Abstract
On October 28th 1943 Winston Churchill said “we shape our buildings, and afterward our buildings shape us” (Humes, 1994). Churchill was pondering how and when to rebuild the British House of Commons, which had been destroyed by enemy bombs on May 10th 1941. The old House had been small and insufficient to hold all its members, but was restored to its original form in 1950 in order to recapture the “convenience and dignity” that the building had shaped into its parliamentary members. The circular loop whereby buildings or dwellings are shaped and go on to shape those that reside in them is also true of pathogens and their hosts. As obligate parasites, pathogens need to alter their cellular host environments to ensure survival. Typically pathogens modify cellular transcription profiles and in doing so, the pathogen in turn is affected, thereby closing the loop. As key orchestrators of gene expression, non-coding RNAs provide a vast and extremely precise set of tools for pathogens to target in order to shape the cellular environment. This review will focus on host non-coding RNAs that are manipulated by the infamous intracellular pathogen, the human immunodeficiency virus (HIV). We will briefly describe both short and long host non-coding RNAs and discuss how HIV gains control of these factors to ensure widespread dissemination throughout the host as well as the establishment of lifelong, chronic infection.
Highlights
The Impact of human immunodeficiency virus (HIV) Infection on Host miRNA Expression ProfilesOver the last decade a number of studies have reported a general perturbation of the host miRNA landscape following HIV infection (Klase et al, 2012; Swaminathan et al, 2014)
Gene Expression and Biophysics Group, Synthetic Biology Emerging Research Area, Council for Scientific and Industrial Research, Building 20, Samantha Barichievy, Discovery Sciences, Research & Development, AstraZeneca, Pepparedsleden 1, Mölndal SE-431, Sweden samantha.barichievy @astrazeneca.com
Specialty section: This article was submitted to Genetics of Aging, a section of the journal Frontiers in Genetics
Summary
Over the last decade a number of studies have reported a general perturbation of the host miRNA landscape following HIV infection (Klase et al, 2012; Swaminathan et al, 2014). HIV may use exosomes to modulate the intracellular levels of RISC-free small RNAs that indirectly inhibit virion production (Chen et al, 2014) This latter observation is intriguing as it involves a novel mechanism in which host miRNAs decrease viral replication. The same effect was observed if AGO2 was depleted thereby leading to a general increase in endogenous small RNA levels These findings have implications for expression-based studies, as a comprehensive evaluation of variations in exosomal-miRNA secretion across different HIV strains and cell types has not been published.
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