Wednesday, June 24, 2009

HIV-1 VPR Protein's Protective Qualities


We have noted that HIV replication increases during the immune activation of opportunistic infection. A study now reveals that HIV-1 VPR protein protects against superantigens and endotoxin assault by moderating inflammatory responses and thus suppressing cell activation and cytokine production.

Even more surprising is the finding that VPR protects T cells against depletion. Says the 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-kappaB. In this regard we sought to test its effects in vivo on an NF-kappaB-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.

Needless to say, this runs quite counter to the assumed role which HIV is commonly believed to play in immune suppression.

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