Fireside conference 11. Common cold.

Abstract

The accepted concept that cold symptoms are usually caused by destruction of the nasal epithelium by virus and that epithelial damage may led to secondary bacterial infection is not supported by this work. Although influenza and adenovirus may destroy the epithelium, no destruction of the nasal epithelium was detected either in vivo during natural or rhinovirus cold on in-vitro in nasal epithelial organ cultures. Infiltration of the nasal mucosa with neutrophils early in the cold does not indicate bacterial infection but may be a direct result of the viral infection. Purulent nasal secretions, which are common in uncomplicated colds, were not accompanied by discernible changes in the aerobic bacterial flora. The nasopharynx may be an important area for further exploration in the study of the pathogenesis of rhinovirus infection since it is a site to which mucus containing virus from the entire nasal mucosa is brought. A prominent feature of the posterior nasopharyngeal wall in both children and adults is a mass of mucosa-associated lymphoid tissue (adenoid or nasopharyngeal tonsils). Preliminary data has suggested that the epithelium overlying the lymphoid tissue expresses ICAM-1 receptors in the normal state, whereas the nasal epithelium does not. This is interesting since the majority of rhinovirus serotypes gain entrance to human cells by this receptor. Symptoms in a rhinovirus cold could result from release of inflammatory and/or neuromediators from the adenoid. Recently, Naclerio et al (8) have demonstrated that kinins and an increased number of neutrophils in nasal secretions correlate with occurrence of symptoms in volunteers with rhinovirus colds.