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GBV-C acute infected cells reveal IL-16 cell mediated downregulation of critical hosts proteins involved in HIV-1 replication

Background

GB virus C (GBV-C) a member of the Flaviviridae, is a non-pathogenic virus, which replicates in lymphocytes and shown to slow viral replication in HIV-1 patients thereby decreasing progression to AIDS. The mechanism by which GBV-C acts remains elusive.

Th1 cytokines are strongly correlated with GBV-C/HIV-1 co-infection, thus allowing for latent seroconversation and longer longevity. IL-16 a potent anti-HIV-1 Th1 cytokine could explain GBV-C role in co-infection. Hijacking host proteins is critical in the replication, infection and expansion of HIV-1 in the human host.

Methods/results

Jurkat T-cells were transfected with (+) strand GBV-C genome and viral load was measured with specific 5'-UTR quantitative digital PCR assay. The GBV-C positive cells were then assayed for IL-16 expression via digital PCR and protein array. The RNA was then hybridized to high density oligonucleotide arrays for total human transcriptome analysis. Over 3000 genes showed differential expression in GBV-C monoinfection however only 20 were critical in HIV-1 replication with significant p-values under (α = 0.05) via two tailed pair wise t-test. The average upregulation of IL-16 in Jurkat T-cells was over 19-fold, p-value 0.001 on the transcription level and secreted protein were similarly upregulated. IL-16 is a known HIV-1 Tat/Rev gene inhibiting cytokine and high density oligonucleotide arrays showed host factors that are 5-fold downregulated that are involved in Tat mediated elongation and Rev mediated importation/exportation. The TAR specific binding protein 1 and the Rev binding protein were both downregulated under GBV-C infection as well as a VPU related binding protein.

Conclusion

GBV-C mediated IL-16 upregulation allows for HIV-1 suppression in co-infected patients. The effects of IL-16 on HIV-1 suppression of Rev/Tat are relativity unknown except that down-regulation of host HIV-1 related proteins give a more conclusive clue to IL-16 suppressive effects. High density oligomicroarrays give new incites to the transcriptome of GBV-C infected patients and their longer longevity when co-infected with HIV-1.

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Correspondence to Richard Allen White III.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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White, R.A., Curr, K. GBV-C acute infected cells reveal IL-16 cell mediated downregulation of critical hosts proteins involved in HIV-1 replication. Retrovirology 6, P95 (2009). https://doi.org/10.1186/1742-4690-6-S2-P95

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Keywords

  • Host Protein
  • Specific Binding Protein
  • High Density Oligonucleotide Array
  • Critical Host
  • Longe Longevity
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