Post-viral atopic airway disease: pathogenesis and potential avenues for intervention

ABSTRACT

Introduction: In early childhood, wheezing due to lower respiratory tract illness is often associated with infection by commonly known respiratory viruses such as respiratory syncytial virus (RSV) and human rhinovirus (RV). How respiratory viral infections lead to wheeze and/or asthma is an area of active research.

Areas covered: This review provides an updated summary of the published information on the development of post-viral induced atopy and asthma and the mechanisms involved. We focus on the contribution of animal models in identifying pathways that may contribute to atopy and asthma following respiratory virus infection, different polymorphisms that have been associated with asthma development, and current options for disease management and potential future interventions.

Expert commentary: Currently there are no prophylactic therapies that prevent infants infected with respiratory viruses from developing asthma or atopy. Neither are there curative therapies for patients with asthma. Therefore, a better understanding of genetic factors and other associated biomarkers in respiratory viral induced pathogenesis is important for developing effective personalized therapies.

KEYWORDS:

• Respiratory syncytial virus (RSV)
• rhinovirus (RV)
• Sendai virus
• pharmacogenetics
• asthma
• atopy
• microRNA
• epigenetics
• machine learning

Declaration of interest

MH Grayson has received research funding from NIH (HL087778 and AI120655) and the Research Institute at Nationwide Children’s Hospital. A Mejias has received research funding from NIH AI112524, Janssen, and the Research Institute at Nationwide Children’s Hospital. Advisory Board fees from Janssen and CME lectures from Abbvie and Novartis. O Ramilo has received research funding from NIH AI112524, Janssen, and the Research Institute at Nationwide Children’s Hospital, and has received fees for participation in Advisory Boards from Janssen, Merck and Sanofi, and for lectures from Merck, Pfizer, and Johnson and Johnson. ME Peeples has received research funding from NIH (AI112524, AI095684, and AI093848), the Cystic Fibrosis Foundation, and Janssen, and has received fees for participating on an Advisory Board for ReViral and a lecture for Pfizer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper is funded by the National Institutes of Health (NIH) grants HL087778 and AI120655, and the Research Institute at Nationwide Children’s Hospital (to MH Grayson) and NIH grant AI112524 (to A Mejias, O Ramilo and ME Peeples)