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Front Immunol. 2019 Mar 26;10:566. doi: 10.3389/fimmu.2019.00566. eCollection 2019.

Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity.

Author information

1
Department of Infectious Diseases, St Jude Children's Research Hospital, Memphis, TN, United States.
2
Department of Biological Sciences, Louisiana State University and School of Veterinary Medicine, Baton Rouge, LA, United States.
3
Department of Comparative Biomedical Sciences, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA, United States.
4
Trellis Bioscience, LLC, Redwood City, CA, United States.
5
Department of Infectious Disease, University of Georgia, Athens, GA, United States.
6
Fundacion INFANT, Buenos Aires, Argentina.

Abstract

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in children <2 years of age. Increased morbidity and mortality have been reported in high-risk patients, such as premature infants, patients with cardiac disease, and severely immune compromised patients. Severe disease is associated with the virulence of the virus as well as host factors specifically including the innate immune response. The role of type I interferons (IFNs) in the response to RSV infection is important in regulating the rate of virus clearance and in directing the character of the immune response, which is normally associated with protection and less severe disease. Two RSV non-structural proteins, NS1 and NS2, as well as the envelope G glycoprotein are known to suppress type I IFN production and a robust type I IFN response to RSV does not occur in human infants or neonatal mouse models of RSV infection. Additionally, presence of type I IFNs are associated with mild symptoms in infants and administration of IFN-α prior to infection of neonatal mice with RSV reduces immunopathology. This evidence has driven RSV prophylaxis and therapeutic efforts to consider strategies for enhancing type I IFN production.

KEYWORDS:

human; infant immunity; mouse; respiratory syncytial virus; type I interferons; vaccine

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