scholarly journals Antiviral innate immune response of RNA interference

2014 ◽  
Vol 8 (07) ◽  
pp. 804-810 ◽  
Author(s):  
Abubaker Sidahmed ◽  
Shaza Abdalla ◽  
Salahedin Mahmud ◽  
Bruce Wilkie

RNA interference (RNAi) is an ancient, natural process conserved among species from different kingdoms. RNAi is a transcriptional and post-transcriptional gene silencing mechanism in which, double-stranded RNA or hairpin RNA is cleaved by an RNase III-type enzyme called Dicer into small interfering RNA duplex. This subsequently directs sequence-specific, homology dependent, Watson-Crick base-pairing post-transcriptional gene silencing by binding to its complementary RNA and initiating its elimination through degradation or by persuading translational inhibition. In plants, worms, and insects, RNAi is the main and strong antiviral defense mechanism. It is clear that RNAi silencing, contributes in restriction of viral infection in vertebrates. In a short period, RNAi has progressed to become a significant experimental tool for the analysis of gene function and target validation in mammalian systems. In addition, RNA silencing has then been found to be involved in translational repression, transcriptional inhibition, and DNA degradation. RNAi machinery required for robust RNAi-mediated antiviral response are conserved throughout evolution in mammals and plays a crucial role in antiviral defense of invertebrates, but despite these important functions RNAi contribution to mammalian antiviral innate immune defense has been underestimated and disputed. In this article, we review the literature concerning the roles of RNAi as components of innate immune system in mammals and how, the RNAi is currently one of the most hopeful new advances toward disease therapy. This review highlights the potential of RNAi as a therapeutic strategy for viral infection and gene regulation to modulate host immune response to viral infection.

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1187
Author(s):  
Michael Wassenegger ◽  
Athanasios Dalakouras

Viroids are plant pathogenic, circular, non-coding, single-stranded RNAs (ssRNAs). Members of the Pospiviroidae family replicate in the nucleus of plant cells through double-stranded RNA (dsRNA) intermediates, thus triggering the host’s RNA interference (RNAi) machinery. In plants, the two RNAi pillars are Post-Transcriptional Gene Silencing (PTGS) and RNA-directed DNA Methylation (RdDM), and the latter has the potential to trigger Transcriptional Gene Silencing (TGS). Over the last three decades, the employment of viroid-based systems has immensely contributed to our understanding of both of these RNAi facets. In this review, we highlight the role of Pospiviroidae in the discovery of RdDM, expound the gradual elucidation through the years of the diverse array of RdDM’s mechanistic details and propose a revised RdDM model based on the cumulative amount of evidence from viroid and non-viroid systems.


2016 ◽  
Vol 4 (41) ◽  
pp. 6620-6639 ◽  
Author(s):  
Jinming Li ◽  
Shanshan Xue ◽  
Zong-Wan Mao

RNA interference (RNAi) is a naturally occurring endogenous regulatory process in which the short double-stranded RNA causes sequence-specific post-transcriptional gene silencing.


2014 ◽  
Vol 5 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Neil A. Youngson ◽  
Pin-Chun Lin ◽  
Shih-Shun Lin

AbstractRecent discoveries in eukaryotes have shown that autophagy-mediated degradation of DICER and ARGONAUTE (AGO), the proteins involved in post-transcriptional gene silencing (PTGS), can occur in response to viral infection and starvation. In plants, a virally encoded protein P0 specifically interacts with AGO1 and enhances degradation through autophagy, resulting in suppression of gene silencing. In HeLa cells, DICER and AGO2 protein levels decreased after nutrient starvation or after treatment to increase autophagy. Environmental exposures to viral infection and starvation have also recently been shown to sometimes not only induce a stress response in the exposed plant but also in their unexposed progeny. These, and other cases of inherited stress response in plants are thought to be facilitated through transgenerational epigenetic inheritance, and the mechanism involves the PTGS and transcriptional gene silencing (TGS) pathways. These recent discoveries suggest that the environmentally-induced autophagic degradation of the PTGS and TGS components may have significant effects on inherited stress responses.


Author(s):  
Elisabetta Ullu ◽  
Appolinaire Djikeng ◽  
Huafang Shi ◽  
Christian Tschudi

In animals and protozoa gene–specific double–stranded RNA triggers the degradation of homologous cellular RNAs, the phenomenon of RNA interference (RNAi). RNAi has been shown to represent a novel paradigm in eukaryotic biology and a powerful method for studying gene function. Here we discuss RNAi in terms of its mechanism, its relationship to other post–transcriptional gene silencing phenomena in plants and fungi, its connection to retroposon silencing and possibly to translation, and its biological role. Among the organisms where RNAi has been demonstrated the protozoan parasite Trypanosoma brucei represents the most ancient branch of the eukaryotic lineage. We provide a synopsis of what is currently known about RNAi in T. brucei and outline the recent advances that make RNAi the method of choice to disrupt gene function in these organisms.


2020 ◽  
Vol 5 (1) ◽  
pp. 41
Author(s):  
Hafiz Ghulam Muhu-Din Ahmed ◽  
Amna . ◽  
Shadab Shaukat ◽  
Iqra Kousar ◽  
Maria Rafiq ◽  
...  

Ribonucleic acid (RNA) silencing, RNA interference (RNAi) or post-transcriptional gene silencing takes place in a variety of eukaryotes and it was discovered firstly in the plants. The RNA silencing process is activated by a trigger from dsRNA predecessor. A very important step in the silencing pathways the conversion of dsRNA into small duplexes of RNA of the representative length and arrangement. Then these small dsRNA monitor RNA silencing by different mechanisms. Post transcriptional gene silencing mechanisms were initially identified as an anti-viral process that give protection to the organisms from the viruses or which inhibit the unsystematic incorporation of transposable components. The basic aim of this review article is to study the mechanism of gene silencing by dsRNA and the roles of certain proteins in cellular post transcriptional RNA silencing machinery and finally we also discuss the RNA silencing as an anti-viral defense mechanism in the plants. 


2019 ◽  
Vol 93 (6) ◽  
Author(s):  
Yunjing Wang ◽  
Yuyao Wu ◽  
Qian Gong ◽  
Asigul Ismayil ◽  
Yuxiang Yuan ◽  
...  

ABSTRACT In plants, RNA-directed DNA methylation (RdDM)-mediated transcriptional gene silencing (TGS) is a natural antiviral defense against geminiviruses. Several geminiviral proteins have been shown to target the enzymes related to the methyl cycle or histone modification; however, it remains largely unknown whether and by which mechanism geminiviruses directly inhibit RdDM-mediated TGS. In this study, we showed that Cotton leaf curl Multan virus (CLCuMuV) V2 directly interacts with Nicotiana benthamiana AGO4 (NbAGO4) and that the L76S mutation in V2 (V2L76S) abolishes such interaction. We further showed that V2, but not V2L76S, can suppresses RdDM and TGS. Silencing of NbAGO4 inhibits TGS, reduces the viral methylation level, and enhances CLCuMuV DNA accumulation. In contrast, the V2L76S substitution mutant attenuates CLCuMuV infection and enhances the viral methylation level. These findings reveal that CLCuMuV V2 contributes to viral infection by interaction with NbAGO4 to suppress RdDM-mediated TGS in plants. IMPORTANCE In plants, the RNA-directed DNA methylation (RdDM) pathway is a natural antiviral defense mechanism against geminiviruses. However, how geminiviruses counter RdDM-mediated defense is largely unknown. Our findings reveal that Cotton leaf curl Multan virus V2 contributes to viral infection by interaction with NbAGO4 to suppress RNA-directed DNA methylation-mediated transcriptional gene silencing in plants. Our work provides the first evidence that a geminiviral protein is able to directly target core RdDM components to counter RdDM-mediated TGS antiviral defense in plants, which extends our current understanding of viral counters to host antiviral defense.


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