Respiratory Syncytial Virus Persistence in Macrophages Upregulates Fcgamma Receptors Expression

Gaona, Jorge; Santiago-Olivares, Carlos; Ortega, Enrique; Gómez, Beatrı́z

doi:10.3390/v6020624

Cited by 12 publications

(8 citation statements)

References 48 publications

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“…AMs can be infected acutely by hRSV, as indicated above [ 151 , 152 ]. Interestingly, infection can occur through the internalization of IC-hRSV via the Fc receptors [ 153 ].…”

Section: Differential Regulation Of the Innate Immune Response By mentioning

confidence: 99%

Innate Immune Components That Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections

Andrade

Pacheco

Gálvez

et al. 2020

Viruses

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The human respiratory syncytial virus (hRSV) and human Metapneumovirus (hMPV) are two of the leading etiological agents of acute lower respiratory tract infections, which constitute the main cause of mortality in infants. However, there are currently approved vaccines for neither hRSV nor hMPV. Moreover, despite the similarity between the pathology caused by both viruses, the immune response elicited by the host is different in each case. In this review, we discuss how dendritic cells, alveolar macrophages, neutrophils, eosinophils, natural killer cells, innate lymphoid cells, and the complement system regulate both pathogenesis and the resolution of hRSV and hMPV infections. The roles that these cells play during infections by either of these viruses will help us to better understand the illnesses they cause. We also discuss several controversial findings, relative to some of these innate immune components. To better understand the inflammation in the lungs, the role of the respiratory epithelium in the recruitment of innate immune cells is briefly discussed. Finally, we review the main prophylactic strategies and current vaccine candidates against both hRSV and hMPV.

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“…AMs can be infected acutely by hRSV, as indicated above [ 151 , 152 ]. Interestingly, infection can occur through the internalization of IC-hRSV via the Fc receptors [ 153 ].…”

Section: Differential Regulation Of the Innate Immune Response By mentioning

confidence: 99%

Innate Immune Components That Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections

Andrade

Pacheco

Gálvez

et al. 2020

Viruses

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“…MΦP passages from 72 to 87 were used in this study. Throughout the passages, the persistence of viral genome was monitored by detecting the mRNA of the gene N by conventional RT-PCR (Gaona et al, 2014). Extracellular viral infectivity titer was 1-2 × 10 2 TCID 50 /ml and no syncytia were observed (Sarmiento et al, 2002).…”

Section: Methodsmentioning

confidence: 99%

“…Total proteins were also extracted from A549 epithelial cells infected for the indicated time as a control (acute infection, A549A). Then, 50 μg of proteins were mixed with Laemmli sample buffer, boiled, separated by 12% SDS-PAGE, and transferred onto PVDF membranes (Amersham, USA) as previously described (Gaona et al, 2014). The commercial antibodies used were anti-NF-κB p65 and anti-NF-κB p100/p52 (Cell Signaling Technol-ogy, USA); anti-RelB, anti-c-Rel, anti-NF-κB p50 and anti-β tubulin (Santa Cruz Biotechnology, USA).…”

Section: Methodsmentioning

confidence: 99%

RSV infection in a macrophage-cell line activates the non-canonical NF-κB pathway and induces pro-inflammatory cytokine expression

Moral-Hernández¹,

Santiago-Olivares²,

Rivera-Toledo³

et al. 2018

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Respiratory syncytial virus (RSV) is a highly prevalent infectious agent that causes severe respiratory tract illnesses in infants and children worldwide. Children who have suffered severe RSV infections during infancy are prone to develop recurrent episodes of wheezing and asthma that may be associated with viral persistence. RSV infections in humans and animal models are characterized by extensive inflammatory responses. Epithelial cell lines acutely infected by RSV have shown activation of the NF-κB signaling through two independent pathways: the canonical pathway, mediated by RelA and p50 subunits, and the non-canonical pathway, mediated by the subunits RelB and p52. Herein, we investigated the state of activation of the canonical and non-canonical NF-κB signaling pathways in macrophages either acutely or persistently infected by RSV and examined the expression of pro-inflammatory mediators. Activation of NF-κB subunits was analyzed through Western blot assays using acutely RSV-infected epithelial cells as a control. The expression levels of two pro-inflammatory cytokines and a chemokine were determined by quantitative RT-PCR and through immunobead assays. The results showed that p52 was abundant during acute and persistent RSV infection, indicating that macrophages predominantly activate the non-canonical pathway. We also observed activation of IL-1β, TNF-α and CCL5/RANTES transcription, though at higher levels in persistently infected macrophages than in acutely infected macrophages. In contrast, the protein levels of these cytokines/chemokine did not correlate with their mRNA transcription, as quantitation displayed higher levels during acute infection than in persistent infection, suggesting post-transcriptional regulation by RSV persistence.

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“…The percentage of FITC-positive cells, as determined by flow cytometry (FACScan; Becton Dickinson, Mountain View, CA, USA) was reported. The expression of N gene mRNA was analyzed by using a primer pair to amplify a 1187-bp segment; as a control, mRNA of the GAPDH gene was determined with a primer pair to amplify a 260-bp segment, as previously described [ 38 ].…”

Section: Methodsmentioning

confidence: 99%

Respiratory Syncytial Virus Persistence in Murine Macrophages Impairs IFN-β Response but Not Synthesis

Rivera-Toledo

Torres-González

Gómez

2015

Viruses

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Type-I interferon (IFN-I) production is an early response to viral infection and pathogenic viruses have evolved multiple strategies to evade this cellular defense. Some viruses can establish and maintain persistent infections by altering the IFN-I signaling pathway. Here, we studied IFN-I synthesis and response in an in vitro model of persistent infection by respiratory syncytial virus (RSV) in a murine macrophage-like cell line. In this model, interferon regulatory factor 3 was constitutively active and located at nuclei of persistently infected cells, inducing expression of IFN-beta mRNA and protein. However, persistently infected macrophages did not respond in an autocrine manner to the secreted-IFN-beta or to recombinant-IFN-beta, since phosphorylated-STAT1 was not detected by western blot and transcription of the interferon-stimulated genes (ISGs) Mx1 and ISG56 was not induced. Treatment of non-infected macrophages with supernatants from persistently infected cells induced STAT1 phosphorylation and ISGs expression, mediated by the IFN-I present in the supernatants, because blocking the IFN-I receptor inhibited STAT1 phosphorylation. Results suggest that the lack of autocrine response to IFN-I by the host cell may be one mechanism for maintenance of RSV persistence. Furthermore, STAT1 phosphorylation and ISGs expression induced in non-infected cells by supernatants from persistently infected macrophages suggest that RSV persistence may trigger a proinflammatory phenotype in non-infected cells as part of the pathogenesis of RSV infection.

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Respiratory Syncytial Virus Persistence in Macrophages Upregulates Fcgamma Receptors Expression

Cited by 12 publications

References 48 publications

Innate Immune Components That Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections

Innate Immune Components That Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections

RSV infection in a macrophage-cell line activates the non-canonical NF-κB pathway and induces pro-inflammatory cytokine expression

Respiratory Syncytial Virus Persistence in Murine Macrophages Impairs IFN-β Response but Not Synthesis

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