scholarly journals Structural and Nonstructural Viral Proteins Are Targets of T-Helper Immune Response against Human Respiratory Syncytial Virus

2016 ◽  
Vol 15 (6) ◽  
pp. 2141-2151 ◽  
Author(s):  
Elena Lorente ◽  
Alejandro Barriga ◽  
Eilon Barnea ◽  
Carmen Mir ◽  
John A. Gebe ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Viral Proteins ◽  
Human Respiratory Syncytial Virus ◽  
T Helper ◽  
Syncytial Virus

scholarly journals siRNA-Mediated Simultaneous Regulation of the Cellular Innate Immune Response and Human Respiratory Syncytial Virus Replication

Biomolecules ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. 165 ◽  
Author(s):  
María Martín-Vicente ◽  
Salvador Resino ◽  
Isidoro Martínez
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Virus Replication ◽  
Innate Immune Response ◽  
Human Respiratory Syncytial Virus ◽  
Innate Immune ◽  
Viral Fusion ◽  
Small Interfering Rnas ◽  
Syncytial Virus ◽  
Nucleoprotein N

Human respiratory syncytial virus (HRSV) infection is a common cause of severe lower respiratory tract diseases such as bronchiolitis and pneumonia. Both virus replication and the associated inflammatory immune response are believed to be behind these pathologies. So far, no vaccine or effective treatment is available for this viral infection. With the aim of finding new strategies to counteract HRSV replication and modulate the immune response, specific small interfering RNAs (siRNAs) were generated targeting the mRNA coding for the viral fusion (F) protein or nucleoprotein (N), or for two proteins involved in intracellular immune signaling, which are named tripartite motif-containing protein 25 (TRIM25) and retinoic acid-inducible gene-I (RIG-I). Furthermore, two additional bispecific siRNAs were designed that silenced F and TRIM25 (TRIM25/HRSV-F) or N and RIG-I (RIG-I/HRSV-N) simultaneously. All siRNAs targeting N or F, but not those silencing TRIM25 or RIG-I alone, significantly reduced viral titers. However, while siRNAs targeting F inhibited only the expression of the F mRNA and protein, the siRNAs targeting N led to a general inhibition of viral mRNA and protein expression. The N-targeting siRNAs also induced a drastic decrease in the expression of genes of the innate immune response. These results show that both virus replication and the early innate immune response can be regulated by targeting distinct viral products with siRNAs, which may be related to the different role of each protein in the life cycle of the virus.

Platelets Modulate Innate Immune Response Against Human Respiratory Syncytial Virus In Vitro

2017 ◽  
Vol 30 (8) ◽  
pp. 576-581 ◽  
Author(s):  
Vesla I. Kullaya ◽  
Quirijn de Mast ◽  
Andre van der Ven ◽  
Hicham elMoussaoui ◽  
Gibson Kibiki ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Innate Immune Response ◽  
Human Respiratory Syncytial Virus ◽  
Innate Immune ◽  
Syncytial Virus

scholarly journals Requirements for Human Respiratory Syncytial Virus Glycoproteins in Assembly and Egress from Infected Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Melissa Batonick ◽  
Gail W. Wertz
Keyword(s):  
Plasma Membrane ◽  
Respiratory Syncytial Virus ◽  
G Proteins ◽  
Matrix Protein ◽  
Protein Localization ◽  
Viral Proteins ◽  
Human Respiratory Syncytial Virus ◽  
The Other ◽  
Infected Cells ◽  
Syncytial Virus

Human respiratory syncytial virus (HRSV) is an enveloped RNA virus that assembles and buds from the plasma membrane of infected cells. The ribonucleoprotein complex (RNP) must associate with the viral matrix protein and glycoproteins to form newly infectious particles prior to budding. The viral proteins involved in HRSV assembly and egress are mostly unexplored. We investigated whether the glycoproteins of HRSV were involved in the late stages of viral replication by utilizing recombinant viruses where each individual glycoprotein gene was deleted and replaced with a reporter gene to maintain wild-type levels of gene expression. These engineered viruses allowed us to study the roles of the glycoproteins in assembly and budding in the context of infectious virus. Microscopy data showed that the F glycoprotein was involved in the localization of the glycoproteins with the other viral proteins at the plasma membrane. Biochemical analyses showed that deletion of the F and G proteins affected incorporation of the other viral proteins into budded virions. However, efficient viral release was unaffected by the deletion of any of the glycoproteins individually or in concert. These studies attribute a novel role to the F and G proteins in viral protein localization and assembly.

scholarly journals Evidence for an intranasal immune response to human respiratory syncytial virus infection in cynomolgus macaques

2015 ◽  
Vol 96 (4) ◽  
pp. 782-792 ◽  
Author(s):  
Clément Grandin ◽  
Marianne Lucas-Hourani ◽  
Marine Clavel ◽  
Fabrice Taborik ◽  
Astrid Vabret ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Virus Infection ◽  
Respiratory Syncytial Virus Infection ◽  
Human Respiratory Syncytial Virus ◽  
Cynomolgus Macaques ◽  
Syncytial Virus

scholarly journals The Viral Transcription Group Determines the HLA Class I Cellular Immune Response Against Human Respiratory Syncytial Virus

2015 ◽  
Vol 14 (4) ◽  
pp. 893-904 ◽  
Author(s):  
Carolina Johnstone ◽  
Elena Lorente ◽  
Alejandro Barriga ◽  
Eilon Barnea ◽  
Susana Infantes ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Cellular Immune Response ◽  
Hla Class I ◽  
Human Respiratory Syncytial Virus ◽  
Class I ◽  
Viral Transcription ◽  
Syncytial Virus ◽  
Cellular Immune

scholarly journals Downregulation of A20 Expression Increases the Immune Response and Apoptosis and Reduces Virus Production in Cells Infected by the Human Respiratory Syncytial Virus

Vaccines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 100
Author(s):  
María Martín-Vicente ◽  
Rubén González-Sanz ◽  
Isabel Cuesta ◽  
Sara Monzón ◽  
Salvador Resino ◽  
...  
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Virus Production ◽  
Antiviral Response ◽  
Human Respiratory Syncytial Virus ◽  
Negative Regulator ◽  
Infected Cells ◽  
Syncytial Virus ◽  
Tract Infections ◽  
The Impact

Human respiratory syncytial virus (HRSV) causes severe lower respiratory tract infections in infants, the elderly, and immunocompromised adults. Regulation of the immune response against HRSV is crucial to limiting virus replication and immunopathology. The A20/TNFAIP3 protein is a negative regulator of nuclear factor kappa B (NF-κB) and interferon regulatory factors 3/7 (IRF3/7), which are key transcription factors involved in the inflammatory/antiviral response of epithelial cells to virus infection. Here, we investigated the impact of A20 downregulation or knockout on HRSV growth and the induction of the immune response in those cells. Cellular infections in which the expression of A20 was silenced by siRNAs or eliminated by gene knockout showed increased inflammatory/antiviral response and reduced virus production. Similar results were obtained when the expression of A20-interacting proteins, such as TAX1BP1 and ABIN1, was silenced. Additionally, downregulation of A20, TAX1BP1, and ABIN1 increased cell apoptosis in HRSV-infected cells. These results show that the downregulation of A20 expression might contribute in the control of HRSV infections by potentiating the early innate immune response and increasing apoptosis in infected cells.

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