Cytomegalovirus (CMV) represents the most prevalent cause of congenital viral infection in newborns and the leading non-genetic etiology of sensorineural hearing loss (SNHL) in children. Notably, only 10–15% of congenitally infected infants possibly present with classic clinical symptoms at birth, including Small for gestational age, Microcephaly, Petechiae or purpura, Blueberry muffin rash, Jaundice, Hepatomegaly, Splenomegaly and abnormal neurologic signs. In contrast, approximately 90% of infected neonates exhibit no apparent symptoms initially. Current research predominantly focuses on symptomatic cases due to their severe acute presentations and high rates of long-term sequelae (40–60%), including SNHL and neurodevelopmental impairments. However, significant controversy persists regarding the management of asymptomatic infants. Emerging evidence reveals that 8–15% of asymptomatic carriers develop Late-onset Hearing Loss (LOHL) beyond the neonatal period. Additionally, 5–10% may manifest neurodevelopmental abnormalities including mild intellectual disability, learning difficulties, or motor coordination disorders. Crucially, given the substantial population of asymptomatic cCMV cases, these delayed complications account for 30–40% of all cCMV-related long-term morbidity, underscoring their considerable public health impact. This review synthesizes current evidence and controversies regarding cCMV-related SNHL in asymptomatic or mildly symptomatic children, with a focus on screening, diagnostic classification, and antiviral management gaps, to heighten clinical awareness of this underrecognized cause of hearing loss.

Cytomegalovirus (CMV) represents the most prevalent cause of congenital viral infection in newborns and the leading non-genetic etiology of sensorineural hearing loss (SNHL) in children. Notably, only 10%-15% of congenitally infected infants possibly present with classic clinical symptoms at birth, including Small for gestational age, Microcephaly, Petechiae or purpura, Blueberry muffin rash, Jaundice, Hepatomegaly, Splenomegaly and abnormal neurologic signs. In contrast, approximately 90% of infected neonates exhibit no apparent symptoms initially. Current research predominantly focuses on symptomatic cases due to their severe acute presentations and high rates of long-term sequelae (40%-60%), including SNHL and neurodevelopmental impairments. However, significant controversy persists regarding the management of asymptomatic infants. Emerging evidence reveals that 8%-15% of asymptomatic carriers develop Late-onset Hearing Loss (LOHL) beyond the neonatal period.Additionally 5%-10% may manifest neurodevelopmental abnormalities including mild intellectual disability, learning difficulties, or motor coordination disorders. Crucially, given the substantial population of asymptomatic cCMV cases, these delayed complications account for 30%-40% of all cCMV-related long-term morbidity, underscoring their considerable public health impact. This review synthesizes current evidence and controversies regarding cCMV-related SNHL in asymptomatic or mildly symptomatic children, with a focus on screening, di-agnostic classification, and antiviral management gaps, to heighten clinical awareness of this underrecognized cause of hearing loss.

Background: Otitis Media with Effusion (OME) is characterized by persistent middle ear effusion without acute infection. Type2 inflammation, mediated by IL-4 and IL-13 signaling through the IL-4Rα receptor, has been implicated in the pathogenesis of chronic rhinosinusitis with nasal polyps, asthma, and possibly OME. Refractory OME in adults remains a therapeutic challenge, as conventional treatments often fail to provide long-term resolution. Targeted biologic therapies that modulate type 2 inflammation may offer a novel therapeutic option. Methods: A 60-year-old man with a 15-year history of allergic rhinitis and chronic rhinosinusitis with nasal polyps, as well as multiple asthma exacerbations, presented with recurrent bilateral aural fullness, hearing loss, and tinnitus. His symptoms persisted despite repeated tympanic punctures, insufflation, and corticosteroid treatment. Otoscopic examination revealed dull tympanic membranes with effusion. Audiometry showed conductive hearing loss with a B-type tympanogram on the left and an A-type curve on the right. Laboratory evaluation demonstrated mildly elevated peripheral eosinophils. Results: The patient was diagnosed with OME, likely secondary to type 2 inflammation. Treatment with Stapokibart (CM310), a humanized anti–IL-4Rα monoclonal antibody, was initiated in March 2025. After nine biweekly injections, the patient experienced complete resolution of aural fullness. Otoscopy and tympanometry normalized, and audiometric thresholds improved significantly. No recurrence of ear symptoms was observed during follow-up. Conclusions: This case illustrates that IL-4Rα blockade with Stapokibart may be effective in refractory OME associated with type 2 inflammation. Early recognition of type 2–driven mechanisms in chronic middle ear disease could facilitate targeted therapy, offering symptom resolution and improved quality of life in patients unresponsive to conventional treatment.ral fullness; otitis media with effusion; allergic rhinitis.

Background and Clinical Significance: Otitis media with effusion (OME) is characterized by persistent middle ear effusion without acute infection. Type 2 inflammation, mediated by IL-4 and IL-13 signaling via the IL-4Rα receptor, has been implicated in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and possibly OME. Refractory OME in adults remains a therapeutic challenge, as conventional treatments often fail to achieve long-term resolution. Targeted biologic therapies that modulate type 2 inflammation may offer a novel treatment option. Case Presentation: We report the case of a 60-year-old man with a 15-year history of allergic rhinitis and CRSwNP, complicated by recurrent asthma exacerbations, who presented with bilateral aural fullness, hearing loss, and tinnitus. His symptoms persisted despite repeated tympanic punctures, Eustachian tube insufflation, and corticosteroid therapy. Otoscopy revealed dull tympanic membranes with effusion, and audiometry showed conductive hearing loss with a B-type tympanogram on the left. Laboratory findings demonstrated mild peripheral eosinophilia. The patient was diagnosed with OME, likely secondary to type 2 inflammation. After nine biweekly injections of Stapokibart (CM310)—a humanized monoclonal antibody targeting IL-4Rα—aural fullness completely resolved. Otoscopic findings and tympanograms normalized, and hearing thresholds improved significantly. Retrospective evaluation using Iino’s diagnostic framework suggested that the patient did not meet the full criteria for eosinophilic otitis media (EOM); nevertheless, marked symptomatic and functional improvement was achieved. No recurrence or adverse effects were observed during follow-up. Conclusions: This case suggests that IL-4Rα blockade with Stapokibart may be effective in treating refractory OME associated with type 2 inflammation, even in patients who do not fulfill the diagnostic criteria for EOM. These findings highlight the potential of anti-IL-4Rα biologics as a novel therapeutic option for middle ear diseases driven by type 2 inflammation.