HIV-1 viral protein-R (VPR) protects against lethal superantigen challenge while maintaining homeostatic T cell levels in vivo

Muthumani, K., Choo, A. Y., Hwang, D. S., Dayes, N. S., Chattergoon, M., Mayilvahanan, S., Thieu, K. P., Buckley, P. T., Emmanuel, J., Premkumar, A., Weiner, D. B. (November 2005) HIV-1 viral protein-R (VPR) protects against lethal superantigen challenge while maintaining homeostatic T cell levels in vivo. Molecular Therapy, 12 (5). pp. 910-921. ISSN 1525-0016

URL: http://www.nature.com/mt/journal/v12/n5/full/mt200...
DOI: 10.1016/j.ymthe.2005.05.009

Abstract

The HIV-1 accessory protein Vpr exhibits many interesting features related to macrophage and T cell biology. As a viral protein or as a soluble molecule it can suppress immune cell activation and cytokine production in vitro in part by targeted inhibition of NF-kappa B. In this regard we sought to test its effects in vivo on an NF-kappa B-dependent immune pathway. We examined the activity of Vpr in a lethal toxin-mediated challenge model in mice. Intravenous delivery of Vpr was sufficient to protect mice from lethal challenge with staphylococcal endotoxin B (SEB). Furthermore, Vpr protected host CD4(+) T cells from in vivo depletion likely by preventing induction of AICD of SEB-exposed cells in a post-toxin-binding fashion. Understanding the biology of Vpr's activities in this model may allow for new insight into potential mechanisms of hyperinflammatory disease and into Vpr pathobiology in the context of HIV infection.

Item Type: Paper
Uncontrolled Keywords: HIV-1 Vpr NF-kappa B T cell activation staphylococcal endotoxin B cytokine sepsis glucocorticoid receptor NF-KAPPA-B immunodeficiency virus type 1 severe sepsis septic shock activation macrophages apoptosis induction receptor VACCINE
Subjects: diseases & disorders > viral diseases > HIV
diseases & disorders > viral diseases
CSHL Authors:
Depositing User: CSHL Librarian
Date: November 2005
Date Deposited: 06 Jan 2012 19:07
Last Modified: 06 Jan 2012 19:07
URI: http://repository.cshl.edu/id/eprint/22660

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