scholarly journals Small Non-coding RNA Expression Following Respiratory Syncytial Virus or Measles Virus Infection of Neuronal Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Abhijeet A. Bakre ◽  
Catherine Duffy ◽  
Hani’ah Abdullah ◽  
S. Louise Cosby ◽  
Ralph A. Tripp
Keyword(s):  
Respiratory Syncytial Virus ◽  
Measles Virus ◽  
Synonymous Codon ◽  
Neuronal Cells ◽  
Synonymous Codon Usage ◽  
Host Responses ◽  
Host Gene Expression ◽  
Non Coding Rna ◽  
Rna Fragments ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) or measles virus (MeV) infection modifies host responses through small non-coding RNA (sncRNA) expression. We show that RSV or MeV infection of neuronal cells induces sncRNAs including various microRNAs and transfer RNA fragments (tRFs). We show that these tRFs originate from select tRNAs (GCC and CAC for glycine, CTT and AAC for Valine, and CCC and TTT for Lysine). Some of the tRNAs are rarely used by RSV or MeV as indicated by relative synonymous codon usage indices suggesting selective cleavage of the tRNAs occurs in infected neuronal cells. The data implies that differentially expressed sncRNAs may regulate host gene expression via multiple mechanisms in neuronal cells.

scholarly journals Chimeric Measles Virus (MV/RSV), Having Ectodomains of Respiratory Syncytial Virus (RSV) F and G Proteins Instead of Measles Envelope Proteins, Induced Protective Antibodies against RSV

Vaccines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 156
Author(s):  
Akihito Sawada ◽  
Takashi Ito ◽  
Yoshiaki Yamaji ◽  
Tetsuo Nakayama
Keyword(s):  
Respiratory Syncytial Virus ◽  
G Proteins ◽  
Cell Lines ◽  
Measles Virus ◽  
Pathological Finding ◽  
Control Group ◽  
Protein Coding ◽  
Virus Growth ◽  
Protective Antibodies ◽  
Syncytial Virus

In our previous study, fusion (F) or glyco (G) protein coding sequence of respiratory syncytial virus (RSV) was inserted at the P/M junction of the measles AIK-C vector (MVAIK), and the recombinant measles virus induced protective immune responses. In the present study, the ectodomains of measles fusion (F) and hemagglutinin (HA) proteins were replaced with those of RSV F and G proteins, and a chimeric MV/RSV vaccine was developed. It expressed F and G proteins of RSV and induced cytopathic effect (CPE) in epithelial cell lines (Vero, A549, and HEp-2 cells), but not in lymphoid cell lines (B95a, Jurkat, and U937 cells). A chimeric MV/RSV grew similarly to AIK-C with no virus growth at 39 °C. It induced NT antibodies against RSV in cotton rats three weeks after immunization through intramuscular route and enhanced response was observed after the second dose at eight weeks. After the RSV challenge with 106 PFU, significantly lower virus (101.4±0.1 PFU of RSV) was recovered from lung tissue in the chimeric MV/RSV vaccine group than in the MVAIK control group with 104.6±0.2 PFU (p < 0.001) and no obvious inflammatory pathological finding was noted. The strategy of ectodomain replacement in the measles virus vector is expected to lead to the development of safe and effective vaccines for other enveloped viruses.

scholarly journals Nasopharyngeal gene expression, a novel approach to study the course of respiratory syncytial virus infection

2014 ◽  
Vol 45 (3) ◽  
pp. 718-725 ◽  
Author(s):  
Corné H. van den Kieboom ◽  
Inge M.L. Ahout ◽  
Aldert Zomer ◽  
Kim H. Brand ◽  
Ronald de Groot ◽  
...  
Keyword(s):  
Gene Expression ◽  
Respiratory Syncytial Virus ◽  
Respiratory Tract ◽  
Pathogen Detection ◽  
Severe Disease ◽  
Host Gene ◽  
Host Gene Expression ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections

Respiratory syncytial virus (RSV) causes mild infections in the vast majority of children. However, in some cases, it causes severe disease, such as bronchiolitis and pneumonia. Development of severe RSV infection is determined by the host response. Therefore, the main aim of this study was to identify biomarkers associated with severe RSV infection.To identify biomarkers, nasopharyngeal gene expression was profiled by microarray studies, resulting in the selection of five genes: ubiquitin D, tetraspanin 8, mucin 13, β-microseminoprotein and chemokine ligand 7.These genes were validated by real-time quantitative PCR in an independent validation cohort, which confirmed significant differences in gene expression between mildly and severely infected and between recovery and acute patients.Nasopharyngeal aspirate samples are regularly taken when a viral respiratory tract infection is suspected. In this article, we describe a method to discriminate between mild and severe RSV infection based on differential host gene expression. The combination of pathogen detection and host gene expression analysis in nasopharyngeal aspirates will significantly improve the diagnosis and prognosis of respiratory tract infections.

scholarly journals Structural basis for human respiratory syncytial virus NS1-mediated modulation of host responses

2017 ◽  
Vol 2 (9) ◽  
Author(s):  
Srirupa Chatterjee ◽  
Priya Luthra ◽  
Ekaterina Esaulova ◽  
Eugene Agapov ◽  
Benjamin C. Yen ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Human Respiratory Syncytial Virus ◽  
Host Responses ◽  
Structural Basis ◽  
Syncytial Virus

scholarly journals Structural basis for IFN antagonism by human respiratory syncytial virus nonstructural protein 2

2021 ◽  
Vol 118 (10) ◽  
pp. e2020587118
Author(s):  
Jingjing Pei ◽  
Nicole D. Wagner ◽  
Angela J. Zou ◽  
Srirupa Chatterjee ◽  
Dominika Borek ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Nonstructural Protein ◽  
Human Respiratory Syncytial Virus ◽  
Host Responses ◽  
Structural Basis ◽  
Downstream Signaling ◽  
Nonstructural Protein 2 ◽  
Syncytial Virus

Human respiratory syncytial virus (RSV) nonstructural protein 2 (NS2) inhibits host interferon (IFN) responses stimulated by RSV infection by targeting early steps in the IFN-signaling pathway. But the molecular mechanisms related to how NS2 regulates these processes remain incompletely understood. To address this gap, here we solved the X-ray crystal structure of NS2. This structure revealed a unique fold that is distinct from other known viral IFN antagonists, including RSV NS1. We also show that NS2 directly interacts with an inactive conformation of the RIG-I–like receptors (RLRs) RIG-I and MDA5. NS2 binding prevents RLR ubiquitination, a process critical for prolonged activation of downstream signaling. Structural analysis, including by hydrogen-deuterium exchange coupled to mass spectrometry, revealed that the N terminus of NS2 is essential for binding to the RIG-I caspase activation and recruitment domains. N-terminal mutations significantly diminish RIG-I interactions and result in increased IFNβ messenger RNA levels. Collectively, our studies uncover a previously unappreciated regulatory mechanism by which NS2 further modulates host responses and define an approach for targeting host responses.

Evidence for Both Respiratory Syncytial Virus and Measles Virus Antigens in the Osteoclasts of Patients with Paget??s Disease of Bone

1984 ◽  
Vol &NA; (183) ◽  
pp. 303???311 ◽  
Author(s):  
BARBARA G. MILLS ◽  
FREDERICK R. SINGER ◽  
LESLIE P. WEINER ◽  
STEPHEN C. SUFFIN ◽  
ELVIRA STABILE ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Measles Virus ◽  
Virus Antigens ◽  
Syncytial Virus

scholarly journals Mutation of Respiratory Syncytial Virus G Protein’s CX3C Motif Attenuates Infection in Cotton Rats and Primary Human Airway Epithelial Cells

Vaccines ◽  
2019 ◽  
Vol 7 (3) ◽  
pp. 69 ◽  
Author(s):  
Binh Ha ◽  
Tatiana Chirkova ◽  
Marina S. Boukhvalova ◽  
He Ying Sun ◽  
Edward E. Walsh ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Host Responses ◽  
Airway Epithelial ◽  
Live Virus ◽  
Human Airway ◽  
Cotton Rats ◽  
Syncytial Virus ◽  
Human Airway Epithelial Cells

Despite being a high priority for vaccine development, no vaccine is yet available for respiratory syncytial virus (RSV). A live virus vaccine is the primary type of vaccine being developed for young children. In this report, we describe our studies of infected cotton rats and primary human airway epithelial cells (pHAECs) using an RSV r19F with a mutation in the CX3C chemokine motif in the RSV G protein (CX4C). Through this CX3C motif, RSV binds to the corresponding chemokine receptor, CX3CR1, and this binding contributes to RSV infection of pHAECs and virus induced host responses that contribute to disease. In both the cotton rat and pHAECs, the CX4C mutation decreased virus replication and disease and/or host responses to infection. Thus, this mutation, or other mutations that block binding to CX3CR1, has the potential to improve a live attenuated RSV vaccine by attenuating both infection and disease pathogenesis.

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