HIV drug nucleoside reverse transcriptase inhibitors as promising anti-inflammation therapeutics by targeting P2X7-dependent large pore formation: one stone for two birds?

Lin-Hua Jiang

doi:10.3389/fphar.2015.00038

Abstract

Nucleoside reverse transcriptase inhibitors (NRTIs) have been the backbones of HIV therapy since introduced in the late 1980s. These HIV drugs act by blocking the viral reverse transcriptase activity that is crucial in the HIV life cycle. In a recent study published by Science, Fowler et al. (2014) have shown that such antiretroviral agents can inhibit P2X7 receptor (P2X7R)-mediated Alu RNA-induced activation of caspase-1 in retinal pigment epithelial (RPE) cells and ATP-induced activation of caspase-1 in macrophage cells, independently of reverse transcriptase inhibition.

Highlights

Edited by: Chiranjib Chakraborty, Galgotias University, India Reviewed by: Rahman M
In a recent study published by Science, Fowler et al (2014) have shown that such antiretroviral agents can inhibit P2X7 receptor (P2X7R)-mediated Alu RNA-induced activation of caspase-1 in retinal pigment epithelial (RPE) cells and ATP-induced activation of caspase1 in macrophage cells, independently of reverse transcriptase inhibition
P2X7R antagonists have been passionately exploited as anti-inflammation therapeutics

Summary

Introduction

Edited by: Chiranjib Chakraborty, Galgotias University, India Reviewed by: Rahman M. In a recent study published by Science, Fowler et al (2014) have shown that such antiretroviral agents can inhibit P2X7 receptor (P2X7R)-mediated Alu RNA-induced activation of caspase-1 in retinal pigment epithelial (RPE) cells and ATP-induced activation of caspase1 in macrophage cells, independently of reverse transcriptase inhibition. They provide evidence to show that NRTIs inhibit P2X7R-mediated activation of caspase-1 in RPE cells and in LPS-primed macrophage cells induced by Alu RNAs and ATP, respectively.

Results

Conclusion