Abstract Respiratory human adenovirus (HAdV) infections pose a significant threat to children’s health. This study investigated the prevalence and molecular epidemiology of respiratory HAdV in children from both hospital and community settings in Shenzhen between 2022 and 2024. Children under 14 years of age with suspected acute respiratory infections were enrolled from eight hospitals between November 2022 and June 2024, as well as from communities between October 2023 and April 2024 in Shenzhen. Respiratory specimens were collected and tested for HAdV. The positive rates of HAdV across different groups were compared using Pearson’s chi-square test with the Bonferroni correction, and phylogenetic analysis was performed on the detected HAdV strains. The positivity proportion of HAdV among children in hospital was 16.7% (83/498) between September 2023 and June 2024, predominantly involving HAdV-B3 (95.2%, 20/21). This rate was significantly higher than that observed from October 2022 to June 2023 (3.4%, 11/321) (χ² = 33.676, P < 0.001), during which HAdV-C1 was the predominant subtype (77.8%, 7/9). The positive proportion of HAdV in hospitalized children was higher than that in outpatient children (χ2 = 0.275, P < 0.001), and the positive proportion of HAdV in boys was lower than that in girls in community (χ2 = 4.843, P = 0.028). No significant difference in the mean age was observed between children infected with HAdV-B and those with HAdV-C (t = 0.670, P = 0.509). The Shenzhen-2023-2-ILI-P600 strain exhibited a deletion in the 362–365 aa region of its Penton base gene. Analysis of global HAdV-C1 strains revealed that aa differences at positions 339 and 472 of the Fiber gene were closely linked to specific evolutionary branches. Global HAdV-B3 strains, while highly conserved, showed branch-associated aa differences at positions 168, 403, and 541 of the Hexon gene. The rise in HAdV positivity among pediatric patients in Shenzhen hospitals from late 2022 to late 2023 coincided with a shift in the dominant type from HAdV-C1 to HAdV-B3. Branch-specific aa differences were identified in the Fiber gene of HAdV-C1 and the Hexon gene of HAdV-B3.
Niu et al. (Wed,) studied this question.