Viral infections and chronic rhinosinusitis

Abstract

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.

Keywords: Chronic rhinosinusitis; airway epithelium; barrier function; genetics; innate immunity; upper respiratory tract infection; virus.

Figure 1.. Antiviral immune response.

Virus binds to sinonasal airway epithelial cells (1), and replicates within the cell. This triggers antiviral interferon responses (2) and cytokine induction that rapidly increases and can transiently induce loss of epithelial barrier function to allow for cell-mediated viral killing (3). These host immune responses than resolve to a homeostatic baseline (4).

Figure 2.. Aberrant antiviral inflammatory response.

Viruses bind to sinonasal airway epithelial cells and can have an increased viral load either due to increased virulence of the virus subtype or enhanced viral binding (1). A delayed interferon response (2) results in increased viral replication and a prolonged interferon response can induce type 2 immune responses characterized by eosinophil and basophil activation (3). The release of interferon and type 2 mediated cytokines can increase epithelial barrier permeability and damage, resulting in a prolonged loss of barrier function (4) and chronic inflammation (5).