1% were positive for GBV-C/ HGV RNA, and 25 of their infants were followed for a median of 12 months. Thirteen infants (52%) were viremic, and infection became persistent in all. Maternal GBV-C/HGV RNA levels of this Group were >10 7 copies/mL. Nucleotide sequence comparison in 5 viremic mother-infant pairs revealed a homoloGy of 93%-98.2%, and none delivered by elective cesarean section. In comparison, of the 12 uninfected infants' mothers, 10 had lower GBV-C/HGV RNA levels (mean, 5 x 10 4 copies/ mL), and the remaininG 2 hiGh-titered mothers had elective cesarean section. Thus, hiGh-titered maternal viremia and mode of delivery are closely associated with the mother-to-infant transmission of GBV-C/HGV to infants, and the infection usually becomes persistent.

  • amplification of Gb Virus c Hepatitis G Virus rna with primers from different reGions of the viral Genome
    Journal of Medical Virology, 1997
    Co-Authors: Jiahorng Kao, Peijer Chen, Wendy Chen, Shengchun Hsiang, Mingyang Lai, Dingshinn Chen
    Abstract:

    GB Virus-C/Hepatitis G Virus (GBV-C/HGV) is a newly identified RNA Virus. The aim of the study was to compare three primer pairs from the 5' untranslated reGion (5'UTR), envelope reGion 2 (E 2) and nonstructural reGion 3 (NS 3) of GBV-C/HGV Genome for their ability to detect GBV-C/HGV RNA by polymerase chain reaction (PCR) assays. By usinG PCR with primers from different reGions of the viral Genome, serum GBV-C/HGV RNA was assayed in 200 at-risk individuals. The sensitivity of this assay was assessed by a titration experiment, and nucleotide sequences of the amplified products were determined directly. Of 200 serum samples, 43 (21.5%) were positive for GBV-C/HGV RNA with at least one of the primer pairs. The positive rates by 5'UTR, NS 3, and E 2 primers were 100%, 98%, and 84%, respectively, and the sensitivity of PCR assays usinG 5'UTR primers was 10 to 100 times more likely to detect GBV-C/HGV RNA than that of NS 3 and E 2 primers. The averaGe homoloGy of amplified tarGets to the prototype HGV Genome was 89%, 80%, and 85% and the similarity between each amplified tarGet was up to 100%, 90%, and 92% in the 5'UTR, E 2, and NS 3 reGions, respectively. Therefore, the 5'UTR of GBV-C/HGV Genome is hiGhly conserved and primers deduced from this reGion can provideva sensitive and specific PCR assay for GBV-C/HGV RNA.

  • Gb Virus c Hepatitis G Virus infection in an area endemic for viral Hepatitis chronic liver disease and liver cancer
    Gastroenterology, 1997
    Co-Authors: Jiahorng Kao, Peijer Chen, Wendy Chen, Mingyang Lai, D P Liu, Janntay Wang, M C Shen, Dingshinn Chen
    Abstract:

    Abstract BACKGROUND & AIMS: GB Virus-C/Hepatitis G Virus (GBV-C/HGV) is a newly identified flaviVirus, and little is known about its clinical siGnificance. GBV-C/HGV was investiGated in different populations, and its coinfection was investiGated in patients with liver disease in Taiwan where Hepatitis B and C are endemic. METHODS: Viral RNA was studied in 70 hiGh-risk individuals, 20 patients with chronic non-B, non-C Hepatitis, 13 with non-A-E fulminant Hepatitis, 100 with asymptomatic Hepatitis B surface antiGen carriaGe, 120 with Hepatitis B surface antiGen-positive chronic liver disease and hepatocellular carcinoma, 100 patients with chronic Hepatitis C, and 100 healthy adults. RESULTS: GBV-C/HGV infection was more frequent in hiGh-risk Groups (15%-30%) and Hepatitis C Virus carriers (10%) than in healthy adults (1%) and Hepatitis B Virus carriers (3.2%). EiGhty-three percent of those infected had underGone blood transfusions previously. The prevalence in Hepatitis B Virus carriers increased with the severity of liver disease, beinG 1% in asymptomatic carriers and 10% in hepatocellular carcinoma. In chronic Hepatitis C, clinical and viroloGical data were comparable between those with and without coinfection. CONCLUSIONS: In Taiwan, GBV-C/HGV infection is common in hiGh-risk Groups, and its coinfection seems to not aGGravate the course of chronic Hepatitis B or C. (GastroenteroloGy 1997 Apr;112(4):1265-70)

  • a prospective study of transfusion transmitted Gb Virus c infection similar frequency but different clinical presentation compared with Hepatitis c Virus
    AH-Scopus to ORCID, 1996
    Co-Authors: Jintown Wang, Peijer Chen, Fengchiao Tsai, Chaze Lee, Jinchuan Sheu, Tehhong Wang, Dingshinn Chen
    Abstract:

    To study the incidence and outcome of GB Virus C (GBV-C) infection in blood recipients. Serum samples collected in a prospective study were examined for GBV-C RNA by a nested polymerase chain reaction assay. AmonG the 400 adults who underwent cardiac surGery, 40 were positive for GBV-C RNA, includinG six whose pretransfusion sera were already positive and seven coinfected with Hepatitis C Virus (HCV) durinG transfusion. The risk of transmission was estimated to be approximately 0.46% per donor. GBV-C viremia was detectable 1 week after transfusion and could persist for 8 years. However, no evident symptoms or siGns were noted in the 25 patients infected by GBV-C alone, and the averaGe peak serum alanine aminotransferase activity was 31 IU/L only (ranGe, 12 to 123), with persistently normal levels in 20 patients. In the seven patients coinfected with HCV, the clinical courses of posttransfusion Hepatitis were similar to those infected by HCV alone. In eiGht patients with posttransfusion non-A approximately E Hepatitis, only one was positive for GBV-C RNA. Sixty samples were chosen to test Hepatitis G Virus (HGV) sequences, 26 of the 30 GBV-C positives were positive for HGV RNA in contrast to none of the 30 GBV-C neGative samples. In conclusion, GBV-C can be transmitted by transfusion in approximately 9% of patients who underwent cardiac surGery. Nevertheless, this Virus does not seem to cause classic Hepatitis in most instances.

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  • miscibility and lanGmuir studies of the interaction of e2 279 298 peptide sequence of Hepatitis G Virus Gb Virus c with dipalmitoylphosphatidyl choline and dimiristoylphosphatidyl choline phospholipids
    Langmuir, 2015
    Co-Authors: J Minones, I Haro, Maria Munoz, Minones J Trillo, Montserrat Busquets, M.a. Alsina
    Abstract:

    Mixed monolayers of E2(279-298), a synthetic peptide belonGinG to the structural protein E2 of the GB Virus C (GBV-C), formerly know as Hepatitis G Virus (HGV), and the phospholipids dipalmitoylphosphatidyl choline (DPPC) and dimiristoylphosphatidyl choline (DMPC),which differ in acyl chains lenGth, were obtained at the A/W interface (monolayers of extension) in order to provide new insiGhts on E2/phospholipids interaction. Analysis of the surface pressure-area isotherms, Brewster anGle microscopy imaGes, relative thickness, and mean areas per molecule has allowed us to establish the conditions under which the mixed components of the monolayer are miscible or immiscible and know how the level of the E2/phospholipid interaction varies with the composition of the mixed films, the surface pressure, and the hydrocarbon chains lenGth of the phospholipids. The steric hindrance caused by the penetration of the polymer strands into the more or less ordered hydrocarbon chains of the phospholipids was suGGested to explain the differences in the peptide interaction with the phospholipids studied. Therefore, the novelty of results obtained with the LanGmuir film balance technique, supplemented with BAM imaGes allow us to achieve a deeper understandinG of the interaction.

  • fluorescence study of the dynamic interaction between e1 145 162 sequence of Hepatitis Gb Virus c and liposomes
    Analytical and Bioanalytical Chemistry, 2009
    Co-Authors: M J Sanchezmartin, I Haro, Asuncion M Alsina, Jose Manuel Amigo, M Pujol, Antonia M Busquets
    Abstract:

    The physicochemical characterization of the peptide sequence E1(145-162) correspondinG to the structural protein E1 of the Hepatitis G Virus was done by studyinG its interaction with model membranes. Small unilamellar vesicles (SUVs) of dimyristoylphosphatidylGlycerol or dimyristoylphosphatidylcholine were chosen as mimetic membranes. Peptide incorporation and location in the phospholipid bilayer was investiGated by fluorescence anisotropy with SUVs labeled with diphenylhexatriene (DPH) or trimethylammonium-DPH. The addition of the peptide E1(145-162) showed siGnificant chanGes in the anisotropy values of the probe located at the air/water interface. These results indicate that the peptide E1(145-162) preferably interacts with the lipid surface without penetratinG inside the bilayer. A series of fluorescence experiments based on tryptophan peptide fluorescence were modeled by means of multivariate curve resolution-alternatinG least squares (MCR-ALS) alGorithm to further study the peptide interaction with bilayers at different temperatures. The preliminary results obtained with MCR-ALS showed how the peptide concentration decay is directly linked to the appearance of a new specie, which corresponds to the lipid-peptide bindinG. These results provide useful information for the desiGn of synthetic immunopeptides that can be incorporated into a liposomal system with potential to promote a direct delivery of the membrane-incorporated immunoGen to the immunocompetent cells, thus increasinG the immuno response from the host.

  • interaction of Gb Virus c Hepatitis G Virus synthetic peptides with lipid lanGmuir monolayers and larGe unilamellar vesicles
    Journal of Physical Chemistry B, 2009
    Co-Authors: Silvia Perezlopez, I Haro, Nuria Vilaromeu, Asuncion Alsina M Esteller, Marta Espina, Christian Mestres
    Abstract:

    In this paper, we aimed to continue the previous study undertaken with one seGment of E1 protein belonGinG to the GB Virus C/Hepatitis G Virus (GBV-C/HGV), specifically between the 53-66 amino acids and their palmitoyl derivative peptide. The sequence selection has been made on the basis of different prediction alGorithms of hydrophobicity and antiGenicity. Their interactions between two different in vitro membrane models, lipid LanGmuir monolayers and vesicles of different lipidic composition, have been evaluated. For this purpose, different lipids, varyinG the charGe and the unsaturations of the hydrocarbon chain 1,2-dipalmitoyl-sn-Glycero-3-phosphocholine (DPPC), 1,2-dioleoyl-sn-Glycero-3-phosphocholine (DOPC), 1,2-dipalmitoyl-sn-Glycero-3-[phospho-rac-(1-Glycerol)] (sodium salt) (DPPG) and 1,2-dioleoyl-sn-Glycero-3-[phospho-rac-(1-Glycerol)] (sodium salt) (DOPG), have been selected. Miscibility and peptides/lipids interactions have been analyzed on the basis of surface pressure (pi)-mean molecular area (A) isotherms, which have been recorded for pure and mixed monolayers of different composition spread at the air/water interface. Furthermore, E1(53-66) sequence and PalmE1(53-66) have been labeled with a fluorescent Group, succinimidyl 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)hexanoate (NBD succinimide), in order to study their behavior in the presence of vesicles. The obtained results are consistent with the existence of electrostatic (attractive) intermolecular interactions between the two positive net charGes of the peptides and the polar heads of neGative-charGed lipids. However, both the lipidic membrane fluidity and the palmitic chain linked to the native peptide play an important role in the balance between the electrostatic forces established at the interface and the hydrophobic ones established inside the membrane. The fluorescence assays have demonstrated that electrostatic forces clearly predominate over the hydrophobic interactions only when the native sequence is retained at the polar interface of DPPG and DOPG vesicles. However, the palmitic tail linked to the peptide helped its penetration in the hydrophobic environment of the membrane, and this process was favored by decreasinG the membrane fluidity.

  • study of adsorption and penetration of e2 279 298 peptide into lanGmuir phospholipid monolayers
    Journal of Physical Chemistry B, 2006
    Co-Authors: C Larios, M.a. Alsina, J Minones, I Haro, M A Busquets, Minones J Trillo
    Abstract:

    The peptide correspondinG to the sequence (279−298) of the Hepatitis G Virus (HGV/GBV-C) E2 protein was synthesized, and surface activity measurements, π−A compression isotherms, and penetration of...

  • interfacial properties of a synthetic peptide derived from Hepatitis G Virus e2 protein interaction with lipid monolayers
    Langmuir, 2006
    Co-Authors: Jorge Casas, I Haro, Marta Espina, Asuncion M Alsina, Marta Haro, F M Royo, Christian Mestres
    Abstract:

    9 paGes, 13 fiGures.-- PMID: 16378428 [PubMed].-- Available online Dec 3, 2005.-- SupportinG information avaliable at: http://pubs.acs.orG/doi/full/10.1021/la051812h