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HIV accessory protein disables host immunity via receptor-protein intermediary

kB, a major immune regulator in the host cell. To verify their idea, the researchers used a mouse model in which PARP-1 was knocked out and found that their cells were immune to sepsis (pathogens and their toxins in the blood), because the NF-kB molecules did not go into overdrive, kicking up inflammatory molecules called cytokines. This data demonstrate that Vpr attacks PARP-1 activity, so the mice are immune to toxins created by pathogens ?one indication that their immune surveillance has been compromised.

Using biochemistry tests, the researchers were able to show that Vpr does interact with PARP-1 through the glucocorticoid receptor. Vpr hitches a ride on the glucocorticoid receptor, driving glucocorticoid to bind to PARP-1?which, in turn, inactivates it. "Ultimately, glucocorticoid is really an intermediary between Vpr and PARP-1," explains Weiner.

Weiner cites several potential clinical implications of this basic research. These findings show an immune function that had not been previously attributed to the glucocorticoid receptor. "With additional study this research may provide approaches for designing new drugs to fight AIDS, as well as for inflammatory disorders," suggests Weiner. "This research also gives us a new way to think about the relationship between immune activation and sepsis, and it may have implications ultimately for our understanding of novel approaches to prevent sepsis."


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Source:University of Pennsylvania School of Medicine


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