Influence of prothymosin-alpha on HIV-1 target cells.

Published

Journal Article (Review)

The important role of CD8(+) T cells in controlling HIV-1 infection through the innate as well as the adaptive immune system is well established. In addition to the major histocompatibility complex (MHC)-dependent cytotoxic activity of CD8(+) T cells, they produce soluble factors that suppress HIV-1 replication in an MHC-independent manner. Several of those factors have been identified, including beta-chemokines, Rantes, MIP-1alpha, MIP-1beta, and MDC. We previously identified that prothymosin alpha (ProTalpha) in the conditioned medium of HVS transformed CD8(+) T cells was a potent inhibitor of HIV-1 replication following proviral integration. In this report we further characterize the anti-HIV-1 activity of ProTalpha by demonstrating its target-cell specificity, distinction from additional inhibitors of HIV-1 transcription in CD8(+) T cell supernatants, as well as the differential regulation of host cell antiviral genes that could impact HIV-1 replication. These genes include a number of transcription factors as well IFN-alpha-inducible genes including PKR, IRF1, and Rantes, in the absence of induction of IFN-alpha. These data suggest that the anti-HIV-1 activity of ProTalpha is mediated through the modulation of a number of genes that have been reported to suppress HIV-1 replication including the dysregulation of transcription factors and the induction of PKR and Rantes mRNA.

Full Text

Duke Authors

Cited Authors

  • Mosoian, A; Teixeira, A; Burns, CS; Khitrov, G; Zhang, W; Gusella, L; Klotman, P; Klotman, M

Published Date

  • September 2007

Published In

Volume / Issue

  • 1112 /

Start / End Page

  • 269 - 285

PubMed ID

  • 17600282

Pubmed Central ID

  • 17600282

Electronic International Standard Serial Number (EISSN)

  • 1749-6632

International Standard Serial Number (ISSN)

  • 0077-8923

Digital Object Identifier (DOI)

  • 10.1196/annals.1415.043

Language

  • eng