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Review
. 2012 Jun;2(3):287-93.
doi: 10.1016/j.coviro.2012.03.008. Epub 2012 Apr 27.

Pathogenesis of rhinovirus infection

Affiliations
Review

Pathogenesis of rhinovirus infection

Joshua L Kennedy et al. Curr Opin Virol. 2012 Jun.

Abstract

Since its discovery in 1956, rhinovirus (RV) has been recognized as the most important virus producing the common cold syndrome. Despite its ubiquity, little is known concerning the pathogenesis of RV infections, and some of the research in this area has led to contradictions regarding the molecular and cellular mechanisms of RV-induced illness. In this article, we discuss the pathogenesis of this virus as it relates to RV-induced illness in the upper and lower airway, an issue of considerable interest in view of the minimal cytopathology associated with RV infection. We endeavor to explain why many infected individuals exhibit minimal symptoms or remain asymptomatic, while others, especially those with asthma, may have severe, even life-threatening, complications (sequelae). Finally, we discuss the immune responses to RV in the normal and asthmatic host focusing on RV infection and epithelial barrier integrity and maintenance as well as the impact of the innate and adaptive immune responses to RV on epithelial function.

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Figures

Figure 1
Figure 1
(A) Rhinovirus is a non-enveloped, spherical virus composed of a protein shell surrounding the naked RNA genome. The protein capsid consists of 4 polypeptides, viral capsid protein 1 (VP1), VP2, VP3, and VP4, in an icosahedral formation. (B) A hydrophobic pocket or “canyon” exists within VP1, which is the likely point of contact for ICAM-1 [4, 64, 65]. VP4 is located on the internal surface of the virus and is important in assembly of the virus during replication and infection of new cells [66].

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