Respiratory viral infections and atopic development: From possible mechanisms to advances in treatment

Abstract

Atopic sensitization and allergic diseases are increasing in modernized countries. These diseases affect millions of individuals, but the mechanisms behind their development are not fully understood. One hypothesis relates to early life respiratory viral infections driving the development of atopic disease including asthma. This review presents the current state of the field, focusing on epidemiologic data supporting a role for early life respiratory viruses in the development of specific IgE, both against aeroallergens and the respiratory virus. Our own work using the Sendai mouse model is then summarized to provide a potential mechanistic explanation for how a respiratory viral infection could drive development of atopic sensitization and disease. We then discuss the components of this mechanistic pathway that have and have not been validated in humans. Finally, we discuss areas ripe for research, as well as potential and current therapeutics that might disrupt the link between respiratory viral infections in early life and atopic sensitization/disease.

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

“…These data are consistent with the notion that early‐life RV infections induce a nonallergic asthma phenotype . It has also been suggested that early‐life RV infections could drive the development of atopic sensitization and subsequent allergic airways disease …”

Heterogeneity and the origins of asthma

“…While essentially all children become infected with Respiratory Syncytial Virus (RSV) in the first two years of life only a small percentage develop severe bronchiolitis and require hospitalization. 35,36 These children tend to be infected in the first 2–6 months of life and have been shown to have a markedly elevated risk for developing asthma (and allergic disease). 35,36 Other studies have shown a similar risk with Metapneumovirus (MPV) and Rhinovirus (RV).…”

Severe Asthma and Allergy: A Pediatric Perspective

“…There is robust evidence concerning the synergistic effect of viral lower respiratory tract infections (LRTI) and IgE sensitization on asthma development, particularly in children predisposed to atopy (72) and asthma exacerbation (73). Increased risks of asthma inception in atopic predisposed children include: the type of virus (more than 10-fold increased risk for asthma development with rhinovirus compared to 5-fold with respiratory syncytial virus); the severity of viral LRTI; and the age during viral LRTI (74). The risk of hospital admission due to asthma exacerbation is increased by the interaction among respiratory viral infections in combination with atopic sensitization and exposure to allergens (75).…”