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Epidemiology, clinical manifestations, and pathogenesis of rhinovirus infections

Diane E Pappas, MD, JD
Section Editors
Martin S Hirsch, MD
Morven S Edwards, MD
Deputy Editor
Jennifer Mitty, MD, MPH


Rhinovirus has long been known as an etiologic agent of colds, which are frequent but otherwise relatively minor and self-limited illnesses. Rhinovirus can also infect the lower respiratory tract and trigger asthma exacerbations in both adults and children, highlighting the fact that this viral pathogen causes greater morbidity than previously recognized [1].

This topic is devoted to the epidemiology, clinical manifestations, and pathogenesis of rhinovirus infections. More general discussions related to the "common cold" are found elsewhere. (See "The common cold in adults: Diagnosis and clinical features" and "The common cold in adults: Treatment and prevention".)


Rhinovirus is the etiologic agent of most common colds and is responsible for one-third to one-half of cases in adults annually [2,3]. More than 100 serotypes have been identified [1,4]. The average adult experiences two to three colds per year, while children average 8 to 12 colds per year [4]. Children are the major reservoir for rhinovirus [4,5].


Rhinovirus is a member of the picornavirus family [6]. It is a small (30 nanometer) single-stranded RNA virus, about the size of a ribosome [4,7]. The capsid has icosahedral symmetry and contains 60 copies each of the four rhinoviral polypeptides (eg, VP1 through VP4) [6]. The full genomes of 99 human rhinoviruses have been fully sequenced [8]. On comparing these sequences, there are highly conserved motifs that may serve as potential targets for antiviral drug development [9].

Most notable is the viral surface, which contains numerous canyons that surround the attachment site for host-cell receptors [6]. Over 90 percent of rhinoviruses use this site to attach to the intercellular adhesion molecule-1 (ICAM-1) receptor expressed on the surface of host cells [6]. Antibody neutralization occurs when IgG binds to the viral surface, which obstructs access of the host-cell receptor to the viral attachment site at the base of the canyon [6].

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Literature review current through: Sep 2017. | This topic last updated: Apr 04, 2016.
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