The role of interferon regulatory factors in the cardiac response to viral infection.
The role of interferon regulatory factors in the cardiac response to viral infection.
复制标题
干扰素调节因子在病毒感染心脏反应中的作用。
DOI：
10.1089/088282402317340206
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Sherry,Barbara
中科院分区：
文献类型：
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作者：
Sherry,Barbara
呼肠孤病毒诱导的小鼠心肌炎为人类疾病提供了极好的模型。心脏组织损伤因呼肠孤病毒株而异，由直接病毒致细胞病变作用引起。一个行列式 病毒引起的心脏组织损伤的主要机制是心脏对病毒感染的干扰素-β（IFN-β）反应。非心肌呼肠孤病毒诱导更多的IFN-β和/或更敏感 IFN-β对心肌细胞的抗病毒作用强于心肌炎呼肠孤病毒。本文综述了干扰素调节因子（IRFs）在病毒感染引起的心脏反应中的作用， 结果提示IRF-3和IRF-1功能可能存在心脏特异性变化。此外，数据显示IRF-2在IFN-β表达调节中的作用是细胞内的， 类型特异性和骨骼肌和心肌细胞之间的差异。总之，结果表明，心脏可能为IRF功能提供了独特的环境，这对于保护免受病毒诱导的炎症至关重要。 心脏损伤
Reovirus-induced murine myocarditis provides an excellent model for the human disease. Cardiac tissue damage varies between reovirus strains, and is caused by a direct viral cytopathogenic effect. One determinant of virus-induced cardiac tissue damage is the cardiac interferon-β(IFN-β) response to viral infection. Nonmyocarditic reoviruses induce more IFN-βand/or are more sensitive to the antiviral effects of IFN-βin cardiac cells than myocarditis reoviruses. The roles of interferon regulatory factors (IRFs) in the cardiac response to viral infection are reviewed, and results suggest possible cardiac-specific variations in IRF-3 and IRF-1 function. In addition, data are presented indicating that the role of IRF-2 in regulation of IFN-βexpression is cell type-specific and differs between skeletal and cardiac muscle cells. Together, results suggest that the heart may provide a unique environment for IRF function, critical for protection against virus-induced cardiac damage.