Respiratory Syncytial Virus (RSV)

Table of Contents

  1. Overview
  2. Virology & Biology
  3. Transmission & Epidemiology
  4. Symptoms in Infants & Young Children
  5. Symptoms in Older Adults & Immunocompromised
  6. Diagnosis
  7. Treatment
  8. Home & Supportive Care
  9. Complications
  10. Prevention, Vaccines & Prophylaxis
  11. Key Research Papers
  12. Connections
  13. Featured Videos

Overview

Respiratory Syncytial Virus (RSV) is the leading cause of acute lower respiratory tract infection (LRTI) in children worldwide. The global burden is staggering: RSV causes an estimated 33 million LRTI episodes per year in children under 5, resulting in approximately 3.6 million hospitalizations and 101,400 deaths — the majority occurring in low- and middle-income countries where intensive supportive care is unavailable (Shi et al., Lancet 2017, PMID 28689664). In the United States alone, RSV drives approximately 2.1 million outpatient visits per year in children under 5, 58,000–80,000 hospitalizations in that same age group, and an underappreciated 6,000–10,000 deaths annually in adults aged 65 and older.

RSV is not only a pediatric pathogen. It is a major cause of serious respiratory illness in elderly adults — second only to influenza as a cause of respiratory-related deaths in that population — and it is particularly dangerous in immunocompromised patients. In hematopoietic stem cell transplant (HSCT) recipients, RSV can progress from an upper respiratory infection to pneumonia in 30–40% of cases, carrying mortality rates of 20–50% once pneumonia is established. Patients with chronic cardiopulmonary diseases such as COPD, congestive heart failure, and chronic lung disease of prematurity face similarly elevated risks of severe disease and hospitalization.

Nearly all children are infected with RSV at least once by their second birthday, and reinfection occurs throughout life because natural immunity is incomplete and wanes over time. Most infections in healthy older children and adults produce a mild cold-like illness lasting one to two weeks. The danger lies at the extremes of age and immune status: young infants whose airways are narrow and whose immune responses are immature, and elderly or immunocompromised adults whose defenses cannot contain viral replication in the lower respiratory tract. The year 2023 marked a historic turning point, with the first RSV vaccines approved for adults and the first long-acting monoclonal antibody (nirsevimab) recommended for all infants — tools that for the first time offer broad population-level protection.

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Virology & Biology

RSV belongs to the family Paramyxoviridae, subfamily Pneumoviridae, genus Orthopneumovirus. It is a non-segmented, negative-sense, single-stranded RNA (ssRNA) virus with a lipid envelope. Unlike influenza, RSV's genome does not segment, which means it does not undergo antigenic shift (reassortment) — but it does accumulate point mutations over time. Two major antigenic subtypes co-circulate in most RSV seasons: RSV-A and RSV-B. Both subtypes cause clinically indistinguishable disease, though some evidence suggests RSV-A is associated with slightly more severe illness in certain seasons. The relative predominance of each subtype varies year to year and geographically.

The two most important surface glycoproteins are the fusion (F) protein and the attachment (G) protein. The G protein helps the virus adhere to the respiratory epithelium of the host. The F protein is the key mediator of infection: it drives fusion of the viral envelope with the host cell membrane, allowing the viral genome to enter the cytoplasm. Crucially, the F protein exists in two structural conformations — the prefusion form (an unstable, spring-loaded conformation present before membrane fusion) and the postfusion form (the stable conformation after fusion has occurred). This structural difference is immunologically critical: the prefusion F protein displays epitopes that elicit far more potent neutralizing antibodies than the postfusion form. This insight, first crystallographically demonstrated by McLellan and colleagues in 2013 (Science, PMID 23618766), revolutionized RSV vaccinology and enabled the development of all effective modern vaccines and nirsevimab. For decades, vaccine efforts had failed because they used the postfusion form, which is less immunogenic and triggered disease-enhancing responses in early formalin-inactivated vaccine trials in the 1960s.

RSV primarily infects ciliated bronchial epithelial cells and type II pneumocytes in the lower respiratory tract. Viral replication causes direct cytopathic effects including the formation of syncytia — large multinucleated giant cells created when the F protein mediates fusion of adjacent cell membranes — which gives the virus its name ("syncytial"). Infection also causes ciliary dysfunction, sloughing of the bronchiolar epithelium, submucosal edema, mucus hypersecretion, and peribronchiolar inflammatory infiltrate. In infants and young children, the resulting bronchiolar obstruction from edema, necrotic debris, and mucus produces the classic bronchiolitis picture: air trapping, atelectasis, ventilation-perfusion mismatch, increased work of breathing, and hypoxia. The narrow airways of young infants amplify these effects dramatically — even small amounts of edema can produce critical airway narrowing.

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Transmission & Epidemiology

RSV is highly contagious. The primary transmission route is direct or close-range contact with large respiratory droplets produced by coughing, sneezing, or talking — these droplets travel short distances and deposit on mucous membranes of the eyes, nose, or mouth. Fomite transmission is also important: RSV survives on hard nonporous surfaces (e.g., countertops, toys, crib rails) for 4–7 hours, and on hands for approximately 30 minutes. This means that an infant can acquire RSV by touching a contaminated surface and then touching their face — making thorough and frequent hand hygiene a cornerstone of household and healthcare prevention. True airborne transmission (droplet nuclei remaining suspended in air) occurs but is considered a less dominant route in most settings compared to direct contact.

In temperate climates of the northern hemisphere, RSV follows a predictable seasonal pattern: circulation begins in October or November, peaks in December through February, and subsides by March or April. In tropical and subtropical climates, RSV circulates year-round with less distinct seasonal peaks. The COVID-19 pandemic disrupted RSV seasonality substantially: public health measures (masking, school closures, social distancing) suppressed RSV in 2020–2021, creating an "immunity debt" in the population — particularly in young children who had never been exposed. When restrictions lifted in 2021–2022, a large off-season summer RSV surge struck the United States and other countries, overwhelming pediatric hospitals. Understanding this immunity debt phenomenon has become relevant to post-pandemic RSV epidemiology planning.

The incubation period from exposure to symptom onset is 2–8 days, most commonly 4–6 days. Infected individuals are typically contagious for 3–8 days; however, infants and immunocompromised individuals may shed virus for 3–4 weeks or longer. In healthcare settings, nosocomial RSV transmission is a serious and underappreciated problem — RSV outbreaks in neonatal intensive care units (NICUs) and pediatric wards can cause significant morbidity. Rigorous contact precautions (gown and gloves), cohorting of infected patients and staff, and meticulous hand hygiene are essential infection control measures during RSV season. Staff can carry RSV on their hands and inadvertently transmit it to vulnerable infants even without personal illness.

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Symptoms in Infants & Young Children

RSV infection in infants and young children typically follows a biphasic course. The upper respiratory phase lasts approximately 1–3 days and is characterized by rhinorrhea (often profuse), nasal congestion, mild cough, and low-grade fever. Importantly, very young infants under 3 months — including premature babies — may not mount a febrile response and can instead present with temperature instability, poor feeding, or lethargy as their first signs of RSV infection. This makes the diagnosis easy to miss unless RSV is considered during peak season. A parent reporting that an infant "just isn't acting right" or is feeding poorly in late fall or winter should prompt consideration of RSV testing.

In moderate to severe disease, a lower respiratory phase develops around days 3–5 as the virus spreads to the bronchioles. Clinical signs include tachypnea (fast breathing), subcostal and intercostal retractions (visible pulling of the skin between the ribs with each breath), nasal flaring, expiratory wheeze, and crackles on auscultation. Hypoxia develops as ventilation-perfusion mismatch worsens. Feeding difficulty is a cardinal sign — increased respiratory rate makes the coordinated suck-swallow-breathe sequence impossible, leading to poor intake and risk of aspiration. Most pediatric RSV hospitalizations are driven by two indications: hypoxia (oxygen saturation below 90–92%) and poor feeding leading to dehydration. Clinicians should assess feeding status carefully at every encounter, not just respiratory parameters.

Apnea deserves special emphasis: RSV-associated apnea (cessation of breathing for more than 20 seconds, or shorter if accompanied by bradycardia or desaturation) is a serious and potentially life-threatening complication, occurring predominantly in premature infants and those under 6–8 weeks of age. Critically, apnea can be the presenting sign of RSV — arriving before the typical catarrhal symptoms develop. A young infant presenting with apnea during RSV season should be tested and admitted for monitoring. The clinician who sees only "apnea" in a 4-week-old and does not obtain RSV testing may miss the diagnosis and send the child home prematurely. Well-appearing infants with mild wheeze ("happy wheezers") can often be managed carefully in the outpatient setting, while those with toxic appearance, poor perfusion, marked retractions, or SpO₂ persistently below 90% require hospitalization. Risk factors for severe RSV in infants include: prematurity (under 36 weeks gestational age), age under 12 weeks, hemodynamically significant congenital heart disease, chronic lung disease of prematurity (bronchopulmonary dysplasia), immunodeficiency, and Down syndrome.

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Symptoms in Older Adults & Immunocompromised

In healthy older children and adults, RSV most commonly causes a typical upper respiratory illness that is clinically indistinguishable from the common cold or other viral URIs. Symptoms include rhinorrhea, nasal congestion, sore throat, low-grade fever, cough, and fatigue lasting 1–2 weeks. Most healthy adults recover without incident and never seek medical care. This relative mildness in healthy adults can create a false sense of security about RSV as "just a cold" — a misconception that has historically led to under-recognition of RSV's enormous burden in vulnerable populations.

In elderly adults aged 65 and older, RSV can cause serious and occasionally life-threatening illness. Lower respiratory tract involvement — bronchitis, pneumonia — occurs in a significant minority of infected elderly patients, particularly those with underlying COPD, asthma, heart failure, or other comorbidities. RSV pneumonia in elderly adults carries substantial mortality. Large epidemiological studies estimate 6,000–10,000 RSV-associated deaths annually in US adults aged 65 and older — comparable to influenza mortality in some seasons (Thompson et al., JAMA 2003, PMID 12517228). Despite this, RSV is dramatically underdiagnosed in elderly patients because clinicians rarely test for it, and the illness is often attributed to influenza or "the flu." RSV also provokes acute exacerbations of COPD and decompensation of underlying heart failure, adding to its clinical impact beyond direct pneumonia deaths. The approval of RSV vaccines for adults aged 60 and older in 2023 is expected to substantially reduce this underappreciated burden.

In immunocompromised patients — particularly recipients of hematopoietic stem cell transplants (HSCT) and those with hematologic malignancies — RSV is a major opportunistic respiratory pathogen. RSV upper respiratory infection in HSCT recipients progresses to pneumonia in 30–40% of cases, and once pneumonia is established, mortality is 20–50%. The highest-risk period is the pre-engraftment phase, when lymphopenia is most profound. Key risk factors for progression to pneumonia include severe lymphopenia (CD4 count below 100 cells/µL), systemic corticosteroid use, high viral load, early transplant timing, and myeloablative conditioning. In solid organ transplant recipients, the risk is lower but still clinically significant, particularly in lung transplant recipients where RSV can trigger bronchiolitis obliterans syndrome. For immunocompromised patients, aggressive diagnostic evaluation (PCR) and early consideration of antiviral therapy are warranted even for what appears to be mild URI.

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Diagnosis

In a healthy full-term infant presenting with classic bronchiolitis during RSV season, the diagnosis can often be made clinically without testing — the American Academy of Pediatrics (AAP) bronchiolitis guidelines explicitly state that testing is not required in straightforward cases. Testing becomes important for hospitalized patients (to guide isolation precautions and cohorting), immunocompromised individuals, very young infants where the diagnosis is uncertain, outbreak investigation, and epidemiological surveillance.

Rapid Antigen Detection Tests (RADTs) are the most widely used point-of-care diagnostic. A nasal wash or nasopharyngeal swab specimen is processed in 15–20 minutes. Sensitivity is 80–90% in young children (who shed high viral loads) but drops to 50–70% in adults and older children who shed less virus. Specificity exceeds 95%. The practical limitation is that a negative rapid test does not rule out RSV in adults or older children — a negative result in a high-suspicion immunocompromised adult should prompt RT-PCR testing.

RT-PCR (reverse transcriptase polymerase chain reaction) is the gold standard for RSV diagnosis. It achieves sensitivity above 95% across all age groups and can identify RSV-A versus RSV-B subtypes. Multiplex molecular panels that simultaneously detect RSV, influenza A and B, SARS-CoV-2, and other respiratory pathogens are now standard in most hospital settings, providing rapid comprehensive results from a single swab. RT-PCR is the preferred test for immunocompromised patients, hospitalized adults, and outbreak investigations. Direct fluorescent antibody (DFA) testing of nasopharyngeal specimens is sensitive in young children and provides rapid results but requires skilled laboratory personnel and specialized equipment. Viral culture is insensitive, slow (results in days to weeks), and is used primarily in reference laboratories for research or surveillance. Chest X-ray in bronchiolitis characteristically shows hyperinflation with increased anteroposterior diameter, peribronchial thickening, and patchy areas of atelectasis — particularly in the right upper lobe, which can be mistaken for consolidative bacterial pneumonia. However, the AAP guideline recommends against routine chest X-ray in typical bronchiolitis, as findings rarely change management and can prompt unnecessary antibiotic use when atelectasis is misread as pneumonia. Pulse oximetry is the most critical bedside tool — continuous monitoring in hospitalized infants guides oxygen supplementation and escalation decisions; a threshold of SpO₂ below 90–92% typically warrants supplemental oxygen.

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Treatment

No approved antiviral agent is available for most RSV patients, and treatment remains primarily supportive. The cornerstone of inpatient management is maintaining adequate oxygenation and hydration. Understanding what does NOT work is as important as knowing what does — several commonly used interventions have been rigorously tested and shown to be ineffective in typical bronchiolitis.

Bronchodilators (inhaled salbutamol/albuterol, ipratropium): Not recommended for routine use in bronchiolitis. Multiple randomized controlled trials and Cochrane reviews have shown no significant impact on hospitalization rates, duration of stay, or clinical outcomes. Transient improvements in auscultatory findings do not translate to meaningful clinical benefit. Some guidelines allow a single trial dose of a bronchodilator with objective reassessment, discontinuing if no response is seen; however, routine use should be avoided. A caveat: older children with documented reactive airway disease who wheeze with RSV may benefit from bronchodilators — the evidence from infant bronchiolitis trials does not directly apply to this group.

Systemic corticosteroids: Not recommended in bronchiolitis. The landmark Plint et al. trial (2009, NEJM) enrolled 800 infants and showed no benefit of combined dexamethasone plus epinephrine, dexamethasone alone, or epinephrine alone over placebo in reducing hospitalization rates. Subsequent meta-analyses have confirmed this null finding. Corticosteroids can worsen viral shedding and carry side effects; they should not be given for routine bronchiolitis regardless of severity. In patients with documented asthma having an RSV-triggered exacerbation, steroids may still be appropriate.

Ribavirin (aerosolized): An antiviral nucleoside analogue approved for severe RSV in infants and used in inhaled form in some immunocompromised patients with RSV lower respiratory tract infection. Evidence for efficacy is limited. The drug is teratogenic (staff exposure requires special precautions including respirators), extremely expensive, and logistically complex to administer. Most centers reserve aerosolized ribavirin for immunocompromised patients with RSV pneumonia — particularly HSCT recipients in the pre-engraftment phase — where the case for treatment is strongest despite the weak evidence base. Some centers use oral ribavirin (off-label) in combination with intravenous immunoglobulin for severe RSV in immunocompromised patients.

High-Flow Nasal Cannula (HFNC) has become standard of care for moderate to severe RSV bronchiolitis requiring respiratory support. Heated, humidified high-flow oxygen (typically 1–2 L/kg/min) reduces the work of breathing, improves oxygenation, and washes out nasopharyngeal dead space. The PARIS trial (Franklin et al., NEJM 2018, PMID 29562151) randomized 1,472 infants with bronchiolitis to HFNC versus standard oxygen. HFNC significantly reduced treatment failure — defined as escalation of care — from 23% to 12% (p < 0.001), though it did not change length of hospital stay or PICU admission rates. HFNC is now used broadly in emergency departments and general wards, reducing the need for PICU transfer. Heliox (a helium-oxygen mixture, typically 70:30 or 80:20) reduces turbulent airflow resistance in the upper airways and may decrease the work of breathing in severe bronchiolitis; it can serve as a temporizing bridge while awaiting intubation in the most severe cases, though evidence for meaningful clinical benefit is limited. Mechanical ventilation is reserved for respiratory failure — practitioners use lung-protective ventilation strategies with permissive hypercapnia and careful titration of PEEP, since dynamic hyperinflation from air trapping is a risk in RSV bronchiolitis. Newer investigational antivirals including presatovir and ziresovir are in active Phase 3 trials and may provide future therapeutic options.

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Home & Supportive Care

The large majority of RSV infections in healthy term infants and children are managed entirely at home with supportive care. Parents and caregivers play a central role in recognizing deterioration early and providing effective symptom relief. The most impactful interventions are simple and require no prescription.

Nasal suctioning is the single most effective practical intervention for infants with RSV congestion. Infants are obligate nasal breathers — nasal obstruction from thick secretions directly causes feeding difficulty and increased work of breathing. A bulb syringe or a device such as a NoseFrida (nasal aspirator) used before each feeding session clears the nasal passages and dramatically improves the infant's ability to feed. Saline nasal drops (1–2 drops in each nostril) instilled 60–90 seconds before suctioning help liquefy thick secretions and improve suction effectiveness. Over-the-counter saline nasal sprays are equally effective and safe. These techniques should be demonstrated to parents and caregivers at the initial visit.

Small frequent feeds are essential for maintaining adequate oral intake when rapid breathing and nasal congestion make normal-volume feeds impossible. Offering smaller amounts every 1–2 hours rather than the usual feeding schedule reduces aspiration risk and allows the infant to breathe more easily between swallows. Breastfeeding provides additional immunological benefit and should be strongly encouraged and supported during RSV illness. Positioning the infant at a 30–45 degree incline may reduce respiratory effort — the supine flat position can worsen nasal congestion and increase the work of breathing. However, elevated positioning must only be used with full caregiver supervision; infants should never be left unattended in infant seats or bouncers during sleep due to positional asphyxiation risk.

Fever management with weight-appropriate doses of acetaminophen (for infants over 3 months) or ibuprofen (for children over 6 months) reduces discomfort and may improve feeding tolerance. Hydration is critical — fever and increased respiratory rate dramatically increase insensible fluid losses. Caregivers should track wet diapers carefully: fewer than 4 wet diapers in 24 hours signals dehydration and warrants medical evaluation. Smoke avoidance is paramount — exposure to secondhand tobacco smoke significantly worsens RSV severity and substantially increases the risk of hospitalization. Any caregiver who smokes should be counseled urgently during RSV illness and ideally connected to cessation resources. Caregivers should return to the emergency department immediately for: respiratory rate above 60 per minute; severe chest retractions or nasal flaring; any episode of apnea or color change (bluish/gray tinge); persistent feeding refusal or fewer than 2 wet diapers; inconsolability or inability to arouse; or SpO₂ below 90% if a home pulse oximeter is available. Over-the-counter decongestants and cough suppressants are not effective in infants and young children and carry risk of harm — they should not be used.

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Complications

Most RSV infections resolve without lasting harm. However, both short-term and long-term complications occur and are important to understand.

Short-term complications include apnea — especially in premature infants under 32 weeks gestational age and term infants under 6–8 weeks. Apnea can be life-threatening and may arrive before classic bronchiolitis symptoms, demanding inpatient monitoring for affected young infants. Respiratory failure requiring mechanical ventilation occurs in 1–5% of hospitalized infants, more commonly in those with the risk factors enumerated above. Bacterial superinfection — most commonly with Streptococcus pneumoniae, Staphylococcus aureus, or Haemophilus influenzae — complicates a minority of RSV pneumonias but significantly increases severity and mortality when it occurs. Nosocomial RSV transmission in NICUs and pediatric wards is an ongoing patient safety concern — premature infants acquiring RSV while hospitalized for other reasons face particularly severe disease.

Long-term complications: The relationship between severe RSV bronchiolitis in infancy and subsequent childhood wheezing and asthma has been an area of intense research and ongoing debate. Epidemiological studies consistently show that infants hospitalized for RSV bronchiolitis in the first year of life have approximately twice the risk of recurrent wheezing and clinically diagnosed asthma by school age compared to controls. The landmark 18-year follow-up study by Sigurs and colleagues (Thorax 2010, PMID 20581410) found that children hospitalized for RSV LRTI in the first year of life had significantly higher rates of asthma and allergic sensitization persisting through age 18. However, the causal direction of this association is genuinely uncertain: RSV may actively induce a wheeze-prone immune phenotype through disruption of normal airway microbiome development or early sensitization, OR children who are genetically predisposed to asthma may be constitutionally more susceptible to severe RSV (the "susceptible host" hypothesis). No intervention has definitively broken the RSV-asthma link — notably, palivizumab prophylaxis in premature infants does not reduce subsequent wheezing risk despite preventing severe RSV bronchiolitis. This remains one of the most actively investigated questions in pediatric respiratory medicine.

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Prevention, Vaccines & Prophylaxis

The year 2023 was transformative for RSV prevention: for the first time in the six-decade history of RSV research, effective tools became available for both infants (nirsevimab) and older adults (two protein subunit vaccines). A third vaccine using mRNA technology was approved in 2024, extending options further.

Nirsevimab (Beyfortus) — a long-acting monoclonal antibody (LAMA) targeting the prefusion F protein — represents a paradigm shift in infant protection. Unlike the older palivizumab, which requires monthly injections and is approved only for high-risk infants, nirsevimab is given as a single intramuscular injection at the start of RSV season and provides protection for the entire season (approximately 5 months). In the pivotal MELODY trial (Hammitt et al., NEJM 2022, PMID 35235726), nirsevimab reduced medically attended RSV LRTI by 74.5% and RSV hospitalizations by 83% compared to placebo. In the Phase 2b DEFINE trial in premature infants, efficacy against RSV LRTI was 78%. The ACIP recommended nirsevimab for all infants under 8 months entering their first RSV season, plus children aged 8–19 months who are at increased risk of severe RSV (premature birth, chronic lung disease, congenital heart disease, immunocompromise). This universal infant recommendation — rather than restriction to high-risk groups — reflects the recognition that even healthy term infants under 6 months can be hospitalized with severe RSV bronchiolitis.

Palivizumab (Synagis) remains available but has been largely superseded by nirsevimab as the preferred prophylactic agent when nirsevimab is available. Palivizumab is a humanized monoclonal antibody against the RSV F protein (postfusion form) given as monthly intramuscular injections throughout the RSV season. In the pivotal 1998 trial (Pediatrics, PMID 9738173), palivizumab reduced RSV hospitalizations by 55% in high-risk infants. The AAP previously recommended it for premature infants under 35 weeks gestational age, infants with hemodynamically significant congenital heart disease, those with chronic lung disease of prematurity, and profoundly immunocompromised children. When nirsevimab is available and affordable, it is preferred due to superior efficacy data and the convenience of a single-dose regimen.

RSV vaccines for adults (approved 2023): Two recombinant prefusion F protein vaccines were approved by the FDA in 2023 for adults aged 60 and older — Abrysvo (Pfizer) and Arexvy (GSK). Arexvy contains RSV-A prefusion F protein combined with the AS01E adjuvant system and demonstrated 82% efficacy against RSV LRTI with at least two symptoms in the pivotal trial. Abrysvo is a bivalent vaccine containing prefusion F proteins from both RSV-A and RSV-B subtypes, showing approximately 89% efficacy against RSV LRTI with two or more symptoms and 94% efficacy against severe RSV LRTI. The ACIP recommended shared clinical decision-making for adults aged 60 and older, meaning patients and providers discuss individual risk factors, expected benefits, and potential side effects to decide together. In 2024, the FDA approved mResvia (Moderna), an mRNA vaccine encoding prefusion F protein, for adults aged 60 and older, with efficacy of 83.7% against RSV LRTI — extending the mRNA platform that proved successful in COVID-19 vaccine development to a new pathogen. Maternal RSV vaccination: Abrysvo also received approval for use in pregnant women at 32–36 weeks of gestational age (maternal RSVpreF). Vaccinating mothers during pregnancy generates high levels of neutralizing antibodies that cross the placenta and protect the newborn through the first months of life. Efficacy against severe RSV LRTI in infants through 90 days postpartum was 69%, and against any medically attended RSV LRTI was 57%. Non-pharmacological prevention remains essential at all ages: frequent and thorough handwashing with soap and water (the most effective environmental control measure); avoiding touching eyes, nose, and mouth; regular disinfection of high-touch surfaces and shared toys; keeping infants away from individuals with respiratory symptoms; excluding symptomatic children from daycare and group settings; and avoiding tobacco smoke exposure.

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Key Research Papers

  1. Shi T, McAllister DA, O'Brien KL, et al. Global, regional, and national disease burden estimates of acute lower respiratory infections due to respiratory syncytial virus in young children in 2015. Lancet. 2017;390:946–958. PMID: 28689664 | DOI: 10.1016/S0140-6736(17)30938-8
  2. Griffiths C, Drews SJ, Marchant DJ. Respiratory Syncytial Virus: Infection, Detection, and New Options for Prevention and Treatment. Clin Microbiol Rev. 2017;30:277–319. PMID: 27903593 | DOI: 10.1128/CMR.00010-16
  3. Hammitt LL, Dagan R, Yuan Y, et al. Nirsevimab for Prevention of RSV in Healthy Late-Preterm and Term Infants. N Engl J Med. 2022;386:837–846. PMID: 35235726 | DOI: 10.1056/NEJMoa2110275
  4. McLellan JS, Chen M, Leung S, et al. Structure of RSV fusion glycoprotein trimer bound to a prefusion-specific neutralizing antibody. Science. 2013;340:1113–1117. PMID: 23618766 | DOI: 10.1126/science.1234914
  5. Higgins D, Trujillo C, Keech C. Advances in RSV vaccine research and development — A global agenda. Vaccine. 2016;34:2870–2875. PMID: 27068190 | DOI: 10.1016/j.vaccine.2016.03.109
  6. Franklin D, Babl FE, Schlapbach LJ, et al. A Randomized Trial of High-Flow Oxygen Therapy in Infants with Bronchiolitis. N Engl J Med. 2018;378:1121–1131. PMID: 29562151 | DOI: 10.1056/NEJMoa1714855
  7. Thompson WW, Shay DK, Weintraub E, et al. Mortality associated with influenza and respiratory syncytial virus in the United States. JAMA. 2003;289:179–186. PMID: 12517228 | DOI: 10.1001/jama.289.2.179
  8. Palivizumab, a humanized respiratory syncytial virus monoclonal antibody, reduces hospitalization from respiratory syncytial virus infection in high-risk infants. Pediatrics. 1998;102:531–537. PMID: 9738173 | DOI: 10.1542/peds.102.3.531
  9. Sigurs N, Aljassim F, Kjellman B, et al. Asthma and allergy patterns over 18 years after severe RSV bronchiolitis in the first year of life. Thorax. 2010;65:1045–1052. PMID: 20581410 | DOI: 10.1136/thx.2009.121582
  10. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis. Pediatrics. 2014;134:e1474–e1502. PMID: 25349312 | DOI: 10.1542/peds.2014-2742
  11. Walsh EE, Frenck RW Jr, Falsey AR, et al. Safety and Immunogenicity of Two RNA-Based Covid-19 Vaccine Candidates. N Engl J Med. 2020;383:2439–2450. PMID: 33053279 | DOI: 10.1056/NEJMoa2027906 (Background for the mRNA vaccine platform applied in mResvia.)
  12. Domachowske JB, Khan AA, Esser MT, et al. Safety, Tolerability and Pharmacokinetics of MEDI-524, a Humanized Monoclonal Antibody for the Prevention of RSV Infection. Pediatr Infect Dis J. 2004;23:812–817. PMID: 15367890 | DOI: 10.1097/01.inf.0000134965.62571.2e

PubMed Topic Searches

  1. RSV bronchiolitis in infants — PubMed
  2. RSV vaccine adults prefusion F protein — PubMed
  3. Nirsevimab RSV prevention infants — PubMed
  4. RSV in immunocompromised HSCT patients — PubMed
  5. High-flow nasal cannula RSV bronchiolitis — PubMed
  6. RSV bronchiolitis and subsequent asthma/wheezing — PubMed
  7. RSV in elderly adults mortality — PubMed
  8. Palivizumab prophylaxis high-risk infants — PubMed

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Connections

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