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Title
Viruses as precipitants of asthma symptoms. II. Physiology and mechanisms.
AuthorBardin PG; Johnston SL; Pattemore PK
AddressImmunopharmacology Group, Southampton General Hospital.
Source
Clin Exp Allergy,
22:
9, 1992 Sep,
809-22
AbstractThe upper and lower airways have complimentary roles in the ultimate object of supplying the body
with oxygen whilst removing waste products of metabolism. Pathology in one area may trigger a response
in another, the physiology of which, in the case of virus-induced asthma exacerbations remains poorly
characterized. Viral infection of the upper airways by common cold viruses frequently triggers a response
in the lower airways leading to prolonged morbidity, especially in subjects with significant pre-existing
airway disease. The induction or amplification of BHR may be an important mechanism whereby asthmatic
symptoms are produced although the cellular and tissue events or reflex mechanisms activated by viral
illnesses and underlying BHR changes are poorly defined and may be dependent on the type and the severity
of infection. Children and asthmatics tend to develop frequent colds setting in motion a sequence of
events culminating in airway obstruction and symptoms of wheezing, coughing and chest tightness. This
may reflect independent inflammatory changes caused by a simply additive effect of viral damage to the
mucosa superimposed upon pre-existing allergic inflammation (Fig. 1). Few if any symptoms will develop
in normal subjects with a mild cold whereas significant symptoms may ensue if the cold is severe and
induces marked lower airway swelling, secretions and smooth muscle contraction; pathology to which children
who have small calibre airways may be particularly susceptible. In asthmatics even a mild cold frequently
induces exacerbation of symptoms, while serious life-threatening asthma attacks may occur associated
with a severe cold. Some studies have suggested that this effect is not only additive but also synergistic
and brought about by release of the mediators already present in increased quantities, the induction
of IgE synthesis, or by the potentiation of neural and epithelial damage. The combined effect of both
asthma and viruses may thus be amplified and result in a sustained and refractory period of airway
obstruction, severe symptoms and unstable asthma. As most hospital admissions for asthma occur over the
winter months and soon after the start of the school terms [115], spread of viruses through the community
to susceptible individuals may be the single most important cause of sustained exacerbations of asthma.
Definition of the pathological and physiological mechanisms involved will lead to better understanding
and may thus provide a basis for prevention and the development of effective forms of treatment for virus-induced
asthma.