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RSV, Virus RSV, Virus

RSV Disease Overview

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RSV – a common cause of respiratory illness

Respiratory syncytial virus (RSV) is a common cause of respiratory disease affecting all ages. Infants, young children and vulnerable adults are at greatest risk of severe RSV infection1

RSV, Infant

RSV is the most common cause of acute lower respiratory infection in infants2

Most children have had an RSV infection by 2 years of age1

RSV, stopwatch

The protective immunity after RSV natural infection is not long-lasting, and re-infection occurs throughout life3,4

RSV, Older patient

Older adults are at risk of severe infection and associated complications due to age-related decline in immunity5

RSV, Patient

Adults with chronic heart, lung disease or weakened immune systems are at greater risk of severe RSV infection1,5,6

Initial stages of infection are facilitated by two surface glycoproteins18

Glycoprotein, Protein, RSV

RSV is a contagious virus with multiple routes of transmission1,20

People infected with RSV are usually contagious for 3 to 8 days. Within families, RSV has been shown to spread rapidly, with older siblings or parents the most likely source of infant RSV infections9,11

There are multiple routes of transmission1,11:

Patient, Cough, RSV

Coughing or sneezing spreads virus-filled droplets that then come into contact with other peoples’ noses, mouths or eyes

RSV, Sneeze,

Direct contact with nasal or oral secretions from infected people

RSV, Surfaces

Indirect contact with nasal or oral secretions from infected people: RSV can survive on hard surfaces for many hours

RSV, Patient, Cough

Typically, RSV infections in adults result in mild, cold-like symptoms which may be indistinguishable from those of other respiratory infections21,22

Frequency of clinical manifestations of respiratory viral infections in older adults, by virus11*

Frequency of clinical manifestations of respiratory viral infections in older adults, by virus RSV, Virus

URTI - Upper Respiratory Tract Infection
LRTI - Lower Respiratory Tract Infection

*These results were published by Kodama F et al. 2017.11 The table was independently created for GSK from the original data

However, RSV is associated to series conditions, such as:

Epidemiology of RSV

RSV seasons vary by region, peaking during winter in temperate climates12,13

Seasonal RSV epidemics lasting up to 5 months occur concurrently with epidemic seasons of other respiratory viruses12,14


Distribution of RSV peak month in the northern hemisphere

The graphs are reproduced from Bloom-Feshbach K et al. 201314 where they were published, free of copyright, under Creative Commons CCO public domain dedication

Pathogenesis and immune response to RSV

Neutrophils and eosinophils contribute to RSV pathogenesis15

RSV replicates almost exclusively in apical ciliated epithelial cells

RSV, Pathogenesis, Inflammation

RSV causes a neutrophil-intensive inflammation of the airways

The degree of inflammation correlates with severity of infection

Lower airway obstructions are caused by cellular inclusions consisting of mucus, DNA, and cell debris that mainly derives from this neutrophil infiltration

RSV, airways, inflammation

RSV infection can also be accompanied by eosinophilia, which is particularly marked in the most severe cases

RSV, eosinophilia

Humoral and cell-mediated immune responses are necessary to clear RSV infection15-17

RSV, Pathogenesis, Inflammation

Neutralising antibodies (nAbs) help prevent RSV infection through the inhibition of viral replication. nAbs inhibit the entry and spread of RSV in the human airway epithelium17

RSV specific T-cell response reduces disease severity through promotion of viral clearance17

APC = antigen-presenting cell; CD8+ T cell = cytotoxic T cell; IgA/E/G = immunoglobulin A/E/G.
Republished with permission of American Society for Microbiology, from Russell CD et al. Clin Microbiol Rev 2017;30:481–502.

Learn more about RSV disease and its burden in adults:


COPD, chronic obstructive pulmonary disorder; CHF, congestive heart failure; DNA, deoxyribonucleic acid


  1. Walsh EE. Clin Chest Med 2017;38:29–36.
  2. Nair H et al. Lancet 2010;375:1545–1555.
  3. Graham BS. Immunol Rev 2011;239:149–166.
  4. Anderson LJ et al. Vaccine 2013;31S:B209–B215.
  5. Stephens LM and Varga SM. Vaccines 2021;9(6):624.
  6. Wyffels V et al. Adv Ther 2020;37(3):1203–1217.
  7. Tian J et al. J Gen Virol 2013;94:1691–1700.
  8. Battles MB, McLellan JS. Nat Rev Microbiol 2019;17:233–245.
  9. Barr R et al. Ther Adv Infect Dis 2019;6:1–9.
  10. Heikkinen T et al. Open Forum Infect Dis 2015;2:ofu118.
  11. Kodama F et al. Infect Dis Clin North Am 2017;31:767–790.
  12. Lehners N et al. PLoS One 2016;11:e0148258.
  13. Baker RE et al. Nat Commun 2019;10:5512.
  14. Bloom-Feshbach K et al. PLoS One 2013;8:e54445.
  15. Griffiths C et al. Clin Microbiol Rev 2017;30:277-319.
  16. Russell CD et al. Clin Microbiol Rev 2017;30:481-502.
  17. Openshaw PJM et al. Annu Rev Immunol 2017;35:501-532.
  18. McLellan JS et al. Curr Top Microbiol Immunol 2013;372:83-104.
  19. Mejias A et al. Ann Allergy Asthma Immunol 2020;125:36-46.
  20. Department of Health Green Book Chapter 27a Respiratory syncytial virus. Accessed September 2023.
  21. Nam HH and Ison MG. BMJ 2019;366:l5021.
  22. Branche AR, Falsey AR. Drugs Aging 2015;32:261–269.

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December 2023 | NX-GB-RSA-WCNT-230009 (V2.0)