Viral and Host Determinants Affecting Respiratory Syncytial Virus Disease 2.0

Dear Colleagues,

This Special Issue is a continuation of our 2021 Special Issue "Viral and Host Determinants Affecting Respiratory Syncytial Virus Disease".

Respiratory syncytial virus (RSV) is the most common cause of infants’ hospitalization for bronchiolitis and confers risk for development of subsequent asthma. In primary RSV infections, disease severity is caused by a complex interaction among viral replication features, other pathogenic or resident microbes, and host immunity. Among the issues that have been investigated are viral replication levels, immune gene expression, and cytokine response in the infant respiratory mucosa and in laboratory-infected peripheral blood mononuclear cells, nasal, and bronchial epithelial cells. High viral load contents producing an exaggerated inflammatory response may contribute to the severity of human disease; however, additional host factors are also likely to contribute. Although the individual’s innate and adaptive immune responses are necessary to control RSV infection, the immune response can also contribute to disease severity of bronchiolitis. Whether the host’s immune response shows predominant type 1 versus type 2 immune characteristics may reflect the genetic heterogeneity of the infected infants or may depend on the specific virus strain that caused the infection. Co-infections with pathogenic bacteria or viruses can have synergistic effects that impact on the immune response and lead to more severe disease and hospitalization. Effects of the infant’s lung or gut microbiome on the immune response to RSV infection are not well known, but recent reports suggest that respiratory microbiota may indeed impact risk for subsequent respiratory sequelae. In addition, during early-life RSV infection, lung function and disease outcomes are also affected by passive smoking and environmental factors. In order to design and implement more effective intervention strategies against RSV infection severity or long-term sequelae such as asthma, it is necessary to gain a better understanding of these interactions. Finally, RSV severe outbreaks has become an additional matter of concern after pandemic restrictions have been lifted.  Several reasons may explain RSV rebound, including waning population immunity, synergistic and antagonistic viral interactions and RSV strain variability.

In this context, many open research issues remain regarding the role of host, immune, and environmental factors as major contributors to disease severity of RSV infection and risk of long-term sequelae. Novel approaches to studying RSV strain virulence will look more broadly at RSV genome variability. Comprehensive clinical data on disease severity, co-infections, microbiota, immune responses, and clinical follow-up of RSV infected infants are important to determine risk mediators for subsequent development of wheezing and asthma.

In this Special Issue, we welcome research articles on RSV infection, related to:

• Bronchiolitis course;
• Pathogenesis;
• RSV genome variability;
• RSV/viral and bacterial co-infection;
• Microbiota characteristics related to RSV infection severity or sequelae;
• Innate and adaptive immune response to RSV;
• Contributing factors to respiratory sequelae from early life RSV infections.

Dr. Alessandra Pierangeli
Guest Editor

Manuscript Submission Information

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• respiratory syncytial virus
• pathogenesis
• host immunity
• viral/bacterial interactions
• wheezing/asthma