ABSTRACT
Introduction: Respiratory syncytial virus (RSV) is the most common cause of acute lower respiratory tract infections in infancy. While many infants are infected with RSV, the nature and severity of the disease vary among individuals. RSV causes bronchiolitis, pneumonia, and asthma exacerbation. However, most children infected with RSV have only mild upper airways disease and may be asymptomatic.
Areas covered: Despite efforts to elucidate mechanisms for the various clinical responses to RSV infection, they remain largely unknown, suggesting that susceptibility and disease are influenced by multiple intrinsic and extrinsic factors. This article reviews the available literature on the field of RSV disease severity and discusses important factors associated to susceptibility and different disease outcome.
Expert opinion: The severity of RSV-induced illness is a phenomenon that depends on a variety of graded mechanisms of interaction between the host, virus, and environment. This may lead to differences in the intensity of immune response in the lung and different courses of the disease. By characterizing, classifying, and grading the affecting factors in high-risk patients versus those who do not fall ill by RSV, we may find therapies or point to disease-limiting medications.
Article highlights
Respiratory syncytial virus (RSV) is responsible for a considerable respiratory disease burden, especially in infants and young children.
Although the severity and case fatality of RSV infection is often associated with underlying conditions, most cases of life-threatening infection occur among previously healthy children.
It is unclear why some people get more severe disease, and which factors are decisive in this variation; host, virus, and/or environment?
The RSV disease phenotype and severity of disease is influenced by a combination of host, viral, and environmental factors.
The influence on RSV immunopathology and disease development by host, virus, and environmental factors, alone or combined, lead to differences in inflammatory and immune response in the lung and a variety of individual courses of the disease.
Declaration of interest
The authors have no 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. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.