Respiratory syncytial virus infection in adults
BMJ 2019; 366 doi: https://doi.org/10.1136/bmj.l5021 (Published 10 September 2019) Cite this as: BMJ 2019;366:l5021- Hannah H Nam, senior fellow,
- Michael G Ison, professor
- Division of Infectious Diseases and Organ Transplantation, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- Correspondence to: M G Ison mgison{at}northwestern.edu
ABSTRACT
Human respiratory syncytial virus (RSV) belongs to the recently defined Pneumoviridae family, Orthopneumovirus genus. It is a negative sense, single stranded RNA virus that results in epidemics of respiratory infections that typically peak in the winter in temperate climates and during the rainy season in tropical climates. Generally, one of the two genotypes (A and B) predominates in a single season, alternating annually, although regional variation occurs. RSV is a cause of disease and death in children, older people, and immunocompromised patients, and its clinical effect on adults admitted to hospital is clarified with expanded use of multiplex molecular assays. Among adults, RSV produces a wide range of clinical symptoms including upper respiratory tract infections, severe lower respiratory tract infections, and exacerbations of underlying disease. Here we discuss the latest evidence on the burden of RSV related disease in adults, especially in those with immunocompromise or other comorbidities. We review current therapeutic and prevention options, as well as those in development.
Footnotes
Series explanation: State of the Art Reviews are commissioned on the basis of their relevance to academics and specialists in the US and internationally. For this reason they are written predominantly by US authors
Contributors: Both authors contributed to the idea for the article, review of primary literature, and writing of the manuscript. Both are guarantors.
Funding: HHN is supported through T32 AI095207.
Competing interests: We have read and understood BMJ policy on declaration of interests and declare the following interests: MGI is a paid member of DSMB for GlaxoSmithKline and Shionogi, has received personal consulting fees from Celltrion, Genentech/Roche, Janssen, Seqirus, Shionogi, Viracor Eurofins, and VirBio, and has served as a non-paid consultant for GlaxoSmithKline, Romark, and Vertex; Northwestern University has received payments for research from AiCuris, Chimerix, Emergent BioScience, Genentech/Roche, Gilead, Janssen, and Shire.
Provenance and peer review: Commissioned; externally peer reviewed.
Patient involvement: No patients were involved in the drafting or review of this manuscript.
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