# paper.pdf ## Metadata - PDFFormatVersion=1.4 - IsLinearized=false - IsAcroFormPresent=false - IsXFAPresent=false - IsCollectionPresent=false - IsSignaturesPresent=false - Custom.CrossmarkMajorVersionDate=2014-12-12 - Custom.CrossmarkDomainExclusive=false - Custom.doi=10.1183/16000617.0179-2025 - Custom.CrossMarkDomains[1]=psychoceramics.labs.crossref.org - CreationDate=D:20260331162157+05'30' - Author=Sachin Ananth - Creator=Arbortext Advanced Print Publisher 10.0.1465/W Unicode - Producer=Acrobat Distiller 8.1.0 (Windows) - ModDate=D:20260404134505+05'30' - Title=Prevalence of respiratory viruses in stable and acute asthma: a systematic review and meta-analysis - xap:creatortool=Arbortext Advanced Print Publisher 10.0.1465/W Unicode - xap:modifydate=2026-04-04T13:45:05+05:30 - xap:createdate=2026-03-31T16:21:57+05:30 - xap:metadatadate=2026-04-04T13:45:05+05:30 - dc:format=application/pdf - dc:identifier=10.1183/16000617.0179-2025 - dc:title=Prevalence of respiratory viruses in stable and acute asthma: a systematic review and meta-analysis - dc:creator=Sachin Ananth,Gioulinta S. Alimani,Cristina Boccabella,Ekaterina Khaleva,Jan Hansel,Ran Wang,Graham Roberts,Chris Kosmidis,Apostolos Bossios,Jørgen Vestbo,Effie Papageorgiou,Nikolaos G. Papadopoulos,Apostolos Beloukas,Alexander G. Mathioudakis - pdf:producer=Acrobat Distiller 8.1.0 (Windows) - xapmm:documentid=uuid:c91ab83d-df46-4ca4-b1c8-d7ae0e29c9bd - xapmm:instanceid=uuid:2fbab7cc-05fb-40a6-b710-7a1de238b2c7 - prism:url=http://dx.doi.org/10.1183/16000617.0179-2025 - prism:doi=10.1183/16000617.0179-2025 - crossmark:doi=10.1183/16000617.0179-2025 - crossmark:crossmarkdomainexclusive=false - crossmark:majorversiondate=2014-12-12 - crossmark:crossmarkdomains=psychoceramics.labs.crossref.org - pdfx:crossmarkdomainexclusive=false - pdfx:crossmarkmajorversiondate=2014-12-12 - pdfx:doi=10.1183/16000617.0179-2025 - pdfx:crossmarkdomains=psychoceramics.labs.crossref.org ## Contents ### Page 1 Prevalence of respiratory viruses in stable and acute asthma: a systematic review and meta-analysis Sachin Ananth 1,2,16 , Gioulinta S. Alimani3,16 , Cristina Boccabella 4 , Ekaterina Khaleva 5 , Jan Hansel 6 , Ran Wang 6,7 , Graham Roberts 5,8,9 , Chris Kosmidis 10 , Apostolos Bossios 11,12,13 , Jørgen Vestbo 6,7 , Effie Papageorgiou 3 , Nikolaos G. Papadopoulos 6,14 , Apostolos Beloukas 3,15,17 and Alexander G. Mathioudakis 6,7,171 London North West University Healthcare NHS Trust, London, UK. 2 National Heart and Lung Institute, Imperial College London, London, UK. 3 Department of Biomedical Sciences, University of West Attica, Athens, Greece. 4 Department of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario. “A Gemelli”—IRCCS, University of the Sacred Heart, Rome, Italy. 5 Faculty of Medicine, University of Southampton, Southampton, UK. 6 Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, The University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. 7 The North West Lung Centre, Wythenshawe Hospital, Manchester University NHS Foundation Trust, Manchester, UK. 8 NIHR Southampton Biomedical Research Centre, University Hospital Southampton NHS Foundation Trust, Southampton, UK. 9 David Hide Asthma and Allergy Centre, Isle of Wight NHS Trust, Newport, UK. 10 Division of Evolution, Infection and Genomics, School of Biological Sciences, The University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. 11 Division of Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. 12 Karolinska Severe Asthma Center, Department of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden. 13 Lung Laboratory, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. 14 Allergy Department, 2nd Paediatric Clinic, National and Kapodistrian University of Athens, Athens, Greece. 15 National AIDS Reference Centre of Southern Greece, University of West Attica, Athens, Greece. 16 Shared first authorship. 17 Shared last authorship. Corresponding author: Alexander G. Mathioudakis (Alexander.mathioudakis@manchester.ac.uk)Shareable abstract (@ERSpublications)This meta-analysis (111 studies) quantifies viral prevalence in acute/stable asthma in children and adults, and highlights links between specific viruses and acute asthma severity. PCR alone may be limited in identifying viral acute asthma triggers. https://bit.ly/4ts91DTCite this article as: Ananth S, Alimani GS, Boccabella C, et al. Prevalence of respiratory viruses in stable and acute asthma: a systematic review and meta-analysis. Eur Respir Rev 2026; 35: 250179 [DOI: 10.1183/16000617.0179-2025].AbstractBackground Respiratory viruses, frequently detected in asthma, are associated with worse outcomes. This meta-analysis systematically quantifies the prevalence of respiratory viruses in stable and acute asthma, across children and adults, and explores factors associated with increased viral burden through meta-regression.Methods This prospectively registered meta-analysis (PROSPERO-CRD42023375108) included studies employing molecular techniques to assess respiratory virus prevalence in asthma. Three databases were searched in August 2024. Risk of bias and certainty of evidence were assessed. We performed random-effects meta-analysis of proportions.Results We included 111 eligible studies. Moderate-certainty evidence indicated a pooled prevalence of any respiratory virus of 33.9% (95% confidence interval 24.8–43.7%) in children and 23.0% (12.9–35.0%) in adults with stable asthma. In acute asthma, prevalence increased to 58.8% (52.5–65.0%) in children and 49.9% (41.2–58.5%) in adults (moderate certainty). Rhinovirus was the most frequently identified virus, especially in acute asthma (45.0% in children versus 21.2% in adults). Respiratory syncytial virus and bocavirus were more common in younger children, while coronavirus and influenza were more frequently detected in adults; respiratory syncytial virus peaked in older adults too. A higher prevalence of influenza virus B and adenovirus in children, and of influenza virus A and parainfluenza 2 in adults with severeversus non-severe acute asthma suggests a potential association with more severe acute attacks.Conclusion Respiratory viruses are common in both stable and acute asthma. This suggests that the diagnostic value of a positive viral test during acute episodes may be limited and could benefit from complementary biomarkers to improve interpretation.Copyright ©The authors 2026 This version is distributed under the terms of the Creative Commons Attribution Non- Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions@ersnet.org Received: 30 July 2025 Accepted: 9 Feb 2026https://doi.org/10.1183/16000617.0179-2025 Eur Respir Rev 2026; 35: 250179EUROPEAN RESPIRATORY REVIEW REVIEW S ANANTH ET AL. ### Page 2 IntroductionAsthma remains a major cause of morbidity, mortality and healthcare expenditure worldwide [1, 2] owing to its complex and heterogeneous nature, which necessitates a personalised approach to assessment and management [3]. Viruses, frequently detected in both stable and acute asthma, represent a potentially treatable trait [3]. Indeed, there are indications that viral presence during stable disease may be associated with poorer asthma control, more frequent acute attacks and reduced lung function [4–6]. Although the mere detection of any virus may not be linked to the severity or recovery from acute attacks, the presence of specific viral pathogens, such as rhinovirus, has been associated with adverse outcomes, including prolonged symptom duration and an increased risk of hospitalisation [7]. Despite growing evidence that viruses play a pivotal role in asthma, data on the prevalence and clinical burden of the various respiratory viruses in this patient group remain insufficient [8]. These data are essential to guide the development of targeted preventive and therapeutic strategies, including vaccines and antivirals for the more prevalent and burdensome viruses. Building on these gaps, previous systematic reviews have addressed the prevalence of viruses in asthma. However, these have focused exclusively on acute attacks and not on stable disease [9–12]. Moreover, some of these reviews are now outdated, and others exhibit methodological shortcomings, such as insufficient literature searches, limited quality appraisal or suboptimal statistical approaches. To address this gap, we performed a systematic review and meta-analysis to quantify the prevalence of respiratory viruses in both acute and stable asthma among children and adults, adhering to rigorous methodological standards. Through meta-regression analyses, we also investigated clinical and methodological factors that may be associated with higher viral prevalence and greater acute asthma severity, aiming to better understand the drivers of viral burden in asthma.MethodsThis systematic review and meta-analysis was prospectively registered with the International Prospective Register for Systematic Reviews (PROSPERO, ID: CRD42023375108) and its protocol was published [8]. The methodology adhered to the Cochrane Collaboration and Grading of Recommendations Assessment, Development and Evaluation (GRADE) guidelines and was reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) framework [13, 14].Search strategy and selection criteriaWe systematically searched MEDLINE, Embase and the Cochrane Library from inception to 31 August 2024, without language restrictions. We used a structured search strategy which aimed to identify studies focusing on asthma and viruses (supplement 1.1). Additionally, we identified relevant studies by screening the reference lists of all included articles and relevant systematic reviews. Duplicate records were removed using EndNote v20 software (Clarivate, Philadelphia, PA, USA) prior to screening. We included studies that assessed the prevalence of respiratory viruses in individuals with stable and/or acute asthma. We accepted any recognised definition of asthma, with a clinician’s diagnosis deemed sufficient for inclusion. We also accepted any recognised definition of acute (exacerbated) asthma. In the absence of reported acute symptoms, asthma was classified as stable. Only studies using molecular techniques, such as PCR or real-time PCR to detect viruses in respiratory samples (e.g. sputum, nasal or pharyngeal swabs, or bronchoalveolar lavage fluid), were considered. We included studies of any design that assessed unselected study participants for the presence of respiratory viruses; we excluded those that selectively tested only individuals with acute asthma based on symptoms suggestive of a viral trigger. We also excluded studies focusing on specific high-risk groups, such as those with known underlying immunodeficiency. To ensure consistency, we excluded studies conducted since the onset of the COVID-19 pandemic owing to potential confounding from altered respiratory virus epidemiology and changes in public health measures and population behaviour [15, 16]. Studies were categorised based on the predominant age of participants: those primarily including participants ⩾16 years were classified as adult studies, while those focusing on participants <16 years were classified as paediatric. This age threshold aligns with the typical transition of asthma patients from paediatric to adult healthcare services.Data extraction and managementTwo authors independently screened titles and abstracts for eligibility, followed by full-text screening of potentially eligible studies. Data extraction was performed using a prospectively designed and pilot-tested spreadsheet. Main study characteristics and baseline data were extracted by one author and verified by ahttps://doi.org/10.1183/16000617.0179-2025 2 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 3 second author, while data around the prevalence of viruses were extracted by two authors independently. Detailed data extraction parameters are available in supplement 1.2. Discrepancies were resolved through discussion, involving a third senior author if necessary.OutcomesThe primary outcome was the prevalence of specific respiratory viruses in stable and acute asthma among paediatric and adult populations. Additionally, we assessed the prevalence of any respiratory virus in studies evaluating at least three viruses, including rhinovirus. As secondary outcomes, we quantified the prevalence of respiratory viruses in severe acute asthma, defined as acute asthma necessitating hospital admission, and in not-necessarily severe acute asthma, defined as asthma attacks that were assessed in the community or the emergency department that may or may not have necessitated a hospital admission. We also examined the proportion of participants testing positive for multiple viruses and compared the viral loads between stable and acute asthma. Planned analyses of seasonal variability in virus prevalence and viral loads were not conducted owing to insufficient comparable data.Risk of bias and certainty of evidence assessmentRisk of bias at the study level was appraised using the HOY et al. [17] tool, specifically designed for prevalence studies, therefore rigorously assessing representativeness of the study participants. Risk of bias assessment was performed in duplicate and disagreements were resolved as described previously. We employed the GRADE methodology to assess the certainty of the evidence on the prevalence of respiratory viruses in stable and acute asthma [14]. Because no official guidance exists for applying GRADE to prevalence studies, and observational designs are optimal for this purpose, we opted to begin our GRADE assessments at a high-certainty assumption.Statistical analysisTo accommodate the anticipated significant clinical and methodological heterogeneity, we performed a random-effects meta-analysis of proportions using the inverse variance method and Freeman–Tukey double arcsine transformation [18, 19]. Heterogeneity was assessed using the I2 statistic. Publication bias was assessed using funnel plots, plotting sample size against viral prevalence, which is more accurate for meta-analyses of proportions [20]. Internal validation was performed using a leave-one-out sensitivity analysis. For the stable asthma analyses, we also performed a sensitivity analysis restricted to studies enrolling participants who were free of any acute respiratory infection or exacerbation symptoms for at least 4 weeks. Meta-regression analyses were performed using random-effect models to evaluate the impact of the following variables on the primary outcomes: participant age, asthma state (stable or acute), acute asthma severity, study publication year, the proportion of samples that were collected during the influenza season, Global Initiative for Asthma (GINA) asthma severity [21], proportion of participants using inhaled corticosteroids (ICS) and the percentage of participants vaccinated for influenza. Meta-regression analyses were conducted using a random-effects model, with inverse-variance weights incorporating between-study variance (τ2 ) estimates from the primary meta-analysis. Statistical significance was assessed using the Knapp–Hartung method. Additionally, sensitivity analyses were conducted by restricting to studies with a low risk of bias and by performing meta-analyses using fixed-effects models. Statistical analysis was performed using R (R Foundation, Vienna, Austria; version 4.4.1). Further details are available in supplement 1.3.ResultsStudy selection and baseline characteristicsAfter deduplication, we screened 25 166 abstracts, identifying 399 as potentially eligible. Following full-text assessment, 280 studies were excluded for reasons detailed in figure 1. Ultimately, 110 reports describing 111 studies were included in our meta-analysis (table S1). The included studies were globally representative (figure 2). Of the included reports, 66 assessed children [7, 22–86] and 46 assessed adults [4–6, 53, 87–127]. In paediatric studies, 28 investigated viruses in stable asthma (overall n=4029 participants; median sample size=137) and 56 in acute asthma (n=9087; median=118). In the adult studies, 20 investigated stable asthma (n=2496; median=93) and 37 investigated acute asthma (n=3988; median=76). Across paediatric and adult populations, 25 studies concurrently evaluated stable and acute asthma within the same cohort.https://doi.org/10.1183/16000617.0179-2025 3 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 4 The main baseline characteristics of study participants are summarised in table S1, although not all variables were consistently reported across the included studies. The definitions of asthma, including stable and acute forms, are summarised in table S2. Based on the available data, among paediatric participants the mean age was 7.5 years and 60.6% were male. The average forced expiratory volume in 1 s (FEV 1 )/ forced vital capacity (FVC) ratio was 0.84 and no participants had a history of smoking. ICS use ranged between 20.0% and 100% across studies (median=68.6%). Adult participants had a mean age of 44.2 years, with 35.2% being male. The average FEV 1/FVC ratio was 0.76. ICS use varied between 8.9% and 100% across studies (median=71.7%). Smoking status was infrequently documented across adult studies, with current smokers comprising 0.0–50.0% of participants, ex-smokers 0.0–48.3% and never-smokers 47.6–100%. Influenza vaccination history and number of acute events during the preceding year were reported very rarely across all included studies.Risk of bias assessmentOverall, 68.5% of studies (76 out of 111) were rated as low risk of bias and 31.5% (35 out of 111) as moderate risk of bias (table S3), with none classified as high risk of bias. However, domain-specific concerns were noted: 96.4% lacked clear random selection of participants, 92.8% had non-response bias risk, 50.5% showed limited sample representativeness and 38.7% had inadequate case definitions.IdentificationScreeningIncluded Records identified from: Databases (n=28702) Reference lists (n=4) Records screened (n=25166) Records excluded (n=24767) Reports sought for retrieval (n=399) Reports not retrieved (n=9) Reports assessed for eligibility (n=390) Studies included in review (n=111) Reports of included studies (n=110) Studies excluded (n=280) Conference abstract (n=168) Not asthma patients (n=28) Not original research (n=14) Did not report virus prevalence data (n=44) Did not use molecular techniques (n=12) Not full-length report (n=12) English translation not possible (n=1) Unfinished work (n=1) Records removed before screening: Duplicate records removed (n=3540)FIGURE 1 Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) flow diagram. https://doi.org/10.1183/16000617.0179-2025 4 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 5 Prevalence of respiratory virusesThe main results of our meta-analysis are summarised in figures 3 and 4, with detailed summaries provided in supplement 1 and full analytical outputs in supplements 2 and 3. Among 21 studies comprising 4238 participants, the prevalence of any respiratory virus in children with stable asthma was estimated at 33.9% (95% confidence interval (CI) 24.8–43.7%). In adults with stable asthma, based on 16 studies with 1363 participants, the prevalence was 23.0% (95% CI 12.9–35.0%). There was no significant difference in the overall viral prevalence between children and adults. Rhinovirus, the most frequently detected virus in stable asthma, was identified more often in children (25.1%, 95% CI 18.1–32.7%) than in adults (11.6%, 95% CI 5.7–19.3%; p=0.001). No other significant differences were observed in the prevalence of various respiratory viruses between children and adults with stable asthma. In stable asthma, the average prevalence of other respiratory viruses did not exceed 10.0%. Among 44 studies comprising 6669 participants, the prevalence of any respiratory virus in children with acute asthma was estimated at 58.8% (95% CI 52.5–65.0%). In adults with acute asthma, based on 29 studies including 2871 participants, the prevalence was 49.9% (95% CI 41.2–58.5%). The overall viral prevalence did not significantly differ between paediatric and adult populations. Rhinovirus was the most frequently detected virus in acute asthma and was significantly more prevalent among children (45.0%, 95% CI 39.0–51.0%) than among adults (21.2%, 95% CI 4.4–28.9%; p<0.001). Respiratory syncytial virus (RSV) was also more common in children (8.7%, 95% CI 6.6–11.2%) than in adults (3.3%, 95% CI 1.8–5.4%; p<0.001). Bocavirus also appeared more prevalent among children (3.4%, 95% CI 1.6–5.8%,versus 0.3%, 95% CI 0.0–1.3%), although this difference did not reach statistical significance ( p=0.064). By contrast, coronavirus was more frequently detected in adults (5.9%, 95% CI 4.0–8.1%) versus children with acute asthma (2.6%, 95% 2.0–3.3%; p<0.001). Influenza also appeared to be more prevalent in adults (8.8%, 95% CI 6.1–11.8%) than in children (5.5%, 95% CI 3.5–7.8%), but the difference did not reach statistical significance ( p=0.062). Our meta-analyses revealed similar prevalence between children and adults in metapneumovirus (3.7%, 95% CI 2.6–4.9% and 3.7%, 95% CI 2.4–5.3%), parainfluenza (3.3%, 95% CI 2.3–4.4% and 3.7%, 95% CI 2.1–5.8%) and adenovirus (2.5%, 95% CI 1.4–3.9% and 1.6%, 95% CI 1.0–2.3%). Our analysis revealed an increased prevalence of viral detection in acute compared with stable asthma, both among children ( p<0.001) and adults ( p<0.001). Among children with acute versus stable asthma, these differences appeared to be driven by an increased prevalence of rhinovirus ( p<0.001), RSV ( p<0.001) and metapneumovirus ( p<0.001). Among adults, only rhinovirus ( p=0.044) was observed significantly more frequently during acute asthma. The prevalence of viruses was similar between cases of acute severe asthma (necessitating hospital admission) and those presenting to primary care or emergency departments (with moderate or severe acute asthma) in both children and adults (figures 5 and 6). Influenza virus B was significantly more prevalent6000 5000 4000 3000 2000 1000 Participants per continentFIGURE 2 Number of participants included in the meta-analyses, per continent. Darker shades of green indicate a higher number of participants from the respective continent. https://doi.org/10.1183/16000617.0179-2025 5 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 6 44 (6669) 21 (4238) 46 (5395) 27 (12 074) 8 (856) 4 (1842) 7 (728) 4 (1842) 9 (887) 4 (1842) 39 (5104) 18 (3671) 18 (2589) 11 (2134) 17 (2407) 11 (2134) 26 (3629) 17 (2842) 41 (5525) 18 (3674) 4 (604) 3 (533) 4 (604) 3 (533) 31 (4378) 14 (3321) 37 (5192) 19 (4211) 12 (1619) 6 (1862) 11 (1565) 6 (1862) 12 (1619) 6 (1862) 3 (377) 3 (489) 37 (5162) 18 (2407) 17 (2368) 11 (1999) Moderate Moderate Moderate Moderate Low Moderate Low Moderate Low Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Low Low Low Low Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Low Low Moderate Moderate Moderate Moderate 95.32 96.73 94.72 95.94 84.89 26.74 44.79 90.55 90.67 83.52 86.8 93.66 88.57 83.32 29.98 0 26.45 70.95 89.65 82.15 91.56 22.46 48.43 61.31 77.86 46.1 75.68 77.9 65.78 19.05 55.44 46.3 78.35 63.79 69.79 0 76.02 95.62 86.5 55.44 58.78 (52.45–64.97) 33.91 (24.76–43.72) 44.97 (39–51.02) 25.05 (18.12–32.69) 16.91 (10.81–24.04) 10.44 (9.07–11.89) 2.88 (1.36–4.93) 5.57 (1.77–11.31) 35.64 (25.74–46.2) 3.76 (1.21–7.64) 5.45 (3.54–7.74) 4.35 (1.52–8.53) 6.01 (3.48–9.17) 3.15 (0.86–6.8) 1.16 (0.7–1.73) 0.6 (0.2–1.05) 2.61 (1.97–3.34) 2.98 (1.7–4.59) 8.73 (6.58–11.15) 2.56 (1.33–4.18) 2.32 (0–8.2) 1.15 (0.14–2.97) 3.41 (1.58–5.88) 1.83 (0.14–5.1) 3.65 (2.59–4.88) 0.9 (0.42–1.54) 3.26 (2.27–4.41) 2.56 (1.46–3.95) 1.16 (0.41–2.28) 0.39 (0.07–0.94) 0.49 (0.07–1.22) 0.33 (0–1.05) 1.9 (0.62–3.82) 0.86 (0.04–2.59) 2.31 (0.19–6.42) 0.03 (0–0.51) 2.47 (1.39–3.85) 5.51 (1.2–12.68) 3.35 (1.56–5.78) 1.37 (0.57–2.49) Any virus Rhinovirus Rhinovirus A Rhinovirus B Rhinovirus C Influenza Influenza A Influenza B Coronavirus Respiratory syncytial virus Respiratory syncytial virus A Respiratory syncytial virus B Metapneumovirus Parainfluenza Parainfluenza 1 Parainfluenza 2 Parainfluenza 3 Parainfluenza 4 Adenovirus Bocavirus Virus Prevalence, % I2 , % CertaintyParticipants, n (N) 60 7050403020100 Prevalence (95% CI)FIGURE 3 Prevalence of respiratory viruses in paediatric asthma (red diamond: acute asthma; blue diamond: stable asthma). Prevalence reported as the percentage estimate with 95% confidence intervals (CIs). I 2 represents the heterogeneity. https://doi.org/10.1183/16000617.0179-2025 6 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 7 29 (2871) 16 (1363) 27 (2664) 17 (1773) 5 (496) 2 (96) 5 (262) 1 (32) 4 (241) 28 (3208) 14 (1213) 15 (1455) 11 (1106) 15 (1385) 11 (1106) 18 (2078) 11 (1085) 25 (2468) 14 (1295) 5 (262) 3 (217) 5 (262) 3 (217) 15 (1609) 9 (686) 26 (2656) 12 (691) 7 (274) 4 (328) 7 (274) 4 (328) 7 (274) 4 (328) 3 (108) 3 (308) 21 (2047) 10 (676) 5 (284) 3 (166) Moderate Moderate Moderate Moderate Low Very low Low Very low Low Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Low Low Low Low Moderate Low Moderate Low Low Low Low Low Low Low Very low Low Moderate Low Low Very low 93.15 94.47 92.24 90.67 77.46 87.51 75.72 0 85.13 87.87 70.29 90.34 25.77 11.32 68.71 84.3 76.13 88.62 40.66 91.23 0 94.07 50.03 71.79 76.58 46.98 27.48 0 3.84 48.93 77.24 55.84 0 14.95 24.6 23.92 0 62.77 49.86 (41.24–58.48) 22.98 (12.86–35) 21.18 (14.35–28.94) 11.64 (5.72–19.28) 15.73 (8.95–23.97) 17.87 (1.56–45.3) 6.43 (1.14–15.36) 9.38 (1.25–22.41) 11.23 (7.54–15.54) 8.75 (6.13–11.79) 4.47 (1.31–9.36) 9.55 (6.61–12.97) 4.57 (0.81–11.09) 1.74 (0.94–2.76) 0.81 (0.25–1.66) 5.88 (4.01–8.08) 4.95 (2.31–8.52) 3.33 (1.75–5.4) 4.24 (0.85–10) 3.76 (1.17–7.63) 8.47 (0–29.39) 1.86 (0.51–3.91) 10.73 (0–38.98) 3.69 (2.36–5.3) 1.56 (0.27–3.77) 3.72 (2.09–5.79) 2.86 (1.4–4.81) 2.46 (0.62–5.35) 0.67 (0.02–1.92) 1.1 (0.07–3.05) 0.77 (0.05–2.07) 7.67 (1.65–17.36) 2.57 (0.39–6.38) 0.26 (0–2.56) 0.38 (0–1.82) 1.62 (1.02–2.34) 1.36 (0.46–2.69) 0.25 (0–1.3) 1.69 (0–6.67) Any virus Rhinovirus Rhinovirus A Rhinovirus B Rhinovirus C Influenza Influenza A Influenza B Coronavirus Respiratory syncytial virus Respiratory syncytial virus A Respiratory syncytial virus B Metapneumovirus Parainfluenza Parainfluenza 1 Parainfluenza 2 Parainfluenza 3 Parainfluenza 4 Adenovirus Bocavirus Virus Prevalence, % I2 , % CertaintyParticipants, n (N) 60 7050403020100 Prevalence (95% CI)FIGURE 4 Prevalence of respiratory viruses in adult asthma (red diamond: acute asthma; blue diamond: stable asthma). Prevalence reported as the percentage estimate with 95% confidence intervals (CIs). I 2 represents the heterogeneity. https://doi.org/10.1183/16000617.0179-2025 7 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 8 19 (3864) 22 (2612) 20 (2788) 23 (2414) 5 (602) 3 (254) 5 (602) 2 (126) 5 (602) 4 (285) 17 (2795) 20 (2143) 10 (1471) 8 (1118) 9 (1132) 8 (1275) 11 (1911) 13 (1552) 18 (2845) 21 (2514) 3 (393) 1 (211) 3 (393) 1 (211) 13 (2209) 16 (2003) 17 (2795) 18 (2231) 4 (562) 8 (1057) 4 (562) 7 (1003) 4 (562) 8 (1057) 2 (323) 1 (54) 15 (2655) 21 (2442) 8 (998) 8 (1305) Moderate Moderate Moderate Moderate Low Low Low Very low Low Low Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Low Low Low Low Moderate Moderate Moderate Moderate Low Moderate Low Moderate Low Moderate Low Very low Moderate Moderate Low Moderate 93.09 96.59 93.56 95.65 48.37 93.86 25.3 58.56 90.7 92.82 88.87 85.49 91.96 74.87 0 25.92 53.19 0 87.63 91.39 93.77 NA 55.16 NA 86.67 66.59 78.65 75.01 83.59 48.17 33.91 66.45 78.29 79.59 83.57 NA 33.27 81.9 90.76 76.4 59.54 (51.84–67.01) 56.01 (45.46–66.28) 49.95 (38.54–55.45) 41.34 (32.45–50.53) 18.01 (13.63–22.85) 14.89 (2.18–35.8) 2.3 (1.1–3.91) 5.18 (0.67–13.02) 38.42 (26.97–50.57) 31.44 (14.15–51.92) 4.67 (2.34–7.74) 6.84 (3.34–11.47) 4.25 (1.39–8.55) 8.43 (5.13–12.44) 0.62 (0.22–1.2) 1.66 (1–2.49) 2.73 (1.54–4.24) 2.57 (1.84–3.42) 8.15 (5.33–11.49) 9.85 (6.52–13.76) 2.31 (0–11.65) 1.9 (0.41–4.27) 3.72 (1.26–7.33) 2.37 (0.67–4.94) 2.74 (1.3–4.67) 4.36 (2.87–6.15) 3.51 (2.07–5.31) 3.34 (1.91–5.16) 1.27 (0–4.45) 1.02 (0.3–2.13) 0.41 (0–1.4) 0.47 (0–1.7) 1.66 (0.1–4.82) 2.06 (0.36–5.02) 1.62 (0–7.59) 3.7 (0.06–10.84) 1.19 (0.64–1.89) 4 (1.7–7.2) 3.74 (0.62–9.25) 3.39 (1.61–5.78) Any virus Rhinovirus Rhinovirus A Rhinovirus B Rhinovirus C Influenza Influenza A Influenza B* Coronavirus Respiratory syncytial virus Respiratory syncytial virus A Respiratory syncytial virus B Metapneumovirus Parainfluenza Parainfluenza 1 Parainfluenza 2 Parainfluenza 3 Parainfluenza 4 Adenovirus* Bocavirus Virus Prevalence, % I2 , % CertaintyParticipants, n (N) 60 7050403020100 Prevalence (95% CI)FIGURE 5 Prevalence of respiratory viruses in severe versus non-severe acute attacks in paediatric asthma (dark red diamond: acute severe asthma; orange diamond: acute moderate/severe asthma). Prevalence reported as the percentage estimate with 95% confidence intervals (CIs). I2 represents the heterogeneity. *: statistically significant difference between severe and non-severe acute asthma attacks. https://doi.org/10.1183/16000617.0179-2025 8 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 9 10 (629) 18 (2217) 10 (617) 16 (2022) 2 (43) 3 (453) 2 (43) 2 (194) 1 (22) 2 (194) 10 (684) 18 (2524) 4 (191) 11 (1264) 4 (191) 11 (1194) 6 (462) 12 (1616) 11 (703) 14 (1765) 2 (86) 3 (176) 2 (86) 3 (176) 4 (177) 11 (1432) 11 (703) 15 (1953) 5 (204) 2 (70) 5 (204) 2 (70) 5 (204) 2 (70) 2 (86) 1 (22) 10 (639) 11 (1408) 2 (92) 3 (192) Low Moderate Low Moderate Very low Low Very low Very low Very low Very low Low Moderate Very low Moderate Very low Moderate Low Moderate Low Moderate Very low Very low Very low Very low Very low Moderate Low Moderate Low Very low Low Very low Low Very low Very low Very low Low Moderate Very low Very low 92.75 93.46 86.53 92.42 0 87 50.36 0 NA 0 82.87 83.76 53.71 67.69 0 31.89 64.14 69.58 85.59 58.28 9.34 64.52 0 0 55.71 51.52 84.2 67.63 27.17 40.16 0 40.16 84.36 0 0 NA 0 50.3 0 0 50.59 (32.88–68.23) 47.17 (38.5–55.92) 16.48 (8.17–26.96) 20.58 (13.29–29) 19.03 (8.53–32.22) 14.47 (5.99–25.8) 11.59 (1.29–28.66) 1.25 (0.07–3.42) 9.09 (0.18–25.49) 11.02 (6.96–15.84) 5.98 (2.38–11.04) 10.29 (7.05–14.05) 3.71 (0.58–9.06) 11.59 (8.39–15.23) 2.77 (0.83–5.65) 1.51 (0.71–2.6) 8.9 (4.56–14.49) 4.83 (2.93–7.17) 4.39 (1.03–9.84) 2.84 (1.63–4.37) 3.33 (0.25–8.88) 3.9 (0.22–11.07) 1.39 (0–5.32) 1.85 (0.25–4.58) 2.56 (0.08–7.6) 3.89 (2.47–5.63) 4.88 (1.27–10.59) 3.18 (1.73–5.03) 1.89 (0.16–5.07) 3.54 (0–12.09) 0.35 (0–1.82) 3.54 (0–12.09) 7.91 (0.26–23.62) 7.63 (2.38–15.19) 0.12 (0–2.63) 0 (0–7.67) 1.17 (0.46–2.17) 1.89 (0.96–3.1) 0.1 (0–2.45) 0.15 (0–1.45) Any virus Rhinovirus Rhinovirus A Rhinovirus B* Rhinovirus C Influenza Influenza A* Influenza B Coronavirus Respiratory syncytial virus Respiratory syncytial virus A Respiratory syncytial virus B Metapneumovirus Parainfluenza Parainfluenza 1 Parainfluenza 2* Parainfluenza 3 Parainfluenza 4 Adenovirus Bocavirus Virus Prevalence, % I2, % CertaintyParticipants, n (N) 60 7050403020100 Prevalence (95% CI)FIGURE 6 Prevalence of respiratory viruses in severe versus non-severe acute attacks in adult asthma (dark red diamond: acute severe asthma; orange diamond: acute moderate/severe asthma). Prevalence reported as the percentage estimate with 95% confidence intervals (CIs). I 2 represents the heterogeneity. *: statistically significant difference between severe and non-severe acute asthma attacks. https://doi.org/10.1183/16000617.0179-2025 9 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 10 among children with acute severe asthma compared with moderate/severe acute asthma (1.7%, 95% CI 1.0–2.5%, versus 0.6%, 95% CI 0.2–1.2%; p=0.02). A statistically significant difference was also observed for adenovirus (4.0%, 95% CI 1.7–7.2%, versus 1.2%, 95% CI 0.6–1.9%; p=0.03). In severe acute asthma in adults, we found increased prevalence compared with moderate/severe asthma of influenza virus A (11.6%, 95% CI 8.4–15.2%, versus 3.7%, 95% CI 0.6–9.1%) and parainfluenza 2 (3.5%, 95% CI 0.0–12.1%,versus 0.4%, 95% CI 0.0–1.8%). Conversely, the prevalence of rhinovirus B was significantly reduced in severe acute asthma compared with moderate/severe asthma (1.3%, 95% CI 0.1–3.4%, versus 11.6%, 95% CI 1.3–28.7%). During stable disease state, co-detection of two or more viruses was infrequent, observed in 2.0% (95% CI 0.0–6.0%) of children and 0.0% (95% CI 0.0–2.0%) of adults. In contrast, during the acute state, co-detection increased significantly, occurring in 9.0% (95% CI 6.0–12.0%) of children (p=0.013) and 3.0% (95% CI 1.0–5.0%) of adults ( p=0.023). Viral load data are summarised in supplement 1.4.Meta-regression and sensitivity analysesHigh I2 estimates and wide prediction intervals across most of the conducted meta-analyses revealed substantial heterogeneity. Meta-regression analyses showed limited effect of accounting for the publication year, baseline ICS use or participant mean age on heterogeneity. Notably, paediatric studies demonstrated a clear association between younger age and a higher prevalence of RSV, metapneumovirus and bocavirus, whereas in adults RSV prevalence was greater in studies involving older populations. Moreover, a higher proportion of participants receiving ICS was strongly associated with a higher prevalence of rhinovirus and parainfluenza in adults with acute asthma ( p=0.008 and 0.003, respectively). Limited availability of data on asthma severity, influenza vaccination status and the proportion of samples collected during influenza season across the included studies rendered the respective analyses ineffective. Our findings remained robust in sensitivity analyses only including studies at a low risk of methodological bias and those performed using fixed-effect models meta-analysis (supplement 3: figures S116 and S117). Sensitivity analyses restricted to studies enrolling participants with stable asthma who were free of acute symptoms for at least 4 weeks were generally consistent with the main analyses, except for some that were based on very small populations (<100 participants), for which estimates were less certain. The only notable difference was a lower rhinovirus prevalence in children with stable asthma (1.1%, 95% CI 0.0–3.8%, compared to 5.5%, 95% CI 1.2–12.7%, in the main analysis), despite this analysis being informed by over 1100 participants.Publication bias, internal validation and certainty of evidenceFunnel plots showed no evidence of publication bias. Most analyses were robust to leave-one-out sensitivity analyses. Only certain viral subtypes, such as RSV A/B, parainfluenza 3 and coronaviruses, were sensitive to the omission of specific studies, likely reflecting small study effects or local epidemic dynamics. The certainty of evidence regarding the prevalence of any virus and regarding most of the specific viral genera assessed was rated as moderate, whereas evidence related to viral species ranged from low to moderate. The primary reason for downgrading the certainty of evidence was inconsistency, attributable to significant variability in viral prevalence estimates across the included studies. Additionally, some meta-analyses of viral species were downgraded due to imprecision, because their estimates were based on very limited study populations.DiscussionThis meta-analysis quantifies the prevalence of respiratory viruses in children and adults with asthma, extensively updating the evidence base for acute asthma while, for the first time, aggregating data on stable asthma. We demonstrate with moderate certainty that respiratory viruses are present in 33.9% (95% CI 24.8–43.7%) of children and 23.0% (95% CI 12.9–35.0%) of adults with stable asthma, compared to detection rates of 58.8% (95% CI 52.5–65.0%) in children and 49.9% (95% CI 41.2–58.5%) of adults with acute asthma. Rhinovirus, predominantly rhinovirus A, was the most frequently identified virus across all patient groups. Notably, our analyses revealed that children with severe acute asthma requiring hospitalisation had a higher prevalence of influenza virus B and adenovirus compared with those managed as outpatients, suggesting an association with more severe attacks. In adults, influenza virus A and parainfluenza 4 were significantly more prevalent in severe cases, whereas rhinovirus B was less frequently detected. In acute asthma, RSV was more common in preschoolers and older adults, bocavirus was most frequently detected in the youngest children, and metapneumovirus was more prevalent in younger than inhttps://doi.org/10.1183/16000617.0179-2025 10 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 11 older children. Conversely, coronavirus and, possibly, influenza appeared more frequently in adults with acute asthma than in children, although the latter did not reach statistical significance. The high prevalence of respiratory viruses in stable asthma suggests that their mere detection in an acute attack does not necessarily imply a viral trigger, because they could also represent an “innocent bystander”. Consequently, the diagnostic value of a positive viral sample during an acute event needs to be further evaluated or strengthened by other biomarkers. Additionally, a positive viral PCR in stable asthma may reflect asymptomatic carriage rather than a true trigger, underscoring the need to better understand its clinical relevance. In parallel, respiratory viruses, particularly rhinoviruses, were more frequently detected in children, likely reflecting both higher exposure (e.g. school, daycare) and age-related differences in innate immunity, such as reduced interferon responses in early childhood [128]. Symptomatic infections represent only a fraction of viral exposures, so asymptomatic carriage is also expected to be more common in children. Interpreting viral prevalence in asthma requires contextualising these findings against baseline rates in the general population. Virus detection rates in acute lower respiratory tract infections do not appear to be lower in the general population than in asthma patients [129, 130]; however, because individuals with asthma experience more frequent acute episodes, their cumulative viral burden is higher [131]. In contrast, during periods without acute illness, respiratory viruses are rarely detected in adults without asthma [132, 133], while detection rates in children remain comparable regardless of asthma status [134, 135]. Notably, the few studies assessing the respiratory virome suggest that eukaryotic viruses may constitute a core component of the virome in both healthy and asthmatic individuals [136, 137]. Thus, it remains unclear whether the presence of viruses in asthma reflects normal viral circulation, an increased susceptibility, delayed viral clearance or an altered immune response, such as an acute or pre-exacerbation state. Notably, there is no evidence supporting persistent airway colonisation by respiratory viruses. These findings underscore the need to interpret viral detection within its clinical context and highlight the importance of developing tailored diagnostic strategies. Current preventive and therapeutic strategies are limited to addressing acute asthma exacerbations associated with influenza, RSV and COVID-19 [138]. Advancing our understanding of how viruses trigger, or fail to trigger, acute attacks, and developing robust methods to accurately identify these viral triggers, is essential for devising novel, targeted interventions. This study adds important new insights into the role of respiratory viruses in asthma. By providing the first large-scale quantification of viral detection in stable asthma, our findings establish baseline rates of PCR positivity and place acute exacerbation data into clearer context. The detailed stratified analyses across asthma state, age group and exacerbation severity revealed virus-specific patterns, such as the differing prevalence of rhinovirus B, adenovirus, RSV and influenza subtypes, that individual studies were underpowered to detect. These patterns offer new perspectives on the potential viral drivers of exacerbation severity and highlight the distinct contributions of different viruses across age groups. Together, these findings refine our understanding of viral epidemiology in asthma and generate hypotheses for future mechanistic and longitudinal research, including work needed to clarify the clinical significance of viral detection during periods of stability. They may also help guide public health planning by identifying which respiratory viruses contribute most to the burden of acute asthma, thereby informing prioritisation of preventive strategies such as vaccination or antiviral development. Previous meta-analyses focused solely on respiratory virus prevalence during acute asthma exacerbations. While their estimates align broadly with ours, they were based on fewer studies and generally had wider confidence intervals [9–12]. FEDDEMA et al. [12] found higher prevalence of any virus, rhinovirus and RSV in younger compared to older individuals, and the opposite trend for influenza; consistent with our findings. That study also reported lower virus-related exacerbation rates in the Northern Hemisphere, while two meta-analyses identified regional differences [10, 12]. However, these analyses pooled heterogeneous populations (adults and children, various time periods and exacerbation severities), increasing risk of bias. Given these limitations, we opted not to perform geographic subgroup analyses in our review to reduce potential sources of bias. This meta-analysis has several limitations. First, significant unexplained heterogeneity in the viral prevalence estimates across the included studies led to downgrading the certainty of evidence of all analyses due to inconsistency. The impact of seasonal fluctuations in viral prevalence (e.g. influenza peaks in winter and rhinovirus in spring/autumn), micro-epidemics, variation in treatments (e.g. higher ICS doseshttps://doi.org/10.1183/16000617.0179-2025 11 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 12 are associated with an increased risk of viral infections) and differences in influenza vaccination history on respiratory viral prevalence are well studied [138]. We attempted to explain the observed variability by accounting for these factors in meta-regression analyses, but these were limited by inconsistent reporting of the relevant data across the included studies. Differences in sampling methods, sample handling and the performance characteristics of viral diagnostic techniques across studies are also likely to have contributed to the observed between-study heterogeneity. Second, while all studies were found to be at low or moderate risk of bias, the vast majority were found to be at a potential risk of selection and non-response bias, and this should be considered in the interpretation of the results. Additionally, several studies lacked clear definitions of acute and stable asthma, underreported key participant characteristics, and provided limited information on the timing of sample collection during acute episodes. Third, most studies employed upper respiratory samples, with only a few small studies assessing lower respiratory tract specimens, precluding a meaningful subgroup analysis. This is a notable limitation, because viral detection in the lower airways is likely to be more clinically relevant in acute events, where the transmission of viruses from the upper to the lower respiratory tract may trigger an asthma attack [138]. Fourth, we relied on clinician-diagnosed asthma, which may introduce some degree of misclassification bias; however, this pragmatic approach reflects real-world practice and is commonly adopted in large epidemiological studies to ensure broader generalisability. Moreover, we used hospitalisation as a surrogate for exacerbation severity, recognising that admission decisions may be influenced by contextual factors such as social and frailty drivers. However, given the predominantly young study populations and the widespread use of hospital admission as a severity marker, we believe this remains an appropriate and inclusive measure for our analysis. Fifth, in the absence of adequate relevant data, we were not able to address some of the prespecified objectives, namely, to compare the viral loads of respiratory viruses during stable and acute asthma and to describe the seasonality of various respiratory viruses. Sixth, low-income countries were absent from our sample, with only two studies originating from lower-middle-income economies per World Bank classifications, and African populations were notably underrepresented. Last, studies conducted after the onset of the COVID-19 pandemic were deliberately excluded to avoid pandemic-related confounding. A future update of this review will be necessary to investigate any shifts in respiratory viral epidemiology attributable to the pandemic. However, this meta-analysis of 111 studies from six continents has several strengths, including a prospective and transparent design that aligns with Cochrane guidance, ensuring methodological rigour, a highly sensitive search strategy, comprehensive quality assessments of the included studies and body of evidence for each outcome, and the application of robust statistical methods. Future research must address the complexities of viral pathogen assessment in asthma through large-scale, prospective cohorts that capture seasonal variability and clinical burden. International collaboration, standardised viral assessments and robust data sharing are essential to build a comprehensive evidence base. Meanwhile, an individual participant data meta-analysis could offer detailed, cost-effective insights to inform targeted preventive and therapeutic strategies, including vaccines and antivirals, ultimately improving global asthma outcomes. In conclusion, this study quantifies respiratory virus prevalence in both acute and stable asthma among adults and children, providing the first aggregate data on stable asthma, and reveals a notable prevalence, with adults exhibiting higher rates compared to healthy individuals. It also offers indirect evidence linking certain viruses to more severe acute attacks, underscoring the complexities of viral involvement in asthma. By integrating stratified analyses and applying a rigorous, prospectively registered methodology, this work enhances the evidence base and identifies key areas for future investigation, ultimately supporting more precise and effective approaches to asthma care.Points for clinical practice• Respiratory viruses are common in both stable and acute asthma, in children and adults.• Rhinovirus is the most frequently detected virus, particularly during an acute asthma attack.• Influenza virus B and adenovirus may be associated with more severe acute asthma in children.• Influenza virus A and parainfluenza 4 may be associated with more severe acute asthma in adults.• The diagnostic value of a positive viral test during acute episodes may be limited and could benefit from complementary biomarkers to improve interpretation. https://doi.org/10.1183/16000617.0179-2025 12 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 13 Data availability: All data extracted from the included studies will be made available on request. Provenance: Submitted article, peer reviewed. The systematic review protocol was registered with PROSPERO (https://www.crd.york.ac.uk/prospero/) with identifier: CRD42023375108. Author contributions: Study conception: S. Ananth, G.S. Alimani, J. Vestbo, A. Beloukas, A.G. Mathioudakis. Study design: S. Ananth, G.S. Alimani, A.G. Mathioudakis. Methodological expertise: A.G. Mathioudakis. Study screening and data extraction: S. Ananth, G.S. Alimani, C. Boccabella, E. Khaleva, J. Hansel, R. Wang. Analysis: S. Ananth, G.S. Alimani, A.G. Mathioudakis. Manuscript preparation: S. Ananth, G.S. Alimani, A.G. Mathioudakis. Critical revision of the manuscript for intellectual content: All authors. All authors had full access to all the data in the study and had final responsibility for the decision to submit the publication. Conflict of interest: S. Ananth, G.S. Alimani, C. Boccabella, E. Khaleva, J. Hansel and R. Wang have nothing to disclose. G. Roberts reports honoraria from ALK-Abello, AstraZeneca, ThermoFisher and Viatris, not related to this work and paid to his institution. C. Kosmidis has nothing to disclose. A. Bossios reports a grant from AstraZeneca; honoraria from Chiesi, GlaxoSmithKline and AstraZeneca; and participation on a Data Safety Advisory Board for AstraZeneca; all paid to his institution and not related to this work. J. Vestbo reports honoraria from AstraZeneca, GlaxoSmithKline, Chiesi and ALK-Abello, not related to this work. E. Papageorgiou has nothing to disclose. N.G. Papadopoulos reports grants from Numil Hellas SA, Vianex and Vibrant America; consulting fees from Abbott Nutrition, HAL Allergy Holding BV, Regeneron Pharmaceuticals Inc and Berlin-Chemie AG; and honoraria from Nestle Nutrition Institute, Numil Hellas SA, GlaxoSmithKline, Menarini International Operations Luxembourg SA, OM Pharma SA and DBV Technologies SA; all paid to his institution and not related to this work. A. Beloukas reports grants or sponsorships from Gilead and GSK/ViiV paid to the University of West Attica; payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Gilead and GSK/ViiV paid to the University of West Attica; support for attending meetings and/or travel from Gilead and GSK/ ViiV; and receipt of equipment, materials, drugs, medical writing, gifts or other services from Cepheid for FOC reagents provided for a research project; all outside the submitted work. A.G. Mathioudakis reports honoraria from GlaxoSmithKline, consulting fees from Sanofi, stock options from Healthy Networks and non-financial support by Verona Pharma, not related to this work. Support statement: J. Hansel, R. Wang, C. Kosmidis and A.G. Mathioudakis were supported by the National Institute for Health and Care Research (NIHR) Manchester Biomedical Research Centre (BRC) (NIHR203308). S. Ananth was supported by an NIHR Academic Clinical Fellowship in Respiratory Medicine, including funding from the NIHR Imperial BRC. J. Hansel was supported by an NIHR Academic Clinical Fellowship in Intensive Care Medicine. A.G. Mathioudakis was supported by an NIHR Clinical Lectureship in Respiratory Medicine (NIHR CL-2021-06-007). R. Wang is funded by NIHR (through an NIHR Clinical Lectureship) and received funding from Asthma+Lung UK (ECSG24\28) and an NIHR Research for Patient Benefit grant (NIHR203591). A. Bossios was supported by a grant from the Swedish Heart and Lung Foundation (HLF 20220478). The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care. The funders had no role in study design, data collection, data analysis, data interpretation or writing of the report. Funding information for this article has been deposited with the Open Funder Registry.References 1 Naghavi M, Ong KL, Aali A, et al. Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021. Lancet 2024; 403: 2100–2132.2 Ferrari AJ, Santomauro DF, Aali A, et al. Global incidence, prevalence, years lived with disability (YLDs), disability-adjusted life-years (DALYs), and healthy life expectancy (HALE) for 371 diseases and injuries in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021. Lancet 2024; 403: 2133–2161.3 Agustí A, Bafadhel M, Beasley R, et al. Precision medicine in airway diseases: moving to clinical practice.Eur Respir J 2017; 50: 1701655.4 Harju TH, Leinonen M, Nokso-Koivisto J, et al. Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma. Thorax 2006; 61: 579–584.5 Walsh LJ, Sullivan A, Ward C, et al. Impact of airway virus in severe asthmatic patients: a pilot study. Allergy Asthma Immunol Res 2023; 15: 406–411.6 Wos M, Sanak M, Soja J, et al. The presence of rhinovirus in lower airways of patients with bronchial asthma. Am J Respir Crit Care Med 2008; 177: 1082–1089. https://doi.org/10.1183/16000617.0179-2025 13 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 14 7 Arden KE, Chang AB, Lambert SB, et al. Newly identified respiratory viruses in children with asthma exacerbation not requiring admission to hospital. J Med Virol 2010; 82: 1458–1461.8 Alimani GS, Ananth S, Boccabella C, et al. Prevalence and clinical implications of respiratory viruses in asthma during stable disease state and acute attacks: protocol for a meta-analysis. PLoS One 2023; 18: e0294416.9 Chen X, Zhang P, Ma Y. Prevalence of acute infection in adults with asthma exacerbation. Ann Thorac Med2023; 18: 132–151.10 Zheng X-Y, Xu Y-J, Guan W-J, et al. Regional, age and respiratory-secretion-specific prevalence of respiratory viruses associated with asthma exacerbation: a literature review. Arch Virol 2018; 163: 845–853.11 Papadopoulos NG, Christodoulou I, Rohde G, et al. Viruses and bacteria in acute asthma exacerbations –A GA 2 LEN-DARE systematic review. Allergy 2011; 66: 458–468.12 Feddema JJ, Claassen E. Prevalence of viral respiratory infections amongst asthmatics: results of a meta-regression analysis. Respir Med 2020; 173: 106020.13 Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021; 372: n71.14 Higgins J, Thomas J, Chandler J, et al. Cochrane Handbook for Systematic Reviews of Interventions version 6.5. Cochrane, 2024. Available from: www.cochrane.org/handbook15 Karcher H, Schoenberger M, Rayban T, et al. Impact of COVID-19 measures on exacerbation rates and healthcare visits in US asthma patients. Allergy Asthma Proc 2023; 44: 422–428.16 Papadopoulos NG, Custovic A, Deschildre A, et al. Impact of COVID-19 on pediatric asthma: practice adjustments and disease burden. J Allergy Clin Immunol Pract 2020; 8: 2592–2599.17 Hoy D, Brooks P, Woolf A, et al. Assessing risk of bias in prevalence studies: modification of an existing tool and evidence of interrater agreement. J Clin Epidemiol 2012; 65: 934–939.18 Munn Z, Moola S, Lisy K, et al. Methodological guidance for systematic reviews of observational epidemiological studies reporting prevalence and cumulative incidence data. Int J Evid Based Healthc 2015; 13: 147–153.19 Barendregt JJ, Doi SA, Lee YY, et al. Meta-analysis of prevalence. J Epidemiol Community Health 2013; 67: 974–978.20 Hunter JP, Saratzis A, Sutton AJ, et al. In meta-analyses of proportion studies, funnel plots were found to be an inaccurate method of assessing publication bias. J Clin Epidemiol 2014; 67: 897–903.21 Reddel HK, Bacharier LB, Bateman ED, et al. Global Initiative for Asthma strategy 2021: executive summary and rationale for key changes. J Allergy Clin Immunol Pract 2022; 10: S1–S18.22 Lopes GP, Amorim ÍPS, Melo B, et al. Identification and seasonality of rhinovirus and respiratory syncytial virus in asthmatic children in tropical climate. Biosci Rep 2020; 40: BSR20200634.23 Jartti T, Liimatainen U, Xepapadaki P, et al. Clinical correlates of rhinovirus infection in preschool asthma.Allergy 2021; 76: 247–254.24 Hassanzad M, Nadji SA, Darougar S, et al. Association of specific viral infections with childhood asthma exacerbations. Interv Med Appl Sci 2019; 11: 17–20.25 Abe N, Yasudo H, Fukano R, et al. Multi-season analyses of causative pathogens in children hospitalized with asthma exacerbation. Pediatr Allergy Immunol 2019; 30: 724–731.26 Merckx J, Ducharme FM, Martineau C, et al. Respiratory viruses and treatment failure in children with asthma exacerbation. Pediatrics 2018; 142: e20174105.27 Robledo Aceves M, Barrón Balderas A, Jaime Ornelas M. Most commonly isolated viruses in asthma exacerbation and their correlation with eosinophil and total serum immunoglobulin E levels. Arch Argent Pediatr 2018; 116: 192–197.28 Deschildre A, Pichavant M, Engelmann I, et al. Virus-triggered exacerbation in allergic asthmatic children: neutrophilic airway inflammation and alteration of virus sensors characterize a subgroup of patients. Respir Res 2017; 18: 191.29 Duenas Meza E, Jaramillo CA, Correa E, et al. Virus and Mycoplasma pneumoniae prevalence in a selected pediatric population with acute asthma exacerbation. J Asthma 2016; 53: 253–260.30 Kato M, Suzuki K, Yamada Y, et al. Virus detection and cytokine profile in relation to age among acute exacerbations of childhood asthma. Allergol Int 2015; 64: S64–S70.31 Stelzer-Braid S, Tovey ER, Willenborg CM, et al. Absence of back to school peaks in human rhinovirus detections and respiratory symptoms in a cohort of children with asthma. J Med Virol 2016; 88: 578–587.32 Prazma CM, Gern JE, Weinstein SF, et al. The association between seasonal asthma exacerbations and viral respiratory infections in a pediatric population receiving inhaled corticosteroid therapy with or without long-acting β-adrenoceptor agonist: a randomized study. Respir Med 2015; 109: 1280–1286.33 Malka J, Covar R, Faino A, et al. The effect of viral infection on exhaled nitric oxide in children with acute asthma exacerbations. J Allergy Clin Immunol Pract 2015; 3: 913–919.34 Amin NM, El Basha NR, El Rifai NM, et al. Viral causes of acute respiratory infection among Egyptian children hospitalized with severe acute asthma exacerbation. J Egypt Public Health Assoc 2013; 88: 52–56. https://doi.org/10.1183/16000617.0179-2025 14 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 15 35 Ozcan C, Toyran M, Civelek E, et al. Evaluation of respiratory viral pathogens in acute asthma exacerbations during childhood. J Asthma 2011; 48: 888–893.36 Rueter K, Bizzintino J, Martin AC, et al. Symptomatic viral infection is associated with impaired response to treatment in children with acute asthma. J Pediatr 2012; 160: 82–87.37 Leung TF, To MY, Yeung ACM, et al. Multiplex molecular detection of respiratory pathogens in children with asthma exacerbation. Chest 2010; 137: 348–354.38 Vallet C, Pons-Catalano C, Mandelcwajg A, et al. Human bocavirus: a cause of severe asthma exacerbation in children. J Pediatr 2009; 155: 286–288.39 Matthew J, Pinto Pereira LM, Pappas TE, et al. Distribution and seasonality of rhinovirus and other respiratory viruses in a cross-section of asthmatic children in Trinidad, West Indies. Ital J Pediatr 2009; 35: 16.40 Chang AB, Clark R, Acworth JP, et al. The impact of viral respiratory infection on the severity and recovery from an asthma exacerbation. Pediatr Infect Dis J 2009; 28: 290–294.41 Saçkesen C, Pinar A, Sekerel BE, et al. Use of polymerase chain reaction for detection of adenovirus in children with or without wheezing. Turk J Pediatr 2005; 47: 227–231.42 Pifferi M, Maggi F, Andreoli E, et al. Associations between nasal torquetenovirus load and spirometric indices in children with asthma. J Infect Dis 2005; 192: 1141–1148.43 Kling S, Donninger H, Williams Z, et al. Persistence of rhinovirus RNA after asthma exacerbation in children.Clin Exp Allergy 2005; 35: 672–678.44 Johnston NW, Johnston SL, Duncan JM, et al. The September epidemic of asthma exacerbations in children: a search for etiology. J Allergy Clin Immunol 2005; 115: 132–138.45 Marin J, Jeler-Kacar D, Levstek V, et al. Persistence of viruses in upper respiratory tract of children with asthma. J Infect 2000; 41: 69–72.46 West JA, Dakhama A, Khan MA, et al. Community study using a polymerase chain reaction panel to determine the prevalence of common respiratory viruses in asthmatic and nonasthmatic children. J Asthma1999; 36: 605–612.47 Freymuth F, Vabret A, Brouard J, et al. Detection of viral, Chlamydia pneumoniae and Mycoplasma pneumoniae infections in exacerbations of asthma in children. J Clin Virol 1999; 13: 131–139.48 Babaei F, Mortazavi HR, Kondori N, et al. Prevalence of respiratory viral infections in children with asthma in Kermanshah. Jundishapur J Microbiol 2021; 14: e100101.49 Jazaeri S, Goldsmith AM, Jarman CR, et al. Nasal interferon responses to community rhinovirus infections are similar in controls and children with asthma. Ann Allergy Asthma Immunol 2021; 126: 690–695.50 Boluk SO, Taskirdi I, Akcal O, et al. Prevalence of viruses in acute asthma exacerbations in childhood in a hospital in west part of turkey. Iran J Allergy Asthma Immunol 2022, 21: 112–118.51 Dinwiddie DL, Kaukis N, Pham S, et al. Viral infection and allergy status impact severity of asthma symptoms in children with asthma exacerbations. Ann Allergy Asthma Immunol 2022; 129: 319–326.52 Sallard E, Schult F, Baehren C, et al. Viral infection and respiratory exacerbation in children: results from a local German pediatric exacerbation cohort. Viruses 2022; 14: 491.53 Bébéar C, Raherison C, Nacka F, et al. Comparison of Mycoplasma pneumoniae infections in asthmatic children versus asthmatic adults. Pediatr Infect Dis J 2014; 33: e71–e75.54 Su YT, Lin YT, Yang CC, et al. High correlation between human rhinovirus type C and children with asthma exacerbations in Taiwan. J Microbiol Immunol Infect 2020; 53: 561–568.55 Lewis TC, Metitiri EE, Mentz GB, et al. Influence of viral infection on the relationships between airway cytokines and lung function in asthmatic children. Respir Res 2018; 19: 228.56 Alsuwaidi AR, Alkalbani AM, Alblooshi A, et al. Nasopharyngeal isolates and their clinical impact on young children with asthma: a pilot study. J Asthma Allergy 2018; 11: 233–243.57 Nguyen-Thi-Dieu T, Le-Thi-Thu H, Le-Thi-Minh H, et al. Study of clinical characteristics and cytokine profiles of asthmatic children with rhinovirus infection during acute asthma exacerbation at national hospital of pediatrics. Can Respir J 2018; 2018: 9375967.58 Costa LDC, Camargos PAM, Brand PLP, et al. Asthma exacerbations in a subtropical area and the role of respiratory viruses: a cross-sectional study. BMC Pulm Med 2018; 18: 109.59 Esquivel A, Busse WW, Calatroni A, et al. Effects of omalizumab on rhinovirus infections, illnesses, and exacerbations of asthma. Am J Respir Crit Care Med 2017; 196: 985–992.60 Zheng SY, Wang LL, Ren L, et al. Epidemiological analysis and follow-up of human rhinovirus infection in children with asthma exacerbation. J Med Virol 2018; 90: 219–228.61 Ducharme FM, Zemek R, Chauhan BF, et al. Factors associated with failure of emergency department management in children with acute moderate or severe asthma: a prospective, multicentre, cohort study.Lancet Respir Med 2016; 4: 990–998.62 Tovey ER, Stelzer-Braid S, Toelle BG, et al. Rhinoviruses significantly affect day-to-day respiratory symptoms of children with asthma. J Allergy Clin Immunol 2015; 135: 663–669. https://doi.org/10.1183/16000617.0179-2025 15 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 16 63 Iwasaki J, Smith WA, Khoo SK, et al. Comparison of rhinovirus antibody titers in children with asthma exacerbations and species-specific rhinovirus infection. J Allergy Clin Immunol 2014; 134: 25–32.64 Yokouchi Y, Katsumori H, Shirakawa S, et al. Protective effects of influenza A (H1N1) pandemic 2009 vaccination against the onset of influenza-like illness and asthma exacerbation in Japanese children.J Asthma 2014; 51: 825–831.65 Kloepfer KM, Lee WM, Pappas TE, et al. Detection of pathogenic bacteria during rhinovirus infection is associated with increased respiratory symptoms and asthma exacerbations. J Allergy Clin Immunol 2014; 133: 1301–1307.66 Leung TF, Chan PKS, Wong GWK, et al. Respiratory viruses and atypical bacteria triggering severe asthma exacerbation in children. Hong Kong Med J 2013; 19: Suppl. 4, 11–14.67 Lee S-l, Chiu S-s, Malik PJS, et al. Is respiratory viral infection really an important trigger of asthma exacerbations in children? Eur J Pediatr 2011; 170: 1317–1324.68 Bizzintino J, Lee WM, Laing IA, et al. Association between human rhinovirus C and severity of acute asthma in children. Eur Respir J 2011; 37: 1037–1042.69 Mandelcwajg A, Moulin F, Menager C, et al. Underestimation of influenza viral infection in childhood asthma exacerbations. J Pediatr 2010; 157: 505–506.70 Maffey AF, Barrero PR, Venialgo C, et al. Viruses and atypical bacteria associated with asthma exacerbations in hospitalized children. Pediatr Pulmonol 2010; 45: 619–625.71 Olenec JP, Kim WK, Lee WM, et al. Weekly monitoring of children with asthma for infections and illness during common cold seasons. J Allergy Clin Immunol 2010; 125: 1001–1006.72 Xepapadaki P, Xatziioannou A, Chatzicharalambous M, et al. Exhaled breath temperature increases during mild exacerbations in children with virus-induced asthma. Int Arch Allergy Immunol 2010; 153: 70–74.73 Ong BH, Gao Q, Phoon MC, et al. Identification of human metapneumovirus and Chlamydophila pneumoniaein children with asthma and wheeze in Singapore. Singapore Med J 2007; 48: 291–293.74 João Silva M, Ferraz C, Pissarra S, et al. Role of viruses and atypical bacteria in asthma exacerbations among children in Oporto (Portugal). Allergol Immunopathol (Madr) 2007; 35: 4–9.75 Khetsuriani N, Kazerouni NN, Erdman DD, et al. Prevalence of viral respiratory tract infections in children with asthma. J Allergy Clin Immunol 2007; 119: 314–321.76 Murray CS, Poletti G, Kebadze T, et al. Study of modifiable risk factors for asthma exacerbations: virus infection and allergen exposure increase the risk of asthma hospital admissions in children. Thorax 2006; 61: 376–382.77 Rawlinson WD, Waliuzzaman Z, Carter IW, et al. Asthma exacerbations in children associated with rhinovirus but not human metapneumovirus infection. J Infect Dis 2003; 187: 1314–1318.78 Thumerelle C, Deschildre A, Bouquillon C, et al. Role of viruses and atypical bacteria in exacerbations of asthma in hospitalized children: a prospective study in the Nord-Pas de Calais region (France). Pediatr Pulmonol 2003; 35: 75–82.79 Akturk H, Sutcu M, Uysalol M, et al. Impact of respiratory viruses on pediatric asthma exacerbations. Çocuk Enfeksiyon Dergisi/Journal of Pediatric Infection 2016; 10: 14–21.80 Brouard J, Freymuth F, Toutain F, et al. Rôle des infections virales et des infections à Chlamydia pneumoniæet à Mycoplasma pneumoniæ au cours de l’asthme du nourrisson et du jeune enfant. À propos d’une étude épidémiologique chez 118 enfants [Role of viral infections and Chlamydia pneumoniae and Mycoplasma pneumoniae infections in asthma in infants and young children. Epidemiologic study of 118 children]. Arch Pediatr 2002; 9: Suppl. 3, 365–371.81 Sauvaget E, Bresson V, Oudyi M, et al. Intérêt de l’identification en routine des agents pathogènes respiratoires chez les enfants hospitalisés pour une exacerbation d’asthme [Value of routine identification of respiratory infectious agents in children hospitalized with an acute asthma exacerbation]. Arch Pediatr 2014; 21: 1173–1179.82 Gao Y, Xepapadaki P, Cui Y, et al. Effect of Haemophilus influenzae, Streptococcus pneumoniae and influenza vaccinations on infections, immune response and asthma control in preschool children with asthma. Allergy2023; 78: 1473–1488.83 Kan-O K, Washio Y, Oki T, et al. Effects of treatment with corticosteroids on human rhinovirus-induced asthma exacerbations in pediatric inpatients: a prospective observational study. BMC Pulm Med 2023; 23: 487.84 Sheikh S, Eisner M, Walum J, et al. Innate immune responses are increased in children with acute asthma exacerbation. Pediatr Allergy Immunol 2024; 35: e14173.85 Usala C, Wilson P. Noninvasive ventilation use in pediatric status asthmaticus. J Asthma 2022; 59: 1338–1342.86 El-Seify M, Al-Fahham M, Salah El-Deen N, et al. Detection of rhinovirus-associated asthma exacerbations using reverse transcriptase-polymerase chain reaction in Egyptian children. Egypt J Pediatr Allergy Immunol2017; 15: 9–15.87 Ko FWS, Chan PKS, Chan RWY, et al. Molecular detection of respiratory pathogens and typing of human rhinovirus of adults hospitalized for exacerbation of asthma and chronic obstructive pulmonary disease.Respir Res 2019; 20: 210. https://doi.org/10.1183/16000617.0179-2025 16 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 17 88 Yoshii Y, Shimizu K, Morozumi M, et al. Detection of pathogens by real-time PCR in adult patients with acute exacerbation of bronchial asthma. BMC Pulm Med 2017; 17: 150.89 Saraya T, Kimura H, Kurai D, et al. The molecular epidemiology of respiratory viruses associated with asthma attacks: a single-center observational study in Japan. Medicine (Baltimore) 2017; 96: e8204.90 Seo KH, Bae DJ, Kim JN, et al. Prevalence of respiratory viral infections in Korean adult asthmatics with acute exacerbations: comparison with those with stable state. Allergy Asthma Immunol Res 2017; 9: 491–498.91 Iikura M, Hojo M, Koketsu R, et al. The importance of bacterial and viral infections associated with adult asthma exacerbations in clinical practice. PLoS One 2015; 10: e0123584.92 Prasetyo AA, Desyardi MN, Tanamas J, et al. Respiratory viruses and torque teno virus in adults with acute respiratory infections. Intervirology 2015; 58: 57–68.93 Murphy VE, Powell H, Wark PAB, et al. A prospective study of respiratory viral infection in pregnant women with and without asthma. Chest 2013; 144: 420–427.94 Althani A, Bushra S, Shaath N, et al. Characterisation of winter respiratory viral infections in patients with asthma and COPD in Qatar. Arch Virol 2013; 158: 1079–1083.95 Denlinger LC, Sorkness RL, Lee WM, et al. Lower airway rhinovirus burden and the seasonal risk of asthma exacerbation. Am J Respir Crit Care Med 2011; 184: 1007–1014.96 Williams JV, Crowe JE, Enriquez R, et al. Human metapneumovirus infection plays an etiologic role in acute asthma exacerbations requiring hospitalization in adults. J Infect Dis 2005; 192: 1149–1153.97 Tan WC, Xiang X, Qiu D, et al. Epidemiology of respiratory viruses in patients hospitalized with near-fatal asthma, acute exacerbations of asthma, or chronic obstructive pulmonary disease. Am J Med 2003; 115: 272–277.98 Corne JM, Marshall C, Smith S, et al. Frequency, severity, and duration of rhinovirus infections in asthmatic and non-asthmatic individuals: a longitudinal cohort study. Lancet 2002; 359: 831–834.99 Xiang X, Qiu D, Chan KP, et al. Comparison of three methods for respiratory virus detection between induced sputum and nasopharyngeal aspirate specimens in acute asthma. J Virol Methods 2002; 101: 127–133.100 Pang YK, Ismail AI, Chan YF, et al. Influenza in Malaysian adult patients hospitalized with community-acquired pneumonia, acute exacerbation of chronic obstructive pulmonary disease or asthma: a multicenter, active surveillance study. BMC Infect Dis 2021; 21: 644.101 Kan-O K, Washio Y, Fujimoto T, et al. Differences in the spectrum of respiratory viruses and detection of human rhinovirus C in exacerbations of adult asthma and chronic obstructive pulmonary disease. Respir Investig 2022; 60: 129–136.102 Pullicino S, DeBattista J, Gouder C, et al. Infective triggers for asthma exacerbations in Malta. Malta Medical Journal 2022; 32: 65–77.103 Clark TW, Medina M-J, Batham S, et al. Adults hospitalised with acute respiratory illness rarely have detectable bacteria in the absence of COPD or pneumonia; viral infection predominates in a large prospective UK sample. J Infect 2014; 69: 507–515.104 Verduyn M, Botto G, Jaubert J, et al. Serum IgG concentrations in adult patients experiencing virus-induced severe asthma exacerbations. J Allergy Clin Immunol Pract 2019; 7: 1507–1513.105 Wardzyńska A, Pawełczyk M, Głobińska A, et al. The profile of respiratory pathogens in induced sputum of elderly and non-elderly asthmatics. Cent Eur J Immunol 2019; 44: 384–389.106 Bjerregaard A, Laing IA, Backer V, et al. High fractional exhaled nitric oxide and sputum eosinophils are associated with an increased risk of future virus-induced exacerbations: a prospective cohort study. Clin Exp Allergy 2017; 47: 1007–1013.107 Bjerregaard A, Laing IA, Poulsen N, et al. Characteristics associated with clinical severity and inflammatory phenotype of naturally occurring virus-induced exacerbations of asthma in adults. Respir Med 2017; 123: 34–41.108 Turchiarelli V, Schinkel J, Molenkamp R, et al. Repeated virus identification in the airways of patients with mild and severe asthma during prospective follow-up. Allergy 2011; 66: 1099–1106.109 Kistler A, Avila PC, Rouskin S, et al. Pan-viral screening of respiratory tract infections in adults with and without asthma reveals unexpected human coronavirus and human rhinovirus diversity. J Infect Dis 2007; 196: 817–825.110 Maggi F, Andreoli E, Pifferi M, et al. Human bocavirus in Italian patients with respiratory diseases. J Clin Virol2007; 38: 321–325.111 Venarske DL, Busse WW, Griffin MR, et al. The relationship of rhinovirus-associated asthma hospitalizations with inhaled corticosteroids and smoking. J Infect Dis 2006; 193: 1536–1543.112 Ferreira A, Williams Z, Donninger H, et al. Rhinovirus is associated with severe asthma exacerbations and raised nasal interleukin-12. Respiration 2002; 69: 136–142.113 Green RM, Custovic A, Sanderson G, et al. Synergism between allergens and viruses and risk of hospital admission with asthma: case-control study. BMJ 2002; 324: 763.114 Atmar RL, Guy E, Guntupalli KK, et al. Respiratory tract viral infections in inner-city asthmatic adults. Arch Intern Med 1998; 158: 2453–2459. https://doi.org/10.1183/16000617.0179-2025 17 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL. ### Page 18 115 Kraft M, Cassell GH, Henson JE, et al. Detection of Mycoplasma pneumoniae in the airways of adults with chronic asthma. Am J Respir Crit Care Med 1998; 158: 998–1001.116 Teichtahl H, Buckmaster N, Pertnikovs E. The incidence of respiratory tract infection in adults requiring hospitalization for asthma. Chest 1997; 112: 591–596.117 Sokhandan M, McFadden ER, Huang YT, et al. The contribution of respiratory viruses to severe exacerbations of asthma in adults. Chest 1995; 107: 1570–1574.118 Allegra L, Blasi F, Centanni S, et al. Acute exacerbations of asthma in adults: role of Chlamydia pneumoniaeinfection. Eur Respir J 1994; 7: 2165–2168.119 Matsuse H, Kondo Y, Saeki S, et al. Naturally occurring parainfluenza virus 3 infection in adults induces mild exacerbation of asthma associated with increased sputum concentrations of cysteinyl leukotrienes. Int Arch Allergy Immunol 2005; 138: 267–272.120 Bjerregaard A, Laing IA, Backer V, et al. Clinical characteristics of eosinophilic asthma exacerbations.Respirology 2017; 22: 295–300.121 Liao H, Yang Z, Yang C, et al. Impact of viral infection on acute exacerbation of asthma in out-patient clinics: a prospective study. J Thorac Dis 2016; 8: 505–512.122 Simpson JL, Moric I, Wark PAB, et al. Use of induced sputum for the diagnosis of influenza and infections in asthma: a comparison of diagnostic techniques. J Clin Virol 2003; 26: 339–346.123 Herrera-García J, Arellano-Montellan E, Paulin-Prado P, et al. Crisis asmática grave asociada con infección viral [Severe asthmatic crisis related to viral infection]. Medicina Interna de México 2017; 33: 159–167.124 Park S, Hwang YI, Lee SW, et al. Isolated respiratory tract microorganisms and clinical characteristics in asthma exacerbation of obese patients: a multicenter study. BMC Pulm Med 2024; 24: 69.125 Paulin-Prado P, Nishimura K, Freimanis-Hance L, et al. Clinical characteristics of asthmatic patients with influenza-like illness and risk of severe exacerbations in Mexico. Ann Allergy Asthma Immunol 2016; 116: 402–407.126 Grissell TV, Powell H, Shafren DR, et al. Interleukin-10 gene expression in acute virus-induced asthma.Am J Respir Crit Care Med 2005; 172: 433–439.127 Öhrmalm L, Malinovschi A, Wong M, et al. Presence of rhinovirus in the respiratory tract of adolescents and young adults with asthma without symptoms of infection. Respir Med 2016; 115: 1–6.128 Georgountzou A, Papadopoulos NG. Postnatal innate immune development: from birth to adulthood. Front Immunol 2017; 8: 957.129 Monto AS, Foster-Tucker JE, Callear AP, et al. Respiratory viral infections from 2015 to 2022 in the HIVE Cohort of American Households: incidence, illness characteristics, and seasonality. J Infect Dis 2024; 231: 795–804.130 Taylor S, Lopez P, Weckx L, et al. Respiratory viruses and influenza-like illness: epidemiology and outcomes in children aged 6 months to 10 years in a multi-country population sample. J Infect 2017; 74: 29–41.131 Belachew AB, Rantala AK, Jaakkola MS, et al. Asthma and respiratory infections from birth to young adulthood. Am J Epidemiol 2023; 192: 408–419.132 Sundell N, Andersson LM, Brittain-Long R, et al. PCR detection of respiratory pathogens in asymptomatic and symptomatic adults. J Clin Microbiol 2019; 57: e00716-18.133 Birger R, Morita H, Comito D, et al. Asymptomatic shedding of respiratory virus among an ambulatory population across seasons. mSphere 2018; 3: e00249-18.134 Walker GJ, Stelzer-Braid S, Shorter C, et al. Viruses associated with acute respiratory infection in a community-based cohort of healthy New Zealand children. J Med Virol 2022; 94: 454–460.135 Most ZM, Perl TM, Sebert M. Respiratory virus infections in symptomatic and asymptomatic children upon hospital admission: new insights. Antimicrob Steward Healthc Epidemiol 2024; 4: e162.136 Megremis S, Constantinides B, Xepapadaki P, et al. Respiratory eukaryotic virome expansion and bacteriophage deficiency characterize childhood asthma. Sci Rep 2023; 13: 8319.137 Mageiros L, Megremis S, Papadopoulos NG. The virome in allergy and asthma: a nascent, ineffable player.J Allergy Clin Immunol 2023; 152: 1347–1351.138 Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2024. 2024. https://doi.org/10.1183/16000617.0179-2025 18 EUROPEAN RESPIRATORY REVIEW ASTHMA | S ANANTH ET AL.