Laboratory of Infectious Diseases, RNA Viruses Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-2007, USA.
Virology. 2012 Nov 25;433(2):320-8. doi: 10.1016/j.virol.2012.08.027. Epub 2012 Sep 7.
Human parainfluenza viruses (PIVs) cause acute respiratory illness in children, the elderly, and immunocompromised patients. PIV3 is a common cause of bronchiolitis and pneumonia, whereas PIV1 and 2 are frequent causes of upper respiratory tract illness and croup. To assess how PIV1, 2, and 3 differ with regard to replication and induction of type I interferons, interleukin-6, and relevant chemokines, we infected primary human airway epithelium (HAE) cultures from the same tissue donors and examined replication kinetics and cytokine secretion. PIV1 replicated to high titer yet did not induce cytokine secretion until late in infection, while PIV2 replicated less efficiently but induced an early cytokine peak. PIV3 replicated to high titer but induced a slower rise in cytokine secretion. The T cell chemoattractants CXCL10 and CXCL11 were the most abundant chemokines induced. Differences in replication and cytokine secretion might explain some of the differences in PIV serotype-specific pathogenesis and epidemiology.
人类副流感病毒(PIVs)可引起儿童、老年人和免疫功能低下患者的急性呼吸道疾病。PIV3 是细支气管炎和肺炎的常见病因,而 PIV1 和 2 则是上呼吸道疾病和哮吼的常见病因。为了评估 PIV1、2 和 3 在复制和诱导 I 型干扰素、白细胞介素-6 和相关趋化因子方面的差异,我们感染了来自同一组织供体的原代人气道上皮(HAE)培养物,并检查了复制动力学和细胞因子分泌。PIV1 复制到高滴度,但直到感染后期才诱导细胞因子分泌,而 PIV2 复制效率较低,但诱导早期细胞因子峰值。PIV3 复制到高滴度,但诱导细胞因子分泌的上升较慢。T 细胞趋化因子 CXCL10 和 CXCL11 是诱导的最丰富的趋化因子。复制和细胞因子分泌的差异可能解释了 PIV 血清型特异性发病机制和流行病学的一些差异。