Infection respiratoire par virus syncytial

Respiratory syncytial virus (RSV), also termed human orthopneumovirus, is a negative-sense, single-stranded RNA virus classified within the Pneumoviridae family (genus Orthopneumovirus), having been discovered in 1956 and historically grouped within Paramyxoviridae ^[2][5][4]. Two antigenic subgroups, RSV-A and RSV-B, generally co-circulate each season, with one genotype often predominating and alternating annually ^[2][5]. The name derives from the large multinucleated syncytia produced when infected cells fuse ^[4].

RSV causes a spectrum of illness ranging from mild upper respiratory tract symptoms—runny nose, sore throat, headache, fatigue, and fever—to severe lower airway disease, including bronchiolitis with small-airway obstruction from accumulated dead cells and mucus, and pneumonia ^[2][5][4]. In infants, RSV characteristically manifests as bronchiolitis, while in adults it more typically produces cold-like illness, though older individuals and those with chronic respiratory or cardiac conditions, or immunocompromise, are prone to severe disease and exacerbations of underlying illness ^[1][5][4]. Reported complications include bronchiolitis, pneumonia, acute otitis media, and conjunctivitis ^[2].

RSV is a leading cause of acute lower respiratory infection in young children worldwide, with an estimated 33 million RSV-associated LRTI episodes, 3.6 million hospitalisations, and roughly 118 200 RSV-attributable deaths annually in children under five years; nearly all children experience at least one infection by their second birthday ^[1][4]. Seasonality is marked by winter peaks in temperate regions and rainy-season peaks in tropical climates, with subgroup predominance alternating annually and considerable regional variation ^[5][4]. RSV produces epidemics that typically peak in winter in temperate climates and during the rainy season in tropical climates, with one of the two genotypes generally predominating in a single season and alternating annually, although regional variation occurs ^[5]. RSV can cause outbreaks in both community and hospital settings, and reinfection remains common throughout life because prior infection does not reliably establish durable immunological memory ^[4].

RSV is highly contagious, with an estimated basic reproduction range of 5 to 25 uninfected persons per infected individual, and spreads through droplets released by coughing or sneezing that contact another person's eyes, nose, or mouth ^[4]. Following entry via the eyes or nasal passages, the virus infects epithelial cells of the upper and lower airways, producing inflammation, cell damage, and airway obstruction ^[4]. Accumulating evidence indicates that RSV is also carried by fine and ultrafine aerosols generated during normal breathing, talking, and coughing, suggesting airborne transmission may occur alongside droplet and contact routes ^[4]. RSV can survive on contaminated surfaces for up to about 25 minutes, and both community and nosocomial outbreaks are well documented ^[4].

RSV is now considered a vaccine-preventable disease following recent approvals of a long-acting monoclonal antibody for protection of all infants and maternal and older-adult vaccines that target the RSV prefusion F protein ^[1][3]. Standard non-pharmaceutical measures include hand hygiene and avoiding close contact with infected individuals, and the emerging recognition of aerosol carriage has prompted consideration of airborne precautions for reliable protection ^[4]. Because no evidence-based antiviral therapy exists, current management is supportive, and prioritising high-risk infants—particularly those in low- and middle-income countries—is advocated as an interim strategy while universal immunisation is pursued ^[1]. Large-scale introduction of these prophylactics underscores the need for active surveillance to monitor population impact and detect potential immune-escape viral mutants ^[3].

1. 1 Mazur NI et al. Severe respiratory syncytial virus infection in children: burden, management, and emerging therapies. Lancet. 2024 Sep 21. PMID: 39265587. doi: 10.1016/S0140-6736(24)01716-1. PubMed: https://pubmed.ncbi.nlm.nih.gov/39265587/
2. 2 World Health Organization. Respiratory syncytial virus - Global [Internet]. cited 12 Aug 2026. Available from: https://www.who.int/health-topics/respiratory-syncytial-virus
3. 3 Langedijk AC et al. Respiratory syncytial virus infection and novel interventions. Nat Rev Microbiol. 2023 Nov. PMID: 37438492. doi: 10.1038/s41579-023-00919-w. PubMed: https://pubmed.ncbi.nlm.nih.gov/37438492/
4. 4 Wikipedia contributors. Respiratory syncytial virus - Wikipedia [Internet]. Wikipedia. cited 3 Sept 2026. Available from: https://en.wikipedia.org/wiki/Respiratory_syncytial_virus
5. 5 Nam HH et al. Respiratory syncytial virus infection in adults. BMJ. 2019 Sep 10. PMID: 31506273. doi: 10.1136/bmj.l5021. PubMed: https://pubmed.ncbi.nlm.nih.gov/31506273/