Murine models of Vpr-mediated pathogenesis

Alexandra Snyder, Michael J. Ross

Research output: Contribution to journalReview article

6 Scopus citations

Abstract

HIV viral protein r (Vpr) exerts a variety of cellular effects, including modulation of transcription and cytokine production, apoptosis, and cell cycle arrest. Vpr induces these affects by mechanisms that include inhibition of NF-kappaB activation, inducing mitochondrial injury, and promoting proteasomal degradation of cellular factor(s) leading to cell cycle arrest. Murine models have provided invaluable contributions to our understanding of HIV pathogenesis, however many of the HIV-1 proteins, including Vpr, differ in their cellular effects depending upon cell type and speciesspecific factors. Since the majority of in vivo studies elucidating the role of Vpr in disease pathogenesis have utilized murine models, it is critical to understand the species-specific factors that may affect Vpr function. In this manuscript, we review the cellular pathways and end organ effects of Vpr that have been studied in murine cell lines and mouse models, and discuss the relevance of these studies to the role of Vpr in disease in persons living with HIV/AIDS.

Original languageEnglish (US)
Pages (from-to)129-135
Number of pages7
JournalCurrent HIV Research
Volume7
Issue number2
DOIs
StatePublished - May 26 2009
Externally publishedYes

Keywords

  • Apoptosis
  • Cell cycle
  • HIV-1
  • HIV-associated nephropathy
  • Immune response
  • Vpr

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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