(Peer-reviewed, Open Access, Fast processing International Journal) Impact Factor : 7.0 , ISSN 0525-1003
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(Peer-reviewed, Open Access, Fast processing International Journal) Impact Factor : 7.0 , ISSN 0525-1003
Volume 07, Issue 2 , February , 2026
Authors & Affiliations
1. Muktarali kyzy Begimai
2.Mohammad Nadeem
3.Ali Haider
4.Gambhir Kumar
(1. Teacher “International Medical Faculty” Osh State University, Osh, Kyrgyzstan.)
(2-4 Student “International Medical Faculty” Osh State University, Osh, Kyrgyzstan.)
Globally, acute asthma flare-ups continue to be a leading cause of pediatric ER visits and hospital stays. The predominant triggering factor, especially in severe episodes and status asthmaticus, is known to be viral respiratory infections. Via intricate immunological and epithelial processes, pathogens such respiratory syncytial virus (RSV), rhinovirus, influenza virus, and more recently SARS - CoV - 2 cause airway inflammation. It is crucial to comprehend these viral triggers in order to enhance child control and prevention tactics.Using the PubMed, Scopus, and Embase databases.
A narrative review of pediatric-focused literature published between 2010 and 2025 was carried out. Included were studies looking at immunologic pathways, clinical outcomes in children, viral infections, and the intensity of asthma flare-ups.
While RSV is closely linked to early-life wheeze and long-term asthma risk, rhinovirus is the most common viral cause of severe pediatric asthma exacerbations. Seasonal increases in severe asthma presentations are partly caused by influenza infection. According to new research, immunological dysregulation and structural airway alterations brought on by post - COVID airway inflammation may increase the severity of asthma. Increased type -2 inflammation, compromised interferon responses, and epithelial damage are common factors.
A major contributing factor to children severe asthma and status asthmaticus is viral infections. Individualized asthma treatment, early detection of virus-induced exacerbations, and preventive vaccination are essential. To better understand the pulmonary effects of COVID -19 in children, longitudinal study is required.
The most prevalent long-term respiratory condition in children and a major contributor to avoidable hospital stays is asthma. Acute exacerbations continue to be a chronic clinical problem, despite the fact that many children attain adequate symptom management with maintenance medication. Severe bouts, especially status asthmaticus, can worsen quickly and necessitate critical care. The bulk of these severe occurrences are preceded by viral respiratory infections, a finding that is consistent across epidemiologic research ( GINA, 2024 ).
Children's airways are particularly vulnerable to viral damage. The clinical effects of viral exposure are increased by immature immune responses, restricted airway diameter, and increased inflammatory reactivity. RSV and rhinovirus are two respiratory viruses that have long been linked to kid and infant wheezing disorders ( Jackson et al., 2013 ). Seasonal increases in severe asthma admissions are a result of influenza, particularly in children who have not received the vaccination ( Kloepfer & Gern, 2016 ). Concerns about chronic airway inflammation and altered immune modulation after infection have been brought up more recently by SARS - CoV - 2.
Although viral triggers have been identified, pediatric practice frameworks still do not fully incorporate their relative roles and mechanisms in causing potentially fatal asthma attacks. Early intervention, vaccine priority, and prevention tactics all benefit from an understanding of these pathways.
With a focus on immunopathology and clinical implications, this study investigates the roles that RSV, rhinovirus, influenza, and post - COVID airway alterations play in children's severe asthma exacerbations and status asthmaticus.
1) Adult - only populations
2) Non - English publications
3) Small case reports lacking outcome data
Relevant articles were screened and categorized by viral pathogen. Due to heterogeneity in study design, findings were synthesized narratively, focusing on clinical applicability and biological plausibility.
Eighty-two papers were categorized by viral pathogen (RSV, rhinovirus, influenza, and SARS - CoV - 2) after meeting inclusion criteria. Increased asthma severity, hospitalization risk, and indicators of airway inflammation were all significantly correlated with viral infection in all groups.
RSV is a well-known precursor to recurrent wheezing and a major cause of lower respiratory tract infections in infants. According to longitudinal cohort studies, infants hospitalized with RSV bronchiolitis are much more likely to experience childhood asthma and persistent wheezing (Sigurs et al., 2010).
RSV increases eosinophilic inflammation and mucus hypersecretion by compromising epithelial integrity and inducing a Th2 - skewed immune response. RSV infection often causes severe exacerbations that necessitate hospitalization in children with preexisting asthma. The severity of the disease over time may be increased by repeated viral damage, which may also lead to airway remodeling.
The most frequent viral cause of asthma flare-ups in school-age children is rhinovirus. Most severe attacks needing emergency care are preceded by rhinovirus infection, according to prospective surveillance studies ( Jackson et al., 2013 ).
According to Contoli et al. (2006), children with asthma exhibit compromised interferon responses to rhinovirus, which results in prolonged viral replication and increased inflammatory signaling. Severe clinical manifestations and enhanced pathogenicity are linked to specific genotypes, especially RV - C.
Airway inflammation is further increased by the combination of viral infection and allergic sensitization. When atopic children are exposed to rhinovirus, their cytokine release, airway hyperresponsiveness, and symptom severity all increase synergistically.
Predictable winter surges in pediatric asthma hospitalizations are partly caused by influenza. Influenza causes both direct airway damage and systemic inflammatory reactions, in contrast to rhinovirus. Following an influenza infection, children with asthma had higher symptom burdens, higher hospitalization rates, and longer recovery times ( Foley et al., 2017 ).
Although vaccination lowers the incidence of influenza and asthma-related complications, uptake in high-risk pediatric populations is still below optimum levels. During influenza outbreaks, secondary bacterial infections and increased airway responsiveness exacerbate the severity of the illness.
Although acute SARS - CoV -2 infection in children is typically mild, new research indicates that some patients may experience long-term respiratory consequences. Coughing, activity intolerance, and wheezing are post - COVID symptoms, especially in children who already have asthma ( Whitaker et al., 2022 ).
Immunologic research shows that after infection, there is persistent interferon activation and T-cell dysregulation, which may compromise antiviral defense and encourage chronic inflammation. In certain cases, imaging and physiologic evaluations show mild airway remodeling.
These results raise concerns that SARS - CoV-2 may act as a modulator of asthma severity rather than a simple temporary trigger, even though long-term pediatric data are still few.
Despite characteristics unique to each disease, common pathways include:
l Disruption of the epithelial barrier
l Reduced interferon signaling against viruses
l Increased inflammation of type 2
l Enhanced hyperresponsiveness of the airways
The rapid escalation of symptoms typical of status asthmaticus is caused by the convergence of these routes.
This summary emphasizes how viral infections are the primary cause of severe asthma flare-ups in children. While RSV contributes to early-life airway sensitivity, rhinovirus is the most common cause, especially in atopic children. SARS - CoV - 2 raises new concerns about long-term airway health, while influenza continues to be a significant seasonal risk.
Impaired antiviral immunity is a major theme. Deficient interferon responses are common in children with asthma, which permits extended viral persistence and severe inflammation. Viral exposure is a powerful amplifier of bronchial hyperreactivity when coupled with allergic airway illness.
Prevention continues to be the best approach from a clinical standpoint. Exacerbation risk is decreased by influenza vaccination, infection management strategies, and controller therapy compliance. Treatment with bronchodilators and anti inflammatory drugs can be promptly intensified when virus-induced deterioration is detected early.
More complexity is introduced in the post COVID era. Clinicians should keep an eye out for prolonged respiratory symptoms in children recovering from SARS CoV - 2 infection, even if conclusive causative routes are still being examined.
This review is constrained by heterogeneity in study design and reliance on observational data. Mechanistic findings may not translate uniformly across pediatric subgroups. Long term post COVID outcomes remain incompletely characterized.
Key priorities include:
Ø Longitudinal pediatric studies on viral – asthma interactions
Ø Biomarkers predicting severe virus induced exacerbations
Ø Targeted immunomodulatory therapies
Ø Expanded vaccination strategies
Understanding host – virus dynamics may allow precision prevention and individualized care.
Children's status asthmaticus and severe asthma flare-ups are primarily caused by viral respiratory infections. Influenza, SARS-CoV-2, RSV, and rhinovirus all have similar but different inflammatory effects that worsen airway dysfunction. Reducing morbidity requires combining early intervention techniques, optimal asthma care, and preventive immunization. In the coming years, pediatric asthma management will be improved by ongoing research into immunological mechanisms and post-viral airway alterations.
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