Intranasal treatment with a novel immunomodulator mediates innate immune protection against lethal pneumonia virus of mice

Martinez, Elisa C.; Garg, Ravendra; Shrivastava, Priyanka; Gomis, Susantha; Hurk, Sylvia van Drunen Littel‐van den

doi:10.1016/j.antiviral.2016.10.008

Cited by 8 publications

(2 citation statements)

References 105 publications

(283 reference statements)

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“…Human respiratory syncytial virus vaccine development studies have been made on this model (Maunder et al., 2015; Martinez et al., 2016) including a model of FI-PVM enhanced respiratory disease, mediated by a Th2-biased response and eosinophil infiltration in lung (Percopo et al., 2009). Most recently, a replication deficient recombinant human adenovirus serotype 5 expressing the M or N protein of PVM pathogenic strain J3666, provided protection in mice, mediated mainly by CD8 + T cells (Maunder et al., 2015).…”

Section: Natural Host Pneumovirus Infectionsmentioning

confidence: 99%

Current Animal Models for Understanding the Pathology Caused by the Respiratory Syncytial Virus

et al. 2019

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The human respiratory syncytial virus (hRSV) is the main etiologic agent of severe lower respiratory tract infections that affect young children throughout the world, associated with significant morbidity and mortality, becoming a serious public health problem globally. Up to date, no licensed vaccines are available to prevent severe hRSV-induced disease, and the generation of safe-effective vaccines has been a challenging task, requiring constant biomedical research aimed to overcome this ailment. Among the difficulties presented by the study of this pathogen, it arises the fact that there is no single animal model that resembles all aspects of the human pathology, which is due to the specificity that this pathogen has for the human host. Thus, for the study of hRSV, different animal models might be employed, depending on the goal of the study. Of all the existing models, the murine model has been the most frequent model of choice for biomedical studies worldwide and has been of great importance at contributing to the development and understanding of vaccines and therapies against hRSV. The most notable use of the murine model is that it is very useful as a first approach in the development of vaccines or therapies such as monoclonal antibodies, suggesting in this way the direction that research could have in other preclinical models that have higher maintenance costs and more complex requirements in its management. However, several additional different models for studying hRSV, such as other rodents, mustelids, ruminants, and non-human primates, have been explored, offering advantages over the murine model. In this review, we discuss the various applications of animal models to the study of hRSV-induced disease and the advantages and disadvantages of each model, highlighting the potential of each model to elucidate different features of the pathology caused by the hRSV infection.

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Section: Natural Host Pneumovirus Infectionsmentioning

confidence: 99%

Current Animal Models for Understanding the Pathology Caused by the Respiratory Syncytial Virus

et al. 2019

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“…Interleukin-6 (IL-6) limits the severity of influenza A virus infection in mice, while it exacerbates disease in PVMinfected mice (26)(27)(28). Multiple mechanisms reduce the severity of both PR8 and PVM infections, including mucin production and inhibition of inflammatory responses (29)(30)(31)(32)(33)(34)(35). Based on these complex differences in immunity to infection with PR8 and PVM, we used a global gene expression approach combined with flow cytometry to evaluate potential mechanisms whereby coinfection with RV reduces the severity of PR8 and PVM.…”

Section: Introductionmentioning

confidence: 99%

Rhinovirus reduces the severity of subsequent respiratory viral infections by interferon-dependent and -independent mechanisms

Leuven

González

Ijezie

et al. 2020

Preprint

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Coinfection by unrelated viruses in the respiratory tract is common and can result in changes in disease severity compared to infection by individual virus strains. We have previously shown that inoculation of mice with rhinovirus (RV) two days prior to inoculation with a lethal dose of influenza A virus (PR8), provides complete protection against mortality. In this study, we extend that finding to a second lethal respiratory virus, pneumonia virus of mice (PVM) and characterize the differences in inflammatory responses and host gene expression in single virus infected vs. coinfected mice. RV prevented mortality and weight loss associated with PVM infection, suggesting that RV-mediated protection is more effective against PVM than PR8. Major changes in host gene expression upon PVM infection were delayed compared to PR8, which likely provides a larger time frame for RV-induced gene expression to alter the course of disease. Overall, RV induced earlier recruitment of inflammatory cells, while these populations were reduced at later times in coinfected mice. Findings common to both coinfection conditions included upregulated expression of mucin-associated genes in RV/PR8 and RV/PVM compared to mock/PR8 and mock/PVM infected mice and dampening of inflammation-related genes late during coinfection. These findings, combined with differences in virus replication levels and disease severity, suggest that the suppression of inflammation in RV/PVM coinfected mice may be due to early suppression of viral replication, while in RV/PR8 coinfected mice may be due to a direct suppression of inflammation. Thus, a mild upper respiratory viral infection can reduce the severity of a subsequent severe viral infection in the lungs through virus-dependent mechanisms.

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Innate immune protection from pneumonia virus of mice induced by a novel immunomodulator is prolonged by dual treatment and mediated by macrophages

Martinez¹,

Garg

Hurk

2019

Antiviral Research

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Intranasal treatment with a novel immunomodulator mediates innate immune protection against lethal pneumonia virus of mice

Cited by 8 publications

References 105 publications

Current Animal Models for Understanding the Pathology Caused by the Respiratory Syncytial Virus

Current Animal Models for Understanding the Pathology Caused by the Respiratory Syncytial Virus

Rhinovirus reduces the severity of subsequent respiratory viral infections by interferon-dependent and -independent mechanisms

Innate immune protection from pneumonia virus of mice induced by a novel immunomodulator is prolonged by dual treatment and mediated by macrophages

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