scholarly journals The Diverse Roles of microRNAs at the Host–Virus Interface

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 440 ◽  
Author(s):  
Annie Bernier ◽  
Selena Sagan
Keyword(s):  
Gene Expression ◽  
Genome Stability ◽  
Viral Infections ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Transcriptional Level ◽  
Cellular Mirnas ◽  
Antiviral Responses ◽  
Dna And Rna ◽  
Rna Accumulation

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections and antiviral responses. Diverse families of DNA and RNA viruses have been shown to take advantage of cellular miRNAs or produce virally encoded miRNAs that alter host or viral gene expression. MiRNA-mediated changes in gene expression have been demonstrated to modulate viral replication, antiviral immune responses, viral latency, and pathogenesis. Interestingly, viruses mediate both canonical and non-canonical interactions with miRNAs to downregulate specific targets or to promote viral genome stability, translation, and/or RNA accumulation. In this review, we focus on recent findings elucidating several key mechanisms employed by diverse virus families, with a focus on miRNAs at the host–virus interface during herpesvirus, polyomavirus, retroviruses, pestivirus, and hepacivirus infections.

scholarly journals Viral miRNAs as Active Players and Participants in Tumorigenesis

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 358 ◽  
Author(s):  
Alessia Gallo ◽  
Vitale Miceli ◽  
Matteo Bulati ◽  
Gioacchin Iannolo ◽  
Flavia Contino ◽  
...  
Keyword(s):  
Viral Infections ◽  
Human Cancer ◽  
Scientific Evidence ◽  
Adaptive Immune System ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Cellular Mirnas ◽  
Viral Mirnas ◽  
Human Cancers ◽  
Cellular Pathways

The theory that viruses play a role in human cancers is now supported by scientific evidence. In fact, around 12% of human cancers, a leading cause of morbidity and mortality in some regions, are attributed to viral infections. However, the molecular mechanism remains complex to decipher. In recent decades, the uncovering of cellular miRNAs, with their invaluable potential as diagnostic and prognostic biomarkers, has increased the number of studies being conducted regarding human cancer diagnosis. Viruses develop clever mechanisms to succeed in the maintenance of the viral life cycle, and some viruses, especially herpesviruses, encode for miRNA, v-miRNAs. Through this viral miRNA, the viruses are able to manipulate cellular and viral gene expression, driving carcinogenesis and escaping the host innate or adaptive immune system. In this review, we have discussed the main viral miRNAs and virally influenced cellular pathways, and their capability to drive carcinogenesis.

Analysis of avian leukosis virus DNA and RNA in bursal tumors: Viral gene expression is not required for maintenance of the tumor state

Cell ◽  
1981 ◽  
Vol 23 (2) ◽  
pp. 311-322 ◽  
Author(s):  
Gregory S. Payne ◽  
Sara A. Courtneidge ◽  
Lyman B. Crittenden ◽  
Aly M. Fadly ◽  
J.Michael Bishop ◽  
...  
Keyword(s):  
Gene Expression ◽  
Viral Gene Expression ◽  
Avian Leukosis Virus ◽  
Viral Gene ◽  
Dna And Rna

scholarly journals A Computational Approach for Predicting Role of Human MicroRNAs in MERS-CoV Genome

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Md Mahmudul Hasan ◽  
Rozina Akter ◽  
Md. Shahin Ullah ◽  
Md. Jaynul Abedin ◽  
G. M. Ahsan Ullah ◽  
...  
Keyword(s):  
Gene Expression ◽  
Middle East ◽  
Viral Replication ◽  
Viral Gene Expression ◽  
Computational Approach ◽  
Viral Gene ◽  
Fatality Rate ◽  
Human Coronavirus ◽  
Cellular Mirnas

The new epidemic Middle East Respiratory Syndrome (MERS) is caused by a type of human coronavirus called MERS-CoV which has global fatality rate of about 30%. We are investigating potential antiviral therapeutics against MERS-CoV by using host microRNAs (miRNAs) which may downregulate viral gene expression to quell viral replication. We computationally predicted potential 13 cellular miRNAs from 11 potential hairpin sequences of MERS-CoV genome. Our study provided an interesting hypothesis that those miRNAs, that is, hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, hsa-miR-6865-5p, and hsa-miR-342-3p, would be antiviral therapeutics against MERS-CoV infection.

scholarly journals Development of “NEC-SD-LAMP,” a New Non-Electrified Infectious Diseases Testing Method

2022 ◽  
Author(s):  
Yusuke Kimura ◽  
Masashi Ikeuchi
Keyword(s):  
Gene Expression ◽  
Melting Point ◽  
Palmitic Acid ◽  
Viral Infections ◽  
Viral Gene Expression ◽  
Isothermal Amplification ◽  
Viral Gene ◽  
Optimal Temperature ◽  
Loop Mediated Isothermal Amplification ◽  
Electric Control

Abstract Here, non-electric-control SalivaDirect loop-mediated isothermal amplification (NEC-SD-LAMP), which can detect infections by analyzing viral gene expression in saliva without electrical control systems, was developed. In this method, viral genes are purified from saliva using SalivaDirect, and gene expression is analyzed by loop-mediated isothermal amplification (LAMP) by adding water to the device, and the results can be visually confirmed. Melting palmitic acid maintains the optimal temperature for the LAMP reaction, as the temperature of palmitic acid is maintained at 62.9°C, its melting point. By taking advantage of the proximity of this melting point to the optimal temperature for LAMP, it is possible to perform LAMP without electricity. Using this method, adenovirus DNA was detected in saliva. Furthermore, the detection limit was 2 copies per µL, indicating that it is possible to detect viral infections in saliva even before the onset of SARS-CoV-2 infection.

scholarly journals Inhibition of Poxvirus Gene Expression and Genome Replication by Bisbenzimide Derivatives

2017 ◽  
Vol 91 (18) ◽  
Author(s):  
Artur Yakimovich ◽  
Moona Huttunen ◽  
Benno Zehnder ◽  
Lesley J. Coulter ◽  
Victoria Gould ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virus Infection ◽  
Vaccinia Virus ◽  
Virus Disease ◽  
Vaccination Campaign ◽  
Antiviral Agents ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Genome Replication ◽  
Dna And Rna

ABSTRACT Virus infection of humans and livestock can be devastating for individuals and populations, sometimes resulting in large economic and societal impact. Prevention of virus disease by vaccination or antiviral agents is difficult to achieve. A notable exception was the eradication of human smallpox by vaccination over 30 years ago. Today, humans and animals remain susceptible to poxvirus infections, including zoonotic poxvirus transmission. Here we identified a small molecule, bisbenzimide (bisbenzimidazole), and its derivatives as potent agents against prototypic poxvirus infection in cell culture. We show that bisbenzimide derivatives, which preferentially bind the minor groove of double-stranded DNA, inhibit vaccinia virus infection by blocking viral DNA replication and abrogating postreplicative intermediate and late gene transcription. The bisbenzimide derivatives are potent against vaccinia virus and other poxviruses but ineffective against a range of other DNA and RNA viruses. The bisbenzimide derivatives are the first inhibitors of their class, which appear to directly target the viral genome without affecting cell viability. IMPORTANCE Smallpox was one of the most devastating diseases in human history until it was eradicated by a worldwide vaccination campaign. Due to discontinuation of routine vaccination more than 30 years ago, the majority of today's human population remains susceptible to infection with poxviruses. Here we present a family of bisbenzimide (bisbenzimidazole) derivatives, known as Hoechst nuclear stains, with high potency against poxvirus infection. Results from a variety of assays used to dissect the poxvirus life cycle demonstrate that bisbenzimides inhibit viral gene expression and genome replication. These findings can lead to the development of novel antiviral drugs that target viral genomes and block viral replication.

scholarly journals Latency Reversing Agents: Kick and Kill of HTLV-1?

2021 ◽  
Vol 22 (11) ◽  
pp. 5545
Author(s):  
Annika P. Schnell ◽  
Stephan Kohrt ◽  
Andrea K. Thoma-Kress
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
Viral Gene Expression ◽  
Cytotoxic T Cell ◽  
Viral Gene ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Reversing Agents ◽  
Ctl Responses

Human T-cell leukemia virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), is a retrovirus, which integrates into the host genome and persistently infects CD4+ T-cells. Virus propagation is stimulated by (1) clonal expansion of infected cells and (2) de novo infection. Viral gene expression is induced by the transactivator protein Tax, which recruits host factors like positive transcription elongation factor b (P-TEFb) to the viral promoter. Since HTLV-1 gene expression is repressed in vivo by viral, cellular, and epigenetic mechanisms in late phases of infection, HTLV-1 avoids an efficient CD8+ cytotoxic T-cell (CTL) response directed against the immunodominant viral Tax antigen. Hence, therapeutic strategies using latency reversing agents (LRAs) sought to transiently activate viral gene expression and antigen presentation of Tax to enhance CTL responses towards HTLV-1, and thus, to expose the latent HTLV-1 reservoir to immune destruction. Here, we review strategies that aimed at enhancing Tax expression and Tax-specific CTL responses to interfere with HTLV-1 latency. Further, we provide an overview of LRAs including (1) histone deacetylase inhibitors (HDACi) and (2) activators of P-TEFb, that have mainly been studied in context of human immunodeficiency virus (HIV), but which may also be powerful in the context of HTLV-1.

scholarly journals The [KIL-d] Element Specifically Regulates Viral Gene Expression in Yeast

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 601-609 ◽  
Author(s):  
Zsolt Tallóczy ◽  
Rebecca Mazar ◽  
Denise E Georgopoulos ◽  
Fausto Ramos ◽  
Michael J Leibowitz
Keyword(s):  
Gene Expression ◽  
Phenotypic Expression ◽  
Viral Gene Expression ◽  
Virus Genome ◽  
Viral Rna ◽  
High Rate ◽  
Viral Gene ◽  
Double Stranded Rna ◽  
Yeast Prions ◽  
Killer Virus

Abstract The cytoplasmically inherited [KIL-d] element epigenetically regulates killer virus gene expression in Saccharomyces cerevisiae. [KIL-d] results in variegated defects in expression of the M double-stranded RNA viral segment in haploid cells that are “healed” in diploids. We report that the [KIL-d] element is spontaneously lost with a frequency of 10−4–10−5 and reappears with variegated phenotypic expression with a frequency of ≥10−3. This high rate of loss and higher rate of reappearance is unlike any known nucleic acid replicon but resembles the behavior of yeast prions. However, [KIL-d] is distinct from the known yeast prions in its relative guanidinium hydrochloride incurability and independence of Hsp104 protein for its maintenance. Despite its transmissibility by successive cytoplasmic transfers, multiple cytoplasmic nucleic acids have been proven not to carry the [KIL-d] trait. [KIL-d] epigenetically regulates the expression of the M double-stranded RNA satellite virus genome, but fails to alter the expression of M cDNA. This specificity remained even after a cycle of mating and meiosis. Due to its unique genetic properties and viral RNA specificity, [KIL-d] represents a new type of genetic element that interacts with a viral RNA genome.

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