Aetiology
Respiratory syncytial virus (RSV) is a member of the Pneumoviridae family. The viral particle plasma membrane originates from the host cell and surrounds a nucleocapsid. The viral genome within the nucleocapsid consists of a single strand of RNA with 10 genes that encode a total of 11 proteins. Two of these direct viral replication, and the remaining 9 function as structural proteins and surface glycoproteins.[31]
RSV has three surface glycoproteins: fusion protein (F), small hydrophobic protein (SH), and glycosylated attachment protein (G). The F and G proteins are the primary targets for the host's antibodies and therefore play a prominent role in the pathophysiology of RSV. The G protein mediates attachment to the host cell, and the F protein facilitates fusion of the host and viral plasma membranes, enabling transit of the viral RNA into the host cell. The F protein also promotes the aggregation of multi-nucleated cells by fusion of their membranes, resulting in the syncytia for which the virus is named.[31] The role of the SH protein is less clear. [Figure caption and citation for the preceding image starts]: Electron micrograph revealing the morphological traits of the RSVCDC/Palmer EL; used with permission [Citation ends].
Pathophysiology
The virus is transmitted by inoculation of the conjunctival or nasopharyngeal mucosa with infected respiratory droplets.[32][33] RSV can remain viable on hard surfaces for up to 6 hours.[34]
The incubation period ranges from 2 to 8 days; 4 to 6 days is most common. [8]
Immunocompetent patients shed the virus, on average for between 3 and 8 days, although this can continue for up to 4 weeks especially in young infants and immunosuppressed children.[8][32][35] Immune deficient patients may shed the virus for 4 to 6 weeks.
Viral replication begins in the nasal epithelium and then progresses downwards through the bronchiolar epithelium and types 1 and 2 alveolar pneumocytes.[36][37] The viral infection is generally limited to the respiratory tract with extrapulmonary disease rarely reported.[38]
Viral replication results in bronchiolar epithelial necrosis, followed by peribronchiolar T-lymphocytic infiltration and submucosal oedema.[39] There may be a genetic predisposition to severe RSV disease involving mutations to interleukin-4, toll-like receptor 4, and CD14 genes.[40][41]
Viscous mucous secretions, primarily neutrophilic inflammation, increase in quantity and mix with cellular debris.[42] The loss of ciliated epithelium makes clearance of these secretions difficult. The end result is dense mucous plugging of the narrowed airways, producing wheeze, cough, air trapping, and ventilation/perfusion ratio mismatch.
Respiratory virus co-infections are commonly reported, but their impact on disease severity is unclear. One systematic review and meta-analysis found no association between co-infection with RSV and other viruses and clinical severity, except for co-infection with RSV and RSV-human metapneumovirus, where co-infection was found to be associated with a higher risk of ICU admission.[43]
Classification
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