scholarly journals The interferon regulatory factor IRF5 is differentially expressed in the blood of patients with viral co-infections.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Influenza A ◽  
Macrophage Polarization ◽  
Cell Lineage ◽  
Interferon Regulatory Factor ◽  
Human Rhinovirus ◽  
Differentially Expressed ◽  
Influenza B ◽  
Regulatory Factor ◽  
Transcriptional Responses ◽  
Human Coronavirus

Co-infection is a process by which the same host can be infected with two pathogens. By mining published microarray data (1), we found that the gene encoding the interferon regulatory factor 5 (IRF5) was among the genes most differentially expressed in the blood of seven patients with viral co-infections: in one patient with human coronavirus OC43 and Influenza A co-infection, in one patient with human coronavirus NL63 and Human Rhinovirus co-infection, and in five patients with Influenza B and Human Rhinovirus co-infection. IRF5 has described functions in macrophage polarization, T-cell lineage specification (2), B-cell development (3), innate immune signal transduction (4) and in transcriptional responses to viral infection (5), and could potentially be relevant to processes underlying viral co-infection.

scholarly journals Differential Expression of Serum Exosome microRNAs and Cytokines in Influenza A and B Patients Collected in the 2016 and 2017 Influenza Seasons

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 149
Author(s):  
Sreekumar Othumpangat ◽  
William G. Lindsley ◽  
Donald H. Beezhold ◽  
Michael L. Kashon ◽  
Carmen N. Burrell ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Influenza A ◽  
Influenza Infection ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Differentially Expressed ◽  
Influenza B ◽  
Airway Epithelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Novel Approach

MicroRNAs (miRNAs) have remarkable stability and are key regulators of mRNA transcripts for several essential proteins required for the survival of cells and replication of the virus. Exosomes are thought to play an essential role in intercellular communications by transporting proteins and miRNAs, making them ideal in the search for biomarkers. Evidence suggests that miRNAs are involved in the regulation of influenza virus replication in many cell types. During the 2016 and 2017 influenza season, we collected blood samples from 54 patients infected with influenza and from 30 healthy volunteers to identify the potential role of circulating serum miRNAs and cytokines in influenza infection. Data comparing the exosomal miRNAs in patients with influenza B to healthy volunteers showed 76 miRNAs that were differentially expressed (p < 0.05). In contrast, 26 miRNAs were differentially expressed between patients with influenza A (p < 0.05) and the controls. Of these miRNAs, 11 were commonly expressed in both the influenza A and B patients. Interferon (IFN)-inducing protein 10 (IP-10), which is involved in IFN synthesis during influenza infection, showed the highest level of expression in both influenza A and B patients. Influenza A patients showed increased expression of IFNα, GM-CSF, interleukin (IL)-13, IL-17A, IL-1β, IL-6 and TNFα, while influenza B induced increased levels of EGF, G-CSF, IL-1α, MIP-1α, and TNF-β. In addition, hsa-miR-326, hsa-miR-15b-5p, hsa-miR-885, hsa-miR-122-5p, hsa-miR-133a-3p, and hsa-miR-150-5p showed high correlations to IL-6, IL-15, IL-17A, IL-1β, and monocyte chemoattractant protein-1 (MCP-1) with both strains of influenza. Next-generation sequencing studies of H1N1-infected human lung small airway epithelial cells also showed similar pattern of expression of miR-375-5p, miR-143-3p, 199a-3p, and miR-199a-5p compared to influenza A patients. In summary, this study provides insights into the miRNA profiling in both influenza A and B virus in circulation and a novel approach to identify the early infections through a combination of cytokines and miRNA expression.

scholarly journals A MicroRNA93–Interferon Regulatory Factor-9–Immunoresponsive Gene-1–Itaconic Acid Pathway Modulates M2-Like Macrophage Polarization to Revascularize Ischemic Muscle

Circulation ◽  
2017 ◽  
Vol 135 (24) ◽  
pp. 2403-2425 ◽  
Author(s):  
Vijay Chaitanya Ganta ◽  
Min Hyub Choi ◽  
Anna Kutateladze ◽  
Todd E. Fox ◽  
Charles R. Farber ◽  
...  
Keyword(s):  
Itaconic Acid ◽  
Macrophage Polarization ◽  
Interferon Regulatory Factor ◽  
Regulatory Factor ◽  
Acid Pathway ◽  
Ischemic Muscle

scholarly journals The COP9 Signalosome Interacts with and Regulates Interferon Regulatory Factor 5 Protein Stability

2012 ◽  
Vol 33 (6) ◽  
pp. 1124-1138 ◽  
Author(s):  
Justyna Korczeniewska ◽  
Betsy J. Barnes
Keyword(s):  
Protein Stability ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Death Receptor ◽  
Interferon Regulatory Factor ◽  
Cop9 Signalosome ◽  
Small Interfering Rnas ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 5 ◽  
Enhanced Degradation

The transcription factor interferon regulatory factor 5 (IRF5) exerts crucial functions in the regulation of host immunity against extracellular pathogens, DNA damage-induced apoptosis, death receptor signaling, and macrophage polarization. Tight regulation of IRF5 is thus warranted for an efficient response toward extracellular stressors and for limiting autoimmune and inflammatory responses. Here we report that the COP9 signalosome (CSN), a general modulator of diverse cellular and developmental processes, associates constitutively with IRF5 and promotes its protein stability. The constitutive CSN/IRF5 interaction was identified using proteomics and confirmed by endogenous immunoprecipitations. The CSN/IRF5 interaction occurred on the carboxyl and amino termini of IRF5; a single internal deletion from amino acids 455 to 466 (Δ455-466) was found to significantly reduce IRF5 protein stability. CSN subunit 3 (CSN3) was identified as a direct interacting partner of IRF5, and knockdown of this subunit with small interfering RNAs resulted in enhanced degradation. Degradation was further augmented by knockdown of CSN1 and CSN3 together. The ubiquitin E1 inhibitor UBEI-41 or the proteasome inhibitor MG132 prevented IRF5 degradation, supporting the idea that its stability is regulated by the ubiquitin-proteasome system. Importantly, activation of IRF5 by the death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in enhanced degradation via loss of the CSN/IRF5 interaction. This study defines CSN to be a new interacting partner of IRF5 that controls its stability.

scholarly journals Deteksi Virus Penyebab Infeksi Saluran Pernafasan Akut di Rumah Sakit (Studi Pendahuluan dengan Uji Fast-Track® Diagnostik)

2018 ◽  
Vol 28 (4) ◽  
pp. 257-262 ◽  
Author(s):  
Vivi Setiawaty ◽  
Maretra Anindya Puspaningrum ◽  
Arie Ardiansyah Nugraha ◽  
Daniel Joko Wahyono
Keyword(s):  
Laboratory Testing ◽  
Fast Track ◽  
Human Adenovirus ◽  
Human Metapneumovirus ◽  
Human Rhinovirus ◽  
Parainfluenza Virus ◽  
Influenza B ◽  
Rt Pcr ◽  
Human Coronavirus ◽  
Human Parainfluenza Virus

Abstract Acute respiratory infections (ARI) is the leading cause of morbidity and mortality in the world and Indonesia. Information on the virus that causes ARI is still limited. The aim of this study was to detect the virus that causes ARI hospitalized cases in three sentinel surveillance hospitals of severe ARI. Laboratory testing of 30 nasal and throat swab specimens from ARI hospitalized cases at Deli Serdang Hospital, Wonosari Hospital and Kanudjoso Djati Hospital during August - September 2016. Laboratory testing were carried out at the Virology Laboratory of the Center for Biomedical Research and Development and Basic Health Technology. This research is a preliminary study using Fast-Track Diagnostics multiplex Real-time RT-PCR to detect 21 viruses. The viruses that have been detected are Human Metapneumovirus (21.2%), Human Parainfluenza Virus 1 (12.1%), Influenza B (6.1%), Human Coronavirus-OC43 (6.1%), Human CoronavirusNL63 (6.1%), Human Parainfluenza Virus 2 (3.0%), Human Rhinovirus (3.0%), and Human Adenovirus (3.0%). Of the 17 samples that tested positive for viruses, 14 of them were single cases of infection while the other three were cases of co-infection between Human Coronavirus-NL63 and Human Parainfluenza Virus 1, Human Metapneumovirus with Human Coronavirus-OC43, and Human Adenovirus with Human Rhinovirus. The most detected virus from ARI hospitalized cases are the Human Metapneumovirus. Abstrak Infeksi saluran pernafasan akut (ISPA) merupakan penyakit menular yang menjadi penyebab utama 1 morbiditas dan mortalitas di dunia dan Indonesia. Informasi virus penyebab ISPA masih terbatas. Tujuan dari penelitian ini adalah mendeteksi virus penyebab kasus ISPA rawat inap di tiga rumah sakit sentinel surveilans ISPA berat. Pemeriksaan pada 30 spesimen swab hidung dan tenggorok dari kasus ISPA rawat inap di RSUD Deli Serdang, RSUD Wonosari, dan RS Kanudjoso Djati selama bulan Agustus–September 2016. Pemeriksaan dilakukan di Laboratorium Virologi Pusat Penelitian dan Pengembangan Biomedis dan Teknologi Dasar Kesehatan. Penelitian ini merupakan penelitian pendahuluan menggunakan FastTrack Diagnostics multiplex Real-time RT-PCR untuk mendeteksi 21 virus. Virus-virus yang berhasil dideteksi adalah Human Metapneumovirus (21,2%). Human Parainfluenza Virus 1 (12,1%), Influenza B (6,1%), Human Coronavirus-OC43 (6,1%), Human Coronavirus-NL63 (6,1%), Human Parainfluenza Virus 2 (3,0%), Human Rhinovirus (3,0%), dan Human Adenovirus (3,0%). Dari 17 sampel yang dinyatakan positif mengandung virus, 14 diantaranya merupakan kasus infeksi tunggal sedangkan tiga lainnya merupakan kas us koinfeksi antara Human Coronavirus-NL63 dengan Human Parainfluenza Virus 1, Human Metapneumovirus dengan Human Coronavirus-OC43, dan Human Adenovirus dengan Human Rhinovirus. Virus yang paling banyak terdeteksi dari spesimen kasus ISPA rawat inap adalah Human Metapneumovirus.

scholarly journals The HLA complex non-coding RNA HCG4 is differentially expressed in the blood of patients with coronavirus co-infections.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Gene Expression ◽  
Influenza A ◽  
Differentially Expressed ◽  
Human Coronavirus ◽  
Gene Encoding ◽  
Non Coding Rna ◽  
Different Types ◽  
Family Gene ◽  
Human Coronaviruses ◽  
One Year

The human coronavirus SARS-CoV-2 (1) has resulted in the death of over 200,000 Americans in less than one year (2). Infection of a person already suffering from a viral infection, a phenomena known as co-infection can potentially pose a problem during the upcoming influenza season. We mined published microarray data (3) to identify genes most differentially expressed in the whole blood of patients suffering from human coronavirus co-infections. We found that the gene encoding the HLA complex non-coding RNA HCG4 was among those whose expression changed most significantly transcriptome-wide when comparing the blood of patients suffering from three different types of co-infections: human coronavirus NL63 and rhinovirus, human coronavirus HKU1 and rhinovirus, as well as in human coronavirus OC43 and influenza A co-infection. We previously reported significant transcriptome-wide changes in HLA family gene expression (4), as well as in changes in gene expression of the cathepsins in viral co-infection (5). Together, these data suggest the process of antigen presentation could be altered during viral co-infections involving the human coronaviruses.

scholarly journals O-GlcNAc transferase promotes influenza A virus–induced cytokine storm by targeting interferon regulatory factor–5

2020 ◽  
Vol 6 (16) ◽  
pp. eaaz7086 ◽  
Author(s):  
Qiming Wang ◽  
Peining Fang ◽  
Rui He ◽  
Mengqi Li ◽  
Haisheng Yu ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Cytokine Production ◽  
Interferon Regulatory Factor ◽  
Clinical Samples ◽  
Cytokine Storm ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 5 ◽  
Key Enzyme ◽  
Glcnac Transferase

In this study, we demonstrated an essential function of the hexosamine biosynthesis pathway (HBP)–associated O-linked β-N-acetylglucosamine (O-GlcNAc) signaling in influenza A virus (IAV)–induced cytokine storm. O-GlcNAc transferase (OGT), a key enzyme for protein O-GlcNAcylation, mediated IAV-induced cytokine production. Upon investigating the mechanisms driving this event, we determined that IAV induced OGT to bind to interferon regulatory factor–5 (IRF5), leading to O-GlcNAcylation of IRF5 on serine-430. O-GlcNAcylation of IRF5 is required for K63-linked ubiquitination of IRF5 and subsequent cytokine production. Analysis of clinical samples revealed that IRF5 is O-GlcNAcylated, and higher levels of proinflammatory cytokines correlated with higher levels of blood glucose in IAV-infected patients. We identified a molecular mechanism by which HBP-mediated O-GlcNAcylation regulates IRF5 function during IAV infection, highlighting the importance of glucose metabolism in IAV-induced cytokine storm.

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