About this Research Topic

Background

Respiratory syncytial virus (RSV) affects approximately 64 million people worldwide, leading to serious infections or death in infants and adults over age 65. RSV has evolved several mechanisms to modify the host response to infection and promote virus replication and transmission. Despite the small genome (encoding 11 proteins), RSV can alter the innate immune response to RSV infection. Examples include RSV NS1 and NS2 which suppress type I IFN production and signaling. Additionally, RSV G reduces the recruitment of innate immune cells by blunting the activity of cytokines, while RSV M has been linked to an impaired host gene transcription, and RSV SH has been classified as a viroporin. These viral proteins help to regulate RSV disease in infected people. One example of RSV-modulated host responses is evident when comparing nasal washes from RSV-infected infants to those infected with other respiratory viruses such as influenza A virus; the RSV patients contain only low to undetectable levels of IFNα and IFN-β in contrast to the robust response to other viruses.

It is becoming clearer that a major strategy used by RSV to outsmart the host is to avoid the innate immune response. This feature may help the virus to repeatedly infect immune people throughout life. A better understanding of the mechanisms that RSV has evolved to circumvent the immune responses of its host is needed to develop better disease interventions.

In this Research Topic, we discuss important questions including:
• Why is immunological memory of RSV so poor?
• Why are anti-RSV antibody titers low?
• How does RSV infection in infancy contribute to childhood asthma-like syndrome?
• Is RSV (re)infection a driver of the dysfunctional airway inflammatory condition?
• How does long-term memory of RSV compare to other respiratory viruses?
• How do memory B cells become activated following RSV infection or vaccination?
• What are the mediators in respiratory epithelial cells produced in response to RSV?
• Is there a need for different vaccine strategies for different ages?

This Research Topic aims to address and highlight critical research needed to facilitate the discovery and development of disease intervention strategies for RSV. We welcome submissions of Original Research, Review/Mini-review, Methods, Opinion, and General Commentary articles.


Dr. Ralph A. Tripp is chief science officer at TrippBio, which is involved in the discovery, development, and commercialization of new antiviral treatments, but Dr. Tripp receives no financial remuneration. Dr. Lawrence Kauvar is founder, senior vice president, and chief scientific officer of Trellis Bioscience (employed full time, with a significant equity stake), which is involved in the development of drugs to treat infectious diseases, including RSV. Dr. Stephania A. Cormier declares no competing interests with regard to the topic theme.

Keywords: Respiratory syncytial virus, RSV, innate immune response, viral infectious diseases, respiratory viruses

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