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Are rhinoviruses implicated in the pathogenesis of sinusitis and chronic rhinosinusitis exacerbations? A
Usmaan Basharat1, Mazen M Aiche1, Marianne M Kim1
1Department of Otolaryngology-Head and Neck Surgery, University of Arizona College of Medicine, Tucson, AZ.
Background:
Rhinovirus (RV) infections are the most common cause of viral upper respiratory infections (URIs), and in the majority of persons they are self-limiting. However, in others, viral URIs can progress to bacterial sinusitis and induce chronic rhinosinusitis (CRS) exacerbations.
Methods:
We conducted a comprehensive Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) review through April 2018 based on MEDLINE, EMBASE, Web of Science-Science Citation Index (SCI), and Conference Proceedings Citation Index- Science (CPCI-S) using keywords: RV, respiratory virus, sinusitis, and airway epithelial cells. The goal of this systematic review was to: (1) determine the prevalence between RV and CRS, (2) study the changes that occur after experimental RV inoculation, (3) investigate the pathophysiologic mechanisms by which RV induces sinonasal inflammation, and (4) explore the treatment options available for RV-associated sinusitis. Data regarding study design, research question, intervention, subjects, outcomes, and biases was extracted.
Results:
The initial search yielded 2395 unique abstracts, of which 614 were selected for full-text review; 147 were included in the final review. We determined that (1) the prevalence of RV infections is increased in those with CRS, (2) humans challenged in vivo with RV secrete local inflammatory mediators with radiographic mucosal thickening, (3) RV species RV-A and RV-C challenges in vitro to sinonasal epithelia produce robust cytokine responses and differential gene changes, and (4) no current therapies have produced consistent and significant resolution of disease.
Conclusion:
RV infections are common in persons with CRS, and incite inflammatory reactions that may result in CRS exacerbations and progression of disease. Further studies assessing RV species, and the host-virome response are required to develop new strategies targeting RV-induced CRS.
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