Etiology of the common cold: Modulating factors

Abstract

The development of a “cold-like illness” (CLI) usually requires infection with an upper respiratory virus such as rhinovirus, influenza virus, respiratory syncytial virus, parainfuluenza virus, coronavirus or adenovirus, among others, and the development of sufficient signs, symptoms and pathophysiologies to qualify as being ill based on personal and cultural definitions. A viral upper respiratory tract infection (vURTI) in the absence of overt illness (subclinical vURTI) will not be made manifest to the individual or to observers and, therefore, will not be diagnosed as a CLI. The degree of illness occurring during a vURTI is directly related to the extent of provoked inflammation, which in turn depends on the engagement of antiviral defense systems. Thus, risk factors for CLI can modulate either the vURTI risk by affecting virus exposure and/or susceptibility to infection, or the CLI risk given a vURTI by affecting immunocompetence, the provoked inflammation and/or the interpretation of ilness as a CLI. In this chapter, we review published studies for evidence of CLI risk-modulating factors and report that climate, crowding and perhaps female gender can affect the probability of exposure to vURTI viruses, that extant immunological factors and age can affect the probability of virus infection given exposure, that stress levels (moderated by social environment), health practices (exercise, tobacco and alcohol consumption, sleep efficiency) and genetics contribute to CLI risk most probably by modulating the immune-inflammatory response to infection, and that other factors such as pollution, home environment and certain personality traits affect CLI risk by biasing illness interpretation for a given set of symptoms and signs.