Amplified rhinovirus colds in atopic subjects. 1994

P G Bardin, and D J Fraenkel, and G Sanderson, and M Dorward, and L C Lau, and S L Johnston, and S T Holgate
Immunopharmacology Group, University Medicine, Southampton General Hospital, UK.

Evidence suggests that atopic individuals may be predisposed to more severe rhinoviral colds coupled to a worsening of existing airway disease than those with asthma. The role of atopy and IgE levels, as well as their relationship to clinical disease expression have not been defined. We hypothesized that an allergic diathesis modulates rhinoviral colds and have initiated studies of normal, atopic and asthmatic subjects employing experimental rhinoviral infection, with measurements of symptom scores, viral shedding and cultures, albumin in nasal washes and serological responses. Twenty-two subjects (11 normal, 5 atopic, 6 atopic and asthmatic) participated and were inoculated with human rhinovirus serotype 16 (HRV 16). Measurements of neutralizing antibody and viral culture were performed at screening, pre-inoculation, during the cold and at 8-10 weeks convalescence. Daily symptoms were noted, nasal washes done, IgE measured and atopy was diagnosed by skin tests. Seventeen volunteers developed clinical colds as assessed by symptom scores, virus shedding was demonstrated (with positive culture) in all subjects and a fourfold or higher seroconversion occurred in 11/22. Neutralizing HRV antibody developed unexpectedly in 10 subjects between screening and inoculation and the presence of absence of this pre-inoculation antibody determined subsequent severity of colds in normal but not in atopic subjects. Atopic antibody positive individuals developed severe clinical colds that were independent of preinoculation antibody in contrast to normal subjects who developed mild colds in the presence of a neutralizing antibody (P = 0.01). Both atopic and normal antibody negative subjects developed severe colds.(ABSTRACT TRUNCATED AT 250 WORDS)

UI MeSH Term Description Entries
D006969 Hypersensitivity, Immediate Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability. Atopic Hypersensitivity,Hypersensitivity, Atopic,Hypersensitivity, Type I,IgE-Mediated Hypersensitivity,Type I Hypersensitivity,Atopic Hypersensitivities,Hypersensitivities, Atopic,Hypersensitivities, IgE-Mediated,Hypersensitivities, Immediate,Hypersensitivities, Type I,Hypersensitivity, IgE-Mediated,IgE Mediated Hypersensitivity,IgE-Mediated Hypersensitivities,Immediate Hypersensitivities,Immediate Hypersensitivity,Type I Hypersensitivities
D007073 Immunoglobulin E An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE). IgE
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D003139 Common Cold A catarrhal disorder of the upper respiratory tract, which may be viral or a mixed infection. It generally involves a runny nose, nasal congestion, and sneezing. Cold, Common,Coryza, Acute,Catarrh,Acute Coryza,Catarrhs,Colds, Common,Common Colds
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D000914 Antibodies, Viral Immunoglobulins produced in response to VIRAL ANTIGENS. Viral Antibodies
D001249 Asthma A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL). Asthma, Bronchial,Bronchial Asthma,Asthmas

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