Pathogenesis of Major Respiratory Viral Infections

Shiva Mani^*
*Correspondence: Shiva Mani, Department Respiratory Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland, Email:

Introduction

In December 2019, a Coronavirus disease 2019 (COVID-19) outbreak occurred in Wuhan, Hubei Province, China. SARS-CoV-2 is a positive singlestranded enveloped RNA virus (ssRNA) of the Coronaviridae family's betacoronavirus genus. Following SARS-CoV-2 infection, a process of recognition by cytotoxic T lymphocytes occurs, resulting in the overproduction of a wide range of proinflammatory mediators, known as a "cytokine storm" (CS), an uncontrolled production of soluble inflammatory markers that, in turn, support an aberrant systemic inflammatory response, which appears to be the main cause of the clinical severity of respiratory infection, u (ARDS) [1].

Description

Mast cells and basophils appear to be involved in the development of CS; in fact, their activation would be able to determine the procoagulant state characteristic of this type of infection.The alarmin interleukin-33 (IL-33), which has traditionally been implicated in allergic and autoimmune diseases (such as rheumatoid arthritis, systemic sclerosis, atopic dermatitis, and food allergies), plays a particularly important role because it is involved in pro-inflammatory processes [2]. IL-33 initiates inflammatory pathways dependent on the myeloid differentiation factor 88 (MyD88) responses and exerts pleiotropic effects by binding to a receptor complex known as the accessory protein of the ST2 and IL-1 receptor, which is expressed on a variety of innate and adaptive immune cells [3].

As a down-regulation mechanism of IL-33, the soluble form of ST2 has been identified as a reliable biomarker of poor prognosis in cardiovascular disease, acute respiratory distress syndrome (ARDS), and other inflammatory conditions. Local activation of the IL-33/ST2 axis, for example, has been linked to a more severe disease progression in children with acute lower respiratory infection (ALRI), necessitating ventilatory support. Recently, a link between IL-33 and lung damage in pulmonary viral infections and chronic lung diseases has been discovered. Indeed, IL-33 has been shown to increase airway inflammation, mucus secretion, and Th2 cytokine synthesis in the lungs following respiratory infections such as influenza, RSV, and rhinovirus infection [4,5]. IL-33, on the other hand, can stimulate the activity of antiviral cytotoxic T cells as well as the production and release of antibodies.

Conclusion

Exposure to the SARS-CoV-2 peptide, like other respiratory virus infections, causes IL-33 expression, which correlates with T cell activation and lung disease severity. Although an increase in IL-33 levels is thought to be a predictor of severe COVID-19, its exact role at different stages of the disease remains unknown. However, the activation role of IL-33 on antiviral CD8 T cells is known, with the virus potentially being eliminated in long-term infections as a result. As a result, using monoclonal antibodies to target the IL-33-ST2 axis could be an effective strategy for controlling the COVID-19 pandemic. Anti-IL-33 antibodies not only reduce bronchial cytokine and chemokine secretion significantly, but they may also be useful in other chronic lung diseases (COPD, IPF), which are frequently characterised by a type-3 inflammatory profile characterised by high neutrophil counts. In this sense, blocking IL-33 could significantly reduce allergic inflammation, making it a promising alternative approach to treating asthma exacerbations caused by respiratory virus infection.

References

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