AI Article Synopsis
- GB virus C (GBV-C) is linked to increased survival rates in HIV patients and its E2 protein can prevent HIV from entering CD4+ T cells.
- A study using Jurkat cell lines showed that a specific 17 amino acid segment of the GBV-C E2 protein significantly inhibited HIV replication across multiple strains, unlike control sequences.
- The E2 protein's ability to inhibit HIV requires it to enter cells, which was only achieved when synthetic peptides were fused with a TAT protein for better cellular uptake.
Article Abstract
GB virus C (GBV-C) infection is associated with prolonged survival in HIV-infected cohorts, and GBV-C E2 protein inhibits HIV entry when added to CD4+ T cells. To further characterize E2 effects on HIV replication, stably transfected Jurkat cell lines expressing GBV-C E2 or control sequences were infected with HIV and replication was measured. HIV replication (all 6 isolates studied) was inhibited in all cell lines expressing a region of 17 amino acids of GBV-C E2, but not in cell lines expressing E2 without this region. In contrast, mumps and yellow fever virus replication was not inhibited by E2 protein expression. Synthetic GBV-C E2 17mer peptides did not inhibit HIV replication unless they were fused to a tat-protein-transduction-domain (TAT) for cellular uptake. These data identify the region of GBV-C E2 protein involved in HIV inhibition, and suggest that this GBV-C E2 peptide must gain entry into the cell to inhibit HIV.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568392 | PMC |
| http://dx.doi.org/10.1016/j.virol.2012.04.019 | DOI Listing |
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