HIV entry inhibition by the envelope 2 glycoprotein of GB virus C

  title={HIV entry inhibition by the envelope 2 glycoprotein of GB virus C},
  author={Susan Jung and Melanie Eichenm{\"u}ller and Norbert Donhauser and Frank Neipel and Alfred M Engel and Georg Hess and Bernhard Prof Dr Fleckenstein and Heide Reil},
Epidemiological studies have revealed an association between GB virus C (GBV-C) long-term viraemia and ameliorated HIV disease progression. We have provided evidence that a single protein of GBV-C, the glycoprotein E2, interferes with early HIV replication steps of both X4- and R5-tropic HIV strains. Preincubation with anti-E2 antibody specifically abrogates the inhibitory effect. Results were confirmed by the in-vitro expression of GBV-C E1/E2 encoding RNA. 
Peptides Derived from a Distinct Region of GB Virus C Glycoprotein E2 Mediate Strain-Specific HIV-1 Entry Inhibition
Findings reveal a new mechanism of viral interference, suggesting that the envelope protein E2 of GBV-C target directly HIV-1 particles to avoid entry of these virions.
HIV-1 Fusion Is Blocked through Binding of GB Virus C E2D Peptides to the HIV-1 gp41 Disulfide Loop
The results of the present study provide initial proof of concept that peptides targeted to the gp41 disulfide loop are able to inhibit HIV fusion and should inspire the development of this new class of HIV-1 entry inhibitors.
Role of GB virus C in modulating HIV disease
There are several reports of a beneficial effect of GBV-C on HIV disease progression in vivo, and different mechanisms to explain these observations have been proposed, including modification of antiviral cytokine production, HIV co-receptor expression, direct inhibition of HIV-1 entry, T-cell activation and Fas-mediated apoptosis.
Effect of synthetic peptides belonging to E2 envelope protein of GB virus C on human immunodeficiency virus type 1 infection.
It is shown how GBV-C E2 domains notably decrease cellular membrane fusion and interfere with the HIV-1 infectivity in a dose-dependent manner, highlighting their potential utility in future anti-HIV-1 therapies.
GB virus C: the good boy virus?
Expression of GB virus C NS5A protein from genotypes 1, 2, 3 and 5 and a 30 aa NS5A fragment inhibit human immunodeficiency virus type 1 replication in a CD4+ T-lymphocyte cell line.
expression of an 85 aa fragment of the GBV-C NS5A phosphoprotein in a CD4+ T cell line (Jurkat) resulted in inhibition of HIV replication, mediated in part by decreased surface expression of the HIV coreceptor CXCR4 and upregulation of SDF-1.
GB Virus Type C Envelope Protein E2 Elicits Antibodies That React with a Cellular Antigen on HIV-1 Particles and Neutralize Diverse HIV-1 Isolates
Data indicate that the GBV-C E2 protein has a structural motif that elicits Abs that cross-react with a cellular Ag present on retrovirus particles, independent of HIV-1 envelope glycoproteins, and provides evidence that a heterologous viral protein can induce HIV–1–neutralizing Abs.


GB virus C: insights into co-infection.
Regulation of CC chemokine receptor 5 in Hepatitis G virus infection
It is demonstrated that an interaction of HGV E2 with CD81 leads to increased RANTES secretion and decreased CCR5 surface expression, which might contribute to the delayed progression of HIV-infection in HGV-coinfected patients.
GB virus C replicates in primary T and B lymphocytes.
GBV-C RNA in purified CD4(+) and CD8(+) T lymphocytes and CD19(+) B lymphocytes removed ex vivo from infected donors is identified and replicated in vitro in these PBMC subsets, suggesting that GBv-C is a panlymphotropic virus.
Characterization of an Immunodominant Antigenic Site on GB Virus C Glycoprotein E2 That Is Involved in Cell Binding
The murine anti-E2 monoclonal antibodies evaluated were evaluated to topologically map immunogenic sites on GBV-C E2 and for the ability to detect or block recombinant E2 binding to various cell lines, suggesting that the epitopes bound by these MAbs are intimately related.
GB virus C infection: is there a clinical relevance for patients infected with the human immunodeficiency virus?
The current knowledge on GB virus C, its role in HIV infection in the HAART era, and the potential mechanisms of its beneficial effect are updated.
Humoral immune response to the E2 protein of hepatitis G virus is associated with long‐term recovery from infection and reveals a high frequency of hepatitis G virus exposure among healthy blood donors
Sequence comparisons showed that E2 is highly conserved among isolates collected worldwide, indicating that immune escape variants are not common in HGV infections.
Cell Surface Heparan Sulfate Is a Receptor for Human Herpesvirus 8 and Interacts with Envelope Glycoprotein K8.1
It is concluded that cell surface glycosaminoglycans play a crucial role in HHV-8 target cell recognition and that HHv-8 envelope protein K8.1 is at least one of the proteins involved.
Inhibition of HIV strains by GB virus C in cell culture can be mediated by CD4 and CD8 T-lymphocyte derived soluble factors
CD4 and CD8 T lymphocytes are stimulated by GBV-C to secrete antiretroviral factors, inhibiting R5- and X4-HIV strains.