Impaired innate host defense causes susceptibility to respiratory virus infections in cystic fibrosis
Impaired innate host defense causes susceptibility to respiratory virus infections in cystic fibrosis
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DOI：
10.1016/s1074-7613(03)00114-6
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发表时间：
2003-05-01
期刊：
影响因子：
32.4
通讯作者：
Erzurum, SC
中科院分区：
文献类型：
--
作者：
Zheng, S;De, BP;Erzurum, SC
病毒感染是囊性纤维化（CF）婴儿呼吸道疾病的主要原因。在这里，我们确定宿主因素允许增加病毒复制和细胞因子的产生，为理解CF中病毒疾病的严重程度提供了一种机制。病毒增加是由于缺乏响应病毒或IFN γ的一氧化氮合酶2（NOS 2）和2 '，5'寡腺苷酸合成酶（OAS）1诱导。这可归因于信号转导和转录激活因子（STAT）1（抗病毒防御的基本组成部分）的激活受损。NO供体或NOS2过表达提供了CF中病毒感染的保护，表明NO足以在人气道中进行抗病毒宿主防御，并且是CF儿童抗病毒治疗的一种策略。
Viral infection is the primary cause of respiratory morbidity in cystic fibrosis (CF) infants. Here, we identify that host factors allow increased virus replication and cytokine production, providing a mechanism for understanding the severity of virus disease in CF. Increased virus is due to lack of nitric oxide synthase 2 (NOS2) and 2', 5' oligoadenylate synthetase (OAS) 1 induction in response to virus or IFNgamma. This can be attributed to impairment of activation of signal transducer and activator of transcription (STAT)1, a fundamental component to antiviral defense. NO donor or NOS2 overexpression provides protection from virus infection in CF, suggesting that NO is sufficient for antiviral host defense in the human airway and is one strategy for antiviral therapy in CF children.