Die Another Way: Interplay between Influenza A Virus, Inflammation and Cell Death

Laghlali, Gabriel; Lawlor, Kate E.; Tate, Michelle D.

doi:10.3390/v12040401

Cited by 46 publications

(56 citation statements)

References 156 publications

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“…The results obtained from mouse models and cell lines infected with IVs demonstrated the production of enhanced levels of ROS, together with an imbalance of antioxidant protection [44,45]. These models indicated the relevance of the redox homeostasis induced by IVs [46][47][48][49][50].…”

Section: Influenza Virus (Iv)mentioning

confidence: 75%

Redox control in the pathophysiology of influenza virus infection

et al. 2020

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Triggered in response to external and internal ligands in cells and animals, redox homeostasis is transmitted via signal molecules involved in defense redox mechanisms through networks of cell proliferation, differentiation, intracellular detoxification, bacterial infection, and immune reactions. Cellular oxidation is not necessarily harmful per se, but its effects depend on the balance between the peroxidation and antioxidation cascades, which can vary according to the stimulus and serve to maintain oxygen homeostasis. The reactive oxygen species (ROS) that are generated during influenza virus (IV) infection have critical effects on both the virus and host cells. In this review, we outline the link between viral infection and redox control using IV infection as an example. We discuss the current state of knowledge on the molecular relationship between cellular oxidation mediated by ROS accumulation and the diversity of IV infection. We also summarize the potential anti-IV agents available currently that act by targeting redox biology/pathophysiology.

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Section: Influenza Virus (Iv)mentioning

confidence: 75%

Redox control in the pathophysiology of influenza virus infection

et al. 2020

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“…The body's natural defense mechanism of inflammation which promotes cell repair and healing [107] was mimicked in our wdNHBE model, with the increased expression of proinflammatory cytokines and chemokines such as TNF, IL1B, IL6, CXCL8 and CXCL10. This suggests that wdNHBE cells recognize IAV and poly(I:C) through binding to pattern recognition receptors (PRRs) such as the Toll-like receptors (TLR3, TLR7, and TLR8), retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein-5 (MDA-5), triggering innate immune response signaling cascades as occurs in vivo [22,54,55,[108][109][110][111][112][113][114]. Antiviral, pro-and anti-inflammatory cytokines and chemokines are then upregulated in the host [27,56,115].…”

Section: Discussionmentioning

confidence: 99%

“…These outbreaks killed an estimated range of between 2.1 and 8.4 million people [18]. Highly pathogenic pandemic IAV strains, plus the avian H5N1 can cause massive viral pneumonia, multiple organ failure and death, due to hyperinflammation caused by the excessive production of cytokines and chemokines, or "cytokine storm" [19][20][21][22]. However, each year there are 1 billion cases of seasonal influenza worldwide and up to 645,000 deaths [23].…”

Section: Introductionmentioning

confidence: 99%

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Pharo

Williams

Boyd

et al. 2020

Viruses

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The respiratory Influenza A Viruses (IAVs) and emerging zoonotic viruses such as Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) pose a significant threat to human health. To accelerate our understanding of the host–pathogen response to respiratory viruses, the use of more complex in vitro systems such as normal human bronchial epithelial (NHBE) cell culture models has gained prominence as an alternative to animal models. NHBE cells were differentiated under air-liquid interface (ALI) conditions to form an in vitro pseudostratified epithelium. The responses of well-differentiated (wd) NHBE cells were examined following infection with the 2009 pandemic Influenza A/H1N1pdm09 strain or following challenge with the dsRNA mimic, poly(I:C). At 30 h postinfection with H1N1pdm09, the integrity of the airway epithelium was severely impaired and apical junction complex damage was exhibited by the disassembly of zona occludens-1 (ZO-1) from the cell cytoskeleton. wdNHBE cells produced an innate immune response to IAV-infection with increased transcription of pro- and anti-inflammatory cytokines and chemokines and the antiviral viperin but reduced expression of the mucin-encoding MUC5B, which may impair mucociliary clearance. Poly(I:C) produced similar responses to IAV, with the exception of MUC5B expression which was more than 3-fold higher than for control cells. This study demonstrates that wdNHBE cells are an appropriate ex-vivo model system to investigate the pathogenesis of respiratory viruses.

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“…An inflammatory response follows with the recruitment of neutrophils, macrophages, and other immune cells. While this response is important for viral clearance, it also plays a role in various disease manifestations [12].…”

Section: Introductionmentioning

confidence: 99%

“…Pleural thickening is a process where the pleura is thickened, usually with scar tissue [47], and it could be caused by acute inflammation of the pleura. The subpleural line is a thin curvilinear opacity of about 1-3 mm in thickness found close to the pleural surface [12]. It is located in the subpleural region and distributed parallel to the pleural surface.…”

mentioning

confidence: 99%

Chest Computed Tomography Findings in COVID-19 and Influenza: A Narrative Review

Onigbinde

Ojo

Fleary

et al. 2020

BioMed Research International

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Objective. The COVID-19 pandemic and annual influenza epidemic are responsible for thousands of deaths globally. With a similarity in clinical as well as laboratory findings, there is a need to differentiate these two conditions on chest CT scan. This paper attempts to use existing literature to draw out differences in chest CT findings in COVID-19 and influenza. Methods. A search was conducted using PubMed. 17 original studies on chest CT findings in COVID-19 and influenza were identified for full-text review and data analysis. Findings. COVID-19 and influenza share similar chest CT findings. The differences found show that COVID-19 ground-glass opacities are usually peripherally located with the lower lobes being commonly involved, while influenza has a central, peripheral, or random distribution usually affecting the five lobes. Vascular engorgement, pleural thickening, and subpleural lines were reported in COVID-19 patients. In contrast, pneumomediastinum and pneumothorax were reported only in studies on influenza. Conclusion and Relevance. COVID-19 and influenza have overlapping chest CT features with few differences which can assist in telling apart the two pathologies. Additional studies are needed to further define the differences and degree between COVID-19 and influenza.

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Die Another Way: Interplay between Influenza A Virus, Inflammation and Cell Death

Cited by 46 publications

References 156 publications

Redox control in the pathophysiology of influenza virus infection

Redox control in the pathophysiology of influenza virus infection

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

Chest Computed Tomography Findings in COVID-19 and Influenza: A Narrative Review

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