This study revealed that viral etiology plays a significant role in the severity of the present ARI and that viral infection affects the host's susceptibility to subsequent ARIs.
Background
Respiratory syncytial virus (RSV) is one of the main viral causes of lower respiratory tract illness (LRTI), especially in young children. RSV vaccines, including maternal and infant vaccines, are under development; however, more epidemiological studies are needed to develop effective vaccination strategies.
Objectives
To estimate detailed age‐specific incidence rates and severity of RSV‐associated LRTI (RSV‐LRTI) using data from a community‐based prospective cohort study in the Philippines.
Patients/Methods
Cohort children who visited health facilities due to acute respiratory symptoms were identified, and nasopharyngeal swabs were collected to detect RSV. The severity of RSV‐LRTI was assessed using the severity definition proposed by the World Health Organization. Risk factors for developing RSV‐LRTI and contribution of SpO
2
measurement were also evaluated.
Results
A total of 395 RSV episodes which occurred in children aged 2‐59 months were categorised as 183 RSV‐LRTI, 72 as severe RSV‐LRTI and 29 as very severe RSV‐LRTI. Children aged 3‐5 months had the highest incidence rate of RSV‐LRTI, at 207.4 per 1000 child‐years (95% CI: 149.0‐279.5). Younger age group, place of living and low educational level of caregivers were associated with developing RSV‐LRTI. Clinical manifestations had low levels of agreement with hypoxaemia as measured by pulse oximeter.
Conclusion
The highest burden of RSV was observed in young infants aged 3‐5 months, whereas the burden was also high in those aged 12‐20 months. Future vaccination strategies should consider the protection of older children, especially those aged one year, as well as young infants.
Autism spectrum disorder (ASD) has phenotypically and genetically heterogeneous characteristics. A simulation study demonstrated that attempts to categorize patients with a complex disease into more homogeneous subgroups could have more power to elucidate hidden heritability. We conducted cluster analyses using the k-means algorithm with a cluster number of 15 based on phenotypic variables from the Simons Simplex Collection (SSC). As a preliminary study, we conducted a conventional genome-wide association study (GWAS) with a data set of 597 ASD cases and 370 controls. In the second step, we divided cases based on the clustering results and conducted GWAS in each of the subgroups vs controls (cluster-based GWAS). We also conducted cluster-based GWAS on another SSC data set of 712 probands and 354 controls in the replication stage. In the preliminary study, which was conducted in conventional GWAS design, we observed no significant associations. In the second step of cluster-based GWASs, we identified 65 chromosomal loci, which included 30 intragenic loci located in 21 genes and 35 intergenic loci that satisfied the threshold of P < 5.0 × 10 −8. Some of these loci were located within or near previously reported candidate genes for ASD: CDH5,
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