RESUMEN
BACKGROUND: Acute exacerbations of chronic rhinosinusitis (AECRS) are thought to arise from common viral infections progressing to secondary bacterial infections. However, the pathophysiology of AECRS remains poorly understood due to a lack of prospective longitudinal studies. METHODS: We conducted a one-year prospective longitudinal study involving chronic rhinosinusitis (CRS) adults. At baseline, we assessed subjective symptom scores using a validated upper respiratory infection questionnaire (WURSS), sinonasal outcome testing scores (SNOT-22), and endoscopic scores (modified Lund-Kennedy score). Every 2 weeks, we contacted subjects to collect WURSS and SNOT-22 scores. If WURSS scores were ≥1 and SNOT-22 scores were ≥ 8.9 compared with baseline, subjects underwent an AECRS assessment. We identified rhinovirus (RV) incidence through viral nasal brushings at each visit and bacterial infection through bacterial swabs if mucus scores were ≥1. RESULTS: Thiry-five of 80 CRS subjects reported at least one AECRS episode during the year, predominantly occurring in the fall and winter seasons. RV infections were detected in 8 of 35 cases, bacterial infections in 17 of 35, and co-occurring infections in 7 of 35. All subjects with AECRS visits exhibited significantly higher endoscopic scores compared with baseline. Subjects with co-occurring RV and bacterial infections demonstrated higher disease severity compared with those with either RV or bacterial infection, or no infection. CONCLUSIONS: In a one-year prospective longitudinal study involving CRS adults, we identified significant risk factors for AECRS including seasonality and the presence of RV and bacterial infections. These data suggest a standard definition of AECRS and the need to target RV and bacterial infections if we are to help reduce disease severity.
RESUMEN
Viral infections are the most common cause of upper respiratory infections; they frequently infect adults once or twice and children 6 to 8 times annually. In most cases, these infections are self-limiting and resolve. However, many patients with chronic rhinosinusitis (CRS) relay that their initiating event began with an upper respiratory infection that progressed in both symptom severity and duration. Viruses bind to sinonasal epithelia through specific receptors, thereby entering cells and replicating within them. Viral infections stimulate interferon-mediated innate immune responses. Recent studies suggest that viral infections may also induce type 2 immune responses and stimulate the aberrant production of cytokines that can result in loss of barrier function, which is a hallmark in CRS. The main purpose of this review will be to highlight common viruses and their associated binding receptors and highlight pathophysiologic mechanisms associated with alterations in mucociliary clearance, epithelial barrier function, and dysfunctional immune responses that might lead to a further understanding of the pathogenesis of CRS.