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<p>Human parainfluenza virus type 3 (HPIV3) is a major cause of severe pediatric respiratory infections in infants, but its association with meteorological factors is not fully understood. This study compared clinical features of HPIV3 and respiratory syncytial virus (RSV) infections and used distributed lag nonlinear models (DLNMs) to identify environmental determinants of HPIV3 transmission. HPIV3 was most prevalent in infants, causing significantly less wheeze, tachypnea (both p &lt; 0.001) and dyspnea (p = 0.044) than RSV. Seasonal prevalence showed a summer peak (46.4%) and a winter minimum (5.9%). High temperatures immediately increased the relative risk (RR) of HPIV3 (RR = 4.258, 95% CI 1.387–13.074), while low temperatures increased the RR after a four-month lag (RR = 3.958, 95% CI 1.858–8.430). PM10 exposure at 140&#xa0;μg/m<sup>3</sup> had the greatest immediate impact (lag 0, RR = 3.335, 95% CI 1.236–8.999). Delayed effects were observed for gaseous pollutants (SO<sub>2</sub> and NO<sub>2</sub>) after five months (SO<sub>2</sub>: RR = 2.047, 95% CI 1.247–3.362; NO<sub>2</sub>: RR = 2.596, 95% CI 1.577–4.273). These findings indicate that HPIV3 shows distinct clinical features and differential environmental sensitivity, with acute responses to heat and particulates and delayed responses to cold and gaseous pollutants. These results support season-focused prevention strategies for vulnerable infants during high-risk periods.</p>

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Environmental lag effects and clinical characteristics of pediatric human parainfluenza virus type 3 infections

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月24日

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  • Dan Hong,
  • Minjuan Zhu,
  • Wanqing Qi,
  • Lingzhi Ping,
  • Meifang Xu,
  • Jian Wu,
  • Renzhen Wang,
  • Zhengrong Chen

摘要

Human parainfluenza virus type 3 (HPIV3) is a major cause of severe pediatric respiratory infections in infants, but its association with meteorological factors is not fully understood. This study compared clinical features of HPIV3 and respiratory syncytial virus (RSV) infections and used distributed lag nonlinear models (DLNMs) to identify environmental determinants of HPIV3 transmission. HPIV3 was most prevalent in infants, causing significantly less wheeze, tachypnea (both p < 0.001) and dyspnea (p = 0.044) than RSV. Seasonal prevalence showed a summer peak (46.4%) and a winter minimum (5.9%). High temperatures immediately increased the relative risk (RR) of HPIV3 (RR = 4.258, 95% CI 1.387–13.074), while low temperatures increased the RR after a four-month lag (RR = 3.958, 95% CI 1.858–8.430). PM10 exposure at 140 μg/m3 had the greatest immediate impact (lag 0, RR = 3.335, 95% CI 1.236–8.999). Delayed effects were observed for gaseous pollutants (SO2 and NO2) after five months (SO2: RR = 2.047, 95% CI 1.247–3.362; NO2: RR = 2.596, 95% CI 1.577–4.273). These findings indicate that HPIV3 shows distinct clinical features and differential environmental sensitivity, with acute responses to heat and particulates and delayed responses to cold and gaseous pollutants. These results support season-focused prevention strategies for vulnerable infants during high-risk periods.