New insights into the molecular mechanisms of Respiratory Syncytial Virus (RSV) disease
Respiratory syncytial virus (RSV) infection is the most common respiratory infection in children and the primary cause of hospital admission in infancy. Also, multiple prospective epidemiologic studies have shown that early infection with this virus is a significant risk factor for wheezing and asthma in childhood and adolescence, even in subjects without atopic predisposition. Indeed, following RSV infection, the release of local pro-inflammatory molecules, the dysfunction of neural pathways, and the compromised epithelial integrity can lead to persistent hyperreactivity and inflammation that manifest clinically with recurrent episodes of airway obstruction. While most research work has been focusing on immune and inflammatory mechanisms, recent evidence has shown changes in the molecular structure of the epithelial and muscular airway cells that can drive airway dysfunction independently from canonic immune-inflammatory mechanisms and pathways. This article summarizes the most recent studies on some of the novel molecular mechanisms involved in the pathophysiology of RSV infection and the consequent predisposition to chronic airway dysfunction and asthma development, with some closing considerations on current and future treatment strategies.
RSV remains the most common respiratory pathogen in infants and young children and the most common cause of hospitalization in early life. Yet, no safe and effective therapy is available. A better understanding of the molecular pathophysiologic mechanisms outlined in this article might open the way to new preventative and therapeutic strategies able to reduce the morbidity and mortality caused by this virus.
Received: Sept 3, 2022
Accepted: 9 Oct, 2022
Published: Nov 1, 2022