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Pathogenesis of Major Respiratory Viral Infections

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href='https://www.hilarispublisher.com/author/shiva-mani-18057' title='Shiva Mani' style='color:#555; border-bottom:1px dotted #CCC;'>Shiva Mani</a><sup><a href='#Shiva_Mani'>*</a></sup> <!-- <div>&nbsp;</div> --> <br/> <div class="mb-2"></div> <a id="Shiva_Mani"></a> <strong><sup>*</sup>Correspondence:</strong> Shiva Mani, Department Respiratory Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland, <strong>Email:</strong> <i class='fa fa-envelope' aria-hidden='true' title='Shivamani999@gmail.com'></i> <div class="clearfix mt-2 mb-3"> <div class="float-left"><a href="#ai" class="btn_cu_color" id="changeicon" data-toggle="collapse" data-target="#au_info"><strong>Author information</strong> <span><i class="fas fa-plus fa-sm"></i></span></a></div> <div class="float-right"> <nav class="nav a-mx-2 med_pdf"> <a href="https://www.hilarispublisher.com/open-access/pathogenesis-of-major-respiratory-viral-infections.pdf" title="View PDF" class="card-link border-bottom-2 yellow-900 border-yellow-900" style="position: relative; right: 5px;"><i class="fas fa-file-pdf"></i> View PDF</a> <a href="https://www.hilarispublisher.com/pdfdownload.php?download=open-access/pathogenesis-of-major-respiratory-viral-infections.pdf&aid=87224" title="Download PDF" class="card-link border-bottom-2 border-blue-900"><i class="fas fa-download"></i> Download PDF</a> </nav> </div> </div> <div id="au_info" class="collapse"> <div class="card bg-light mb-3"> <div class="card-body p-2 pb-0"> Department Respiratory Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland<br> <!-- <div>&nbsp;</div> --> <p> <strong>Received: </strong>05-Mar-2022, Manuscript No. jcrdc-22-58576; <strong>Editor assigned: </strong>07-Mar-2022, Pre QC No. P-58576; <strong>Reviewed: </strong>10-Mar-2022, QC No. Q-58576; <strong>Revised: </strong>15-Mar-2022, Manuscript No. R-58576; <strong>Published:</strong> 20-Mar-2022 , <strong>DOI:</strong> 10.4172/ jcrdc.2022.08.203 <br> <strong>Citation:</strong> Mani, Shiva. “Pathogenesis of Major Respiratory Viral Infections.” Clin Respir Dis Care 8 (2022): 203. DOI: 10.4172/ jcrdc.2022.08.203 <br> <strong>Copyright:</strong> © 2022 Mani S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. </p> </div> </div> </div> <h4>Introduction</h4> <p>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 &quot;cytokine storm&quot; (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) [<a href="#1" title="1">1</a>].</p> <h4>Description</h4> <p>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 [<a href="#2" title="2">2</a>]. 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 [<a href="#3" title="3">3</a>].</p> <p>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 [<a href="#4" title="4">4</a>,<a href="#5" title="5">5</a>]. IL-33, on the other hand, can stimulate the activity of antiviral cytotoxic T cells as well as the production and release of antibodies.</p> <h4>Conclusion</h4> <p>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.</p> <h4>References</h4> <ol> <li><a name="1" id="1"></a>Cavalcanti, Alexandre Biasi, &Eacute;rica Aranha Suzumura, Ligia Nasi Laranjeira, and Denise de Moraes Paisani, et al. <a href="https://jamanetwork.com/journals/jama/article-abstract/2654894" target="_blank">&ldquo;Effect of lung recruitment and titrated positive end-expiratory pressure (PEEP) vs low PEEP on mortality in patients with acute respiratory distress syndrome: A randomized clinical trial.&rdquo;</a> <em>JAMA</em> 318 (2017): 1335&ndash;1345.</li> <p align="right"><a 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