Respiratory syncytial virus, commonly abbreviated as RSV, is an enveloped, negative-sense, single-stranded RNA virus belonging to the family Pneumoviridae and the genus Orthopneumovirus. It is a major respiratory pathogen and one of the leading causes of lower respiratory tract disease in infants, older adults, and individuals with underlying health conditions.

RSV enters host cells through interactions between viral surface glycoproteins and host-cell receptors, followed by fusion of the viral envelope with the host-cell membrane. RSV replicates entirely in the cytoplasm: following entry, the viral genome is released into the cytoplasm, where viral replication and transcription occur within specialised cytoplasmic inclusion bodies often referred to as viral factories. Newly formed viral components assemble at the plasma membrane, and progeny virions acquire their envelope by budding from the infected cell.

The RSV genome is approximately 15 kb in length and encodes 11 viral proteins. These include structural proteins required for viral replication, assembly, and virion formation, as well as non-structural proteins that help modulate host innate immune responses. Two major surface glycoproteins, the fusion protein and the attachment protein, play central roles in RSV infection. The attachment protein supports viral binding to host cells, while the fusion protein mediates fusion between viral and host-cell membranes. The fusion protein can also promote the formation of multinucleated syncytia, a characteristic feature of RSV infection and the basis of the virus’s name.

RSV is divided into two major antigenic subgroups, RSV-A and RSV-B, both of which circulate globally and may co-circulate during seasonal outbreaks. Although infection stimulates an immune response, protective immunity is incomplete and relatively short-lived. As a result, reinfections can occur throughout life. Viral genetic diversity, strain variation, and differences in host immune responses all contribute to the continued global burden of RSV disease.

RSV is transmitted primarily through respiratory droplets, close person-to-person contact, and contact with contaminated surfaces. It is highly contagious and typically causes seasonal outbreaks, particularly during the winter months in temperate regions. In healthy adults and older children, RSV infection often causes mild upper respiratory tract illness, with symptoms such as cough, nasal congestion, fever, and wheezing. However, RSV can cause severe lower respiratory tract disease, including bronchiolitis and pneumonia, especially in infants, older adults, and individuals with chronic cardiopulmonary disease or weakened immune systems.

RSV is estimated to cause approximately 64 million infections and more than 100,000 deaths globally each year, with the greatest disease burden occurring at the extremes of age. Nearly all children are infected with RSV by two years of age, and primary infection during infancy is a leading cause of hospitalisation due to bronchiolitis. In older adults and high-risk populations, RSV infection can worsen existing respiratory or cardiovascular conditions and contribute to substantial morbidity, mortality, and healthcare burden.

Preventive strategies for RSV have historically been limited. More recently, new RSV vaccines and long-acting monoclonal antibody therapies have been developed to reduce severe disease in vulnerable populations, including infants and older adults. However, direct-acting antiviral treatment options for RSV remain limited, and there is still a need for improved therapeutic strategies, broader prevention approaches, and continued research into RSV pathogenesis and immune protection.

Overall, RSV is a highly contagious and clinically important respiratory virus. Its ability to cause repeated infections throughout life, together with its major impact on infants, older adults, and high-risk groups, makes it an important focus for antiviral discovery, vaccine development, and respiratory virus research.