- Article
- Source: Campus Sanofi
- Jan 2, 2025
Understanding Viral Shedding in RSV
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The first step of viral shedding is when the virus enters the body and infects host cells.1 The virus particles are then released from the infected cells primarily via budding, exocytosis, or cell death.2,3
For example, RSV virions undergo budding. After replication, RSV virions are assembled near the plasma membrane, where F proteins may bind and attract M proteins, starting filament budding. Filament formation may also begin inside the cell, with vesicles developing into filaments and loading with nucleocapsids before fusing with the plasma membrane.4,5 This process leads to the release of new viral particles from various cellular membranes.5,6
These newly released virions may either infect other healthy cells or be dispersed into the environment through actions such as coughing, sneezing, or other similar occurrences that infect healthy individuals.6
How long does viral shedding last?
The duration of viral shedding varies depending on the type of virus, the host, and whether the patient is symptomatic or asymptomatic.6
For example, adults will shed RSV for 3 to 7 days following the infection, while infants generally shed for up to 14 days in mild infections, although this could be as long as 3 weeks in infants with severe infection and several months for those who are immunocompromised.6
The duration of RSV viral shedding is estimated to be longer in symptomatic individuals compared with asymptomatic individuals, approximately 13 days versus 7 days, respectively.10
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Read more on how to prevent the transmission of RSV or keep learning about RSV pathophysiology.
Frequently asked questions
The occurrence of viral shedding varies depending on the type of virus and the host. For example, in RSV, viral shedding could potentially occur 3 to 4 days before the onset of symptoms.12
Both viral load and viral shedding relate to the presence and transmission of viruses in and from the host, but they focus on different aspects of the viral infection process.
Viral load refers to the amount of virus present in a specific volume of a host's bodily fluid; for example, the RSV concentration in a single nasal wash collection is termed a viral load.14 Viral shedding involves the release of infectious virions (virus particles) from an infected host into the environment, facilitating transmission to new hosts.1
Viral shedding generally decreases over time.15 In the early stages of infection, viral shedding is often at its peak, increasing its potential for transmission.10 This decline can vary depending on the virus and the individual's immune response.6
References
1. Louten J. Virus transmission and epidemiology. Essential Human Virology. 1st ed. Academic Press; 2016:71-92. 2. Ryu WS. Virus life cycle. Molecular Virology of Human Pathogenic Viruses. Academic Press; 2017:31-45. 3. Payne S. Virus interactions with the cell. Viruses. 1st ed. Academic Press; 2017:23-35. 4. Förster A, Maertens GN, Farrell PJ, Bajorek M. Dimerization of matrix protein is required for budding of respiratory syncytial virus. J Virol. 2015;89(8):4624-4635. 5. Battles MB, McLellan JS. Respiratory syncytial virus entry and how to block it. Nat Rev Microbiol. 2019;17(4):233-245. 6. Kaler J, Hussain A, Patel K, Hernandez T, Ray S. Respiratory syncytial virus: A comprehensive review of transmission, pathophysiology, and manifestation. Cureus. 2023;15(3):e36342. 7. Okiro EA, White LJ, Ngama M, Cane PA, Medley GF, Nokes DJ. Duration of shedding of respiratory syncytial virus in a community study of Kenyan children. BMC Infect Dis. 2010;10:15. 8. Symptoms and care of RSV. Centers for Disease Control and Prevention. August 30, 2024. Accessed December 10, 2024. https://www.cdc.gov/rsv/symptoms/index.html 9. Eiland LS. Respiratory syncytial virus: diagnosis, treatment and prevention. J Pediatr Pharmacol Ther. 2009;14(2):75-85. 10. Munywoki PK, Koech DC, Agoti CN, Bett A, Cane PA, Medley GF, et al. Frequent asymptomatic respiratory syncytial virus infections during an epidemic in a rural Kenyan household cohort. J Infect Dis. 2015;212(11):1711-1718. 11. Barker J, Stevens D, Bloomfield SF. Spread and prevention of some common viral infections in community facilities and domestic homes. J Appl Microbiol. 2001;91(1):7-21. 12. Otomaru H, Sornillo JBT, Kamigaki T, et al. Risk of transmission and viral shedding from the time of infection for respiratory syncytial virus in households. Am J Epidemiol. 2021;190(12):2536-2543. 13. Zhang L, Peeples ME, Boucher RC, Collins PL, Pickles RJ. Respiratory syncytial virus infection of human airway epithelial cells is polarized, specific to ciliated cells, and without obvious cytopathology. J Virol. 2002;76(11):5654-5666. 14. DeVincenzo JP, Wilkinson T, Vaishnaw A, et al. Viral load drives disease in humans experimentally infected with respiratory syncytial virus. Am J Respir Crit Care Med. 2010;182(10):1305-1314. 15. Walsh EE, Peterson DR, Kalkanoglu AE, Lee FEH, Falsey AR. Viral shedding and immune responses to respiratory syncytial virus infection in older adults. J Infect Dis. 2013;207(9):1424-1432.
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