Identification of host miRNAs that may limit human rhinovirus replication

Bondanese, Victor P.; Francisco-Garcia, Ana S.; Bedke, Nicole; Davies, Donna E.; Sánchez-Elsner, Tilman

doi:10.4331/wjbc.v5.i4.437

Cited by 41 publications

(39 citation statements)

References 88 publications

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“…However, in vitro studies have demonstrated that has-miR155 transfection suppresses RV replication in the human cell line BEAS-2B (derived from normal human bronchial epithelial cells). [ 23 ] In this elegant work Bondanese and colleagues also observed viral RNA co-immunoprecipitated with argonaute 2 protein (crucial component of the miR silencing complex) confirming the functional direct action of miRs against RV. In agreement with our current findings, bioinformatics predictions and subsequent experiments demonstrated that hsa-miR155 is the key miR orchestrating host immune responses against RV.…”

Section: Discussionmentioning

confidence: 76%

“…We focused on the targetome analysis of hsa-miR-155 , given our current observations and recent evidence demonstrating the antiviral effect of hsa-miR-155 against RV in vitro . [ 23 ]…”

Section: Resultsmentioning

confidence: 99%

“…In agreement with our current findings, bioinformatics predictions and subsequent experiments demonstrated that hsa-miR155 is the key miR orchestrating host immune responses against RV. [ 23 ] Similarly, miR-155 has been previously identified by other groups to be a key player in antiviral responses in the respiratory system[ 5 , 40 ] as well in other systems,[ 41 – 43 ] being critical for host defense against numerous viruses such as influenza, hepatitis C, herpes and HTLV-1 infections. [ 9 , 44 , 45 ]…”

Section: Discussionmentioning

confidence: 99%

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Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood

et al. 2016

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BackgroundInnate immune responses are fine-tuned by small noncoding RNA molecules termed microRNAs (miRs) that modify gene expression in response to the environment. During acute infections, miRs can be secreted in extracellular vesicles (EV) to facilitate cell-to-cell genetic communication. The purpose of this study was to characterize the baseline population of miRs secreted in EVs in the airways of young children (airway secretory microRNAome) and examine the changes during rhinovirus (RV) infection, the most common cause of asthma exacerbations and the most important early risk factor for the development of asthma beyond childhood.MethodsNasal airway secretions were obtained from children (≤3 yrs. old) during PCR-confirmed RV infections (n = 10) and age-matched controls (n = 10). Nasal EVs were isolated with polymer-based precipitation and global miR profiles generated using NanoString microarrays. We validated our in vivo airway secretory miR data in an in vitro airway epithelium model using apical secretions from primary human bronchial epithelial cells (HBEC) differentiated at air-liquid interface (ALI). Bioinformatics tools were used to determine the unified (nasal and bronchial) signature airway secretory miRNAome and changes during RV infection in children.ResultsMultiscale analysis identified four signature miRs comprising the baseline airway secretory miRNAome: hsa-miR-630, hsa-miR-302d-3p, hsa- miR-320e, hsa-miR-612. We identified hsa-miR-155 as the main change in the baseline miRNAome during RV infection in young children. We investigated the potential biological relevance of the airway secretion of hsa-mir-155 using in silico models derived from gene datasets of experimental in vivo human RV infection. These analyses confirmed that hsa-miR-155 targetome is an overrepresented pathway in the upper airways of individuals infected with RV.ConclusionsComparative analysis of the airway secretory microRNAome in children indicates that RV infection is associated with airway secretion of EVs containing miR-155, which is predicted in silico to regulate antiviral immunity. Further characterization of the airway secretory microRNAome during health and disease may lead to completely new strategies to treat and monitor respiratory conditions in all ages.

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Section: Discussionmentioning

confidence: 76%

“…We focused on the targetome analysis of hsa-miR-155 , given our current observations and recent evidence demonstrating the antiviral effect of hsa-miR-155 against RV in vitro . [ 23 ]…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood

et al. 2016

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“…The miR-128 and miR-155 miRNAs were identified as possible regulators of the innate immune response against RV-1B [33], since they have as targets the genetic material from RV. A report demonstrated that gene silencing of these miRNAs increases RV replication by~50% [34]. miR-23b is involved in the immune response against RV, as it downregulates LPR5 and VLDLR transmembrane receptor expression [4].…”

Section: Rhinovirus (Rv)mentioning

confidence: 99%

microRNAs in viral acute respiratory infections: immune regulation, biomarkers, therapy, and vaccines

Leon-Icaza

Zeng

Rosas-Taraco

2019

ExRNA

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MicroRNAs (miRNAs) are single-stranded RNAs of 17-24 nt. These molecules regulate gene expression at the posttranscriptional level and are differentially expressed in viral acute respiratory infections (ARIs), which are responsible for high morbidity and mortality around the world. In recent years, miRNAs have been studied in order to discover anti-viral ARI drug targets as well as biomarkers for diagnosis, severity, and prognosis. This review presents an analysis of the regulatory response to viral ARIs of miRNAs, including their participation in the innate immune response, their utility as biomarkers, and their potential for future therapies and vaccine development.

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“…Third, host miRNAs can also directly target pathogen mRNAs to regulate pathogen replication, latency, and virulence. For example, miR‐128 and miR‐155 can decrease the replication of human rhinovirus by binding to viral RNA . Several cellular miRNAs can target viral mRNA genes in resting CD4 + cells to maintain HIV‐1 latency .…”

Section: Mirnas Regulate T Cell Immunity During Pathogen Infectionmentioning

confidence: 99%

Roles of microRNAs in T cell immunity: Implications for strategy development against infectious diseases

Giri

Mahato

Cheng

2018

Medicinal Research Reviews

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T cell immunity plays a vital role in pathogen infections.MicroRNA (miRNAs) are small, single-stranded noncoding RNAs that regulate T cell immunity by targeting key transcriptional factors, signaling proteins, and cytokines associated with T cell activation, differentiation, and function. The dysregulation of miRNA expression in T cells may lead to specific immune responses and can provide new therapeutic opportunities against various infectious diseases. Here, we summarize recent studies that focus on the roles of miRNAs in T cell immunity and highlight miRNA functions in prevalent infectious diseases. Additionally, we also provide insights into the functions of extracellular vesicle miRNAs and attempt to delineate the mechanism of miRNA sorting into extracellular vesicles and their immunomodulatory functions. Moreover, methodologies and strategies for miRNA delivery against infectious diseases are summarized. Finally, potential strategies for miRNAbased therapies are proposed.

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Identification of host miRNAs that may limit human rhinovirus replication

Abstract: Taken together, our results suggest that pathological changes in microRNA expression, as already reported for asthma or chronic obstructive pulmonary disease have the potential to affect Rhinovirus replication and therefore may play a role in virus-induced exacerbations.

Cited by 41 publications

References 88 publications

Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood

Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood

microRNAs in viral acute respiratory infections: immune regulation, biomarkers, therapy, and vaccines

Roles of microRNAs in T cell immunity: Implications for strategy development against infectious diseases

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