Since late 2021, the Omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has undergone rapid evolutionary diversification, givi

Background: The post-acute respiratory consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in individuals with asthma remain incompletely understood. While early coronavirus disease 2019 (COVID-19) research focused on acute infection severity, less is known about asthma control and exacerbation risk following recovery, particularly beyond the acute phase. Objectives: To systematically evaluate asthma control and exacerbation risk following SARS-CoV-2 infection in the post-acute COVID-19 phase among pediatric and adult populations. Methods: We conducted a systematic review in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines and a prospectively registered PROSPERO protocol (CRD420261290371). PubMed, Embase, CINAHL, Scopus, and Web of Science were searched from 1 January 2020 to 21 January 2026. Observational studies evaluating asthma control or exacerbation outcomes assessed ≥ 4 weeks after confirmed SARS-CoV-2 infection were included. Comparators comprised uninfected asthma controls, within-individual pre–post analyses, or population-level controls. Data were synthesised narratively due to substantial clinical and methodological heterogeneity. Results: Eleven observational studies involving children and adults with asthma met the eligibility criteria. Evidence regarding post-acute asthma control was heterogeneous. Several studies reported short-term worsening of asthma control following SARS-CoV-2 infection, particularly within the first one to three months, whereas larger longitudinal and registry-based studies generally demonstrated stability or recovery of asthma control over longer follow-up. In contrast, asthma exacerbation risk showed a more consistent pattern, with large population-based studies demonstrating approximately a two- to five-fold increase in post-acute exacerbation risk among individuals hospitalised with COVID-19 (adjusted hazard ratios ranging from 2.78 to 5.12), while risk was lower and more variable among non-hospitalised cases (hazard ratios approximately 1.8–2.1). Findings were more variable and often null among patients with mild infection. No consistent evidence of sustained deterioration in asthma control was observed across longer-term follow-up. Conclusion: Post-acute asthma outcomes following SARS-CoV-2 infection are heterogeneous and appear to vary according to acute COVID-19 severity, follow-up duration, and study design. While transient worsening of asthma control may occur, particularly after more severe infection, the available evidence does not consistently demonstrate sustained deterioration in asthma control. These findings suggest that post-COVID asthma management may benefit from consideration of infection severity, while highlighting the need for high-quality longitudinal research to better define long-term outcomes.

Inborn errors of immunity, including primary immunodeficiency disorders (PIDs), comprise a heterogeneous group of genetic conditions characterized by immune system dysfunction. One such rare PID is CD137 deficiency, which results from TNFRSF9 mutations. CD137, also known as 4-1BB, plays a pivotal role in immune system regulation and co-stimulation. This literature review explores CD137 deficiency and its implications, emphasizing its association with EBV-associated lymphoproliferative disease and potential therapeutic targets. We present the case of a 21-year-old female patient with CD137 deficiency who experienced recurrent infections, autoimmunity, and lymphoma. Genetic analysis revealed that the patient had a homozygous TNFRSF9 variant. The patient subsequently developed severe Epstein–Barr virus (EBV)-associated lymphoproliferative disease, which is one of the clinical manifestations associated with CD137 deficiency. Additionally, this review discusses similar cases in the literature and details the clinical manifestations and immune abnormalities associated with CD137 deficiency. Understanding the genetic complexity of CD137 deficiency and the immune system dysregulation it causes provides insights into potential therapeutic interventions for affected individuals. This review highlights the role of CD137 as a crucial regulator of immune homeostasis and a potential target for immunotherapy in autoimmune diseases and malignancies.