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Human respiratory syncytial virus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Human respiratory syncytial virus (RSV) is a negative-sense, single-stranded RNA virus of the family Paramyxoviridae, which includes common respiratory viruses such as those causing measles and mumps. RSV is a member of the paramyxovirus subfamily Pneumovirinae.

Diagnosis

History and Symptoms

For most people, RSV produces only mild symptoms, often indistinguishable from common colds and minor illnesses.

Treatment

Primary Prevention

As the virus is ubiquitous in all parts of the world, avoidance of infection is not possible.

References

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Overview

Respiratory syncytial virus was first isolated in chimpanzees with respiratory tract infections 1956. A year later, two infants with respiratory illnesses had an identical virus. The virus was first referred to as chimpanzee coryza agent but later was renamed to ”respiratory syncytial virus” given its characteristic epithelial cells, which clump together when cultured to form syncytia.

Historical Perspective

  • Respiratory syncytial virus was first identified in 1956. The virus was isolated in chimpanzees with respiratory tract infections and was therefore referred to as chimpanzee coryza agent[1].
  • In 1957, two similar viruses were isolated in infants with respiratory illnesses, which demonstrated to be indistinguishable from chimpanzee coryza agent. The virus was confirmed in humans and to be associated with respiratory illnesses in children[2][3].
  • The virus was renamed in subsequent years to ”respiratory syncytial virus” given the characteristic cytopathic effect on tissue culture cells by which the infected epithelial cells clump together to form large cell-like structure known as syncytia [4][5][6].

References

  1. BLOUNT RE, MORRIS JA, SAVAGE RE (1956). “Recovery of cytopathogenic agent from chimpanzees with coryza”. Proc Soc Exp Biol Med. 92 (3): 544–9. doi:10.3181/00379727-92-22538. PMID 13359460.
  2. CHANOCK R, ROIZMAN B, MYERS R (1957). “Recovery from infants with respiratory illness of a virus related to chimpanzee coryza agent (CCA). I. Isolation, properties and characterization”. Am J Hyg. 66 (3): 281–90. doi:10.1093/oxfordjournals.aje.a119901. PMID 13478578.
  3. BEEM M, WRIGHT FH, HAMRE D, EGERER R, OEHME M (1960). “Association of the chimpanzee coryza agent with acute respiratory disease in children”. N Engl J Med. 263: 523–30. doi:10.1056/NEJM196009152631101. PMID 13798226.
  4. CHANOCK RM, KIM HW, VARGOSKO AJ, DELEVA A, JOHNSON KM, CUMMING C; et al. (1961). “Respiratory syncytial virus. I. Virus recovery and other observations during 1960 outbreak of bronchiolitis, pneumonia, and minor respiratory diseases in children”. JAMA. 176: 647–53. PMID 13692354.
  5. “Human Respiratory Syncytial Virus – an overview | ScienceDirect Topics”.
  6. Hall CB, McBride JT (1991). “Respiratory syncytial virus–from chimps with colds to conundrums and cures”. N Engl J Med. 325 (1): 57–8. doi:10.1056/NEJM199107043250110. PMID 2046710.
Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Overview

Respiratory syncytial virus (RSV) is a negative sense, single stranded RNA virus, member of Pneumoviridae family, Orthopneumovirus genus. It is spread by direct contact with infectious sections or by self-inoculation after touching contaminated surfaces. The virus infects the ciliated epithelial cells of the respiratory tract triggering an intense inflammatory response.

Transmission

  • Respiratory syncytial virus is spread by
    • Direct contact with an infected individual
    • Self-inoculation after touching contaminated surfaces[1]
    • Infectious sections in form of large-particle aerosols or fomites[2]
  • The virus infects the ciliated epithelial cells of the respiratory tract, specifically the bronchioles. It may also infect the basal cells, targeting the airway epithelium[3].
  • Upon infection, an intense inflammatory response is triggered, mediated initially by the infected airway epithelial cells[4][5].

Genetics

  • RSV is an enveloped, negative sense, single stranded RNA virus. It is member of Pneumoviridae family, Orthopneumovirus genus[5].
  • The viral genome encodes 11 proteins. The G protein is responsible for viral attachment to cells, and the F protein promotes syncytia formation[4].

References

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Overview

Influenza infection is caused by the influenza virus that belong to the family Orthomyxoviridae. Three types of influenza virus have been reported to cause clinical illness in humans: types A, B, and C. Influenza virus can be found in humans, as well as in poultry, pigs, and bats.

Taxonomy

  • The scientific name of the virus is respiratory syncytial virus (hRSV)
    • Other names include human orthopneumovirus or respiratory syncytial virus (RSV)[1].
  • Member of the Pneumoviridae family and Orthopneumovirus genus.
  • Enveloped, negative sense, single stranded RNA virus[2].
  • Main subtypes are A and B. Most evidence suggests no difference in disease severity between both subtypes[3].
  • Lineage: Viruses > Riboviria > Orthornavirae > Negarnaviricota > Haploviricotina > Monjiviricetes > Mononegavirales (negative-sense genome single-stranded RNA viruses) > Pneumoviridae > Orthopneumovirus[1].
  • Natural hosts for hRSV are humans and chimpanzees[4].
  • Transmission directly through large droplets via nasal or oral secretions or indirectly through contact with contaminated surfaces[5][6].

References

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Differentiating Human Respiratory Syncytial Virus from other Diseases

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References

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Epidemiology and Demographics

Incidence

  • In the 2016–2020 season, the incidence of RSV-associated hospitalizations was estimated to be 42-53 per 100,000 individuals.[1]
  • In the 2022-2023 season, the incidence of RSV-associated hospitalizations was estimated to be 43.4 per 100,000 individuals.[2]

Age

  • RSV infection can occur in patients of all ages.
  • Infants and young children are most commonly affected by RSV.
  • 55% of RSV cases occur in individuals under 1 year of age.[3]
  • 8% of RSV cases occur in individuals aged ≥65 years.[3]

Mortality Rate

The overall crude mortality rate due to RVS (cause of death unspecified) in the United States was 7.8 per 100,000 individuals. A breakdown of the mortality rate by age group revealed that the rate was highest among individuals aged 65 years or older, at 46.8 per 100,000. The mortality rate was also elevated among those aged 50-64 years, at 11.8 per 100,000. In contrast, the mortality rate was lower among individuals aged 1-4 years, at 1.1 per 100,000, and even lower among those aged one year or less, at 2.7 per 100,000. [4]

RSV circulation in the United States (except Floria and Hawai) and similar climates typically starts in fall and peaks in winter:[5]

  • Season onset ranged from mid-September to mid-November.
  • Season peak ranged from late December to mid-February.
  • Season offset ranged from mid-April to mid-May.

Prior to 2020, RSV seasonal patterns in the United States were consistent, but have been disrupted since the onset of the COVID-19 pandemic.[6]

References

  1. “www.cdc.gov” (PDF). Retrieved 2023-01-16.
  2. “RSV-NET Interactive Dashboard | CDC”. Retrieved 2023-01-16.
  3. 3.0 3.1 Staadegaard L, Caini S, Wangchuk S, Thapa B, de Almeida WAF, de Carvalho FC; et al. (2021). “The Global Epidemiology of RSV in Community and Hospitalized Care: Findings From 15 Countries”. Open Forum Infect Dis. 8 (7): ofab159. doi:10.1093/ofid/ofab159. PMC 8320297 Check |pmc= value (help). PMID 34337092 Check |pmid= value (help).
  4. Hansen CL, Chaves SS, Demont C, Viboud C (2022). “Mortality Associated With Influenza and Respiratory Syncytial Virus in the US, 1999-2018”. JAMA Netw Open. 5 (2): e220527. doi:10.1001/jamanetworkopen.2022.0527. PMC 8886548 Check |pmc= value (help). PMID 35226079 Check |pmid= value (help).
  5. “Respiratory Syncytial Virus Seasonality — United States, 2014–2017 | MMWR”. Retrieved 2023-01-16.
  6. “Changes in Influenza and Other Respiratory Virus Activity During the COVID-19 Pandemic — United States, 2020–2021 | MMWR”. Retrieved 2023-01-16.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Risk factors

Patient Groups at High Risk for Severe RSV Disease:[1]

  • Prematurity
  • Bronchopulmonary Dysplasia
  • Congenital Heart Disease
  • Neuromuscular Impairment
  • Immunodeficiency
  • Immunosuppression
  • Down Syndrome
  • Age < 6 months at the beginning of the RSV season
  • Multiple birth
  • Male sex
  • Low socio-economic status and parental education
  • Crowded living conditions/siblings
  • Maternal smoking and indoor smoke pollution
  • Malnutrition/small for gestational age
  • Family history of atopy of asthma
  • Low cord serum antibody titers
  • Living at altitude

Risk Factors for Acquisition of RSV:[1]

  • Birth before or during RSV season
  • Day care attendance/older siblings in school or day-care
  • Lack of breastfeeding

References

  1. 1.0 1.1 1.2 Sommer C, Resch B, Simões EA (2011). “Risk factors for severe respiratory syncytial virus lower respiratory tract infection”. Open Microbiol J. 5: 144–54. doi:10.2174/1874285801105010144. PMC 3258650. PMID 22262987.
Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Bassel Almarie M.D.[2]

Natural History

RSV primarily infects the ciliated epithelial cells of the airways, causing bronchiolitis characterized by mucus in the airways, sloughed epithelial cell debris, and abundant neutrophils. The accumulation of mucus in the airways is a hallmark of RSV-induced lower respiratory infections (LRIs) and can lead to pulmonary obstruction.[1]

Complications

  • Bronchiolitis[2]
  • Pneumonia[2]
  • Asthma exacerbation[3]
  • Otitis media[4]
  • Apnea[5]
  • RSV encephalitis
  • Near-miss sudden infant death syndrome
  • RSV myocarditis[6][7]

References

  1. Meng J, Stobart CC, Hotard AL, Moore ML (2014). “An overview of respiratory syncytial virus”. PLoS Pathog. 10 (4): e1004016. doi:10.1371/journal.ppat.1004016. PMC 3999198. PMID 24763387.
  2. 2.0 2.1 Piedimonte G, Perez MK (2014). “Respiratory syncytial virus infection and bronchiolitis”. Pediatr Rev. 35 (12): 519–30. doi:10.1542/pir.35-12-519. PMC 5029757. PMID 25452661.
  3. Wu P, Hartert TV (2011). “Evidence for a causal relationship between respiratory syncytial virus infection and asthma”. Expert Rev Anti Infect Ther. 9 (9): 731–45. doi:10.1586/eri.11.92. PMC 3215509. PMID 21905783.
  4. Phillips M, Finelli L, Saiman L, Wang C, Choi Y, Patel J (2020). “Respiratory Syncytial Virus-associated Acute Otitis Media in Infants and Children”. J Pediatric Infect Dis Soc. 9 (5): 544–550. doi:10.1093/jpids/piaa094. PMID 32886769 Check |pmid= value (help).
  5. “Apnea Induced by Respiratory Syncytial Virus Infection is no… : The Pediatric Infectious Disease Journal”. Retrieved 2023-01-16.
  6. Mori M, Kawashima H, Nakamura H, Nakagawa M, Kusuda S, Saji T; et al. (2011). “Nationwide survey of severe respiratory syncytial virus infection in children who do not meet indications for palivizumab in Japan”. J Infect Chemother. 17 (2): 254–63. doi:10.1007/s10156-010-0121-1. PMID 20872156.
  7. Kawashima H, Inagaki N, Nakayama T, Morichi S, Nishimata S, Yamanaka G; et al. (2021). “Cardiac Complications Caused by Respiratory Syncytial Virus Infection: Questionnaire Survey and a Literature Review”. Glob Pediatr Health. 8: 2333794X211044114. doi:10.1177/2333794X211044114. PMC 8436282 Check |pmc= value (help). PMID 34527765 Check |pmid= value (help).
Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X ray | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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References

References

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