Increased susceptibility to pentobarbital following mouse cytomegalovirus infection: relative roles of viral-induced interferon and viral infection of the liver.
Increased susceptibility to pentobarbital following mouse cytomegalovirus infection: relative roles of viral-induced interferon and viral infection of the liver.
复制标题
小鼠巨细胞病毒感染后对戊巴比妥的敏感性增加：病毒诱导的干扰素和肝脏病毒感染的相对作用。
DOI：
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发表时间：
1989
期刊：
影响因子：
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通讯作者：
M. Selgrade
中科院分区：
文献类型：
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作者：
J. Catignani;M. Ménache;M. Selgrade
本研究的目的是确定病毒诱导的干扰素（IFN）和病毒感染的肝脏在小鼠巨细胞病毒（MCMV）诱导的细胞色素P-450（cyt P-450）水平的下降和戊巴比妥诱导的睡眠时间（PEN-ST）的增加的相对作用。这是通过建立IFN应答、肝脏病毒感染、抑制细胞色素P-450水平和增强PEN-ST之间的时间关系，通过确定抗IFN抗体治疗对所有这些应答的影响，以及通过操纵已知影响病毒发病机制和宿主对病毒应答的因素，如动物年龄、病毒毒力和病毒剂量来实现的。在一般情况下，操纵这些因素对增加刺激宿主免疫反应导致更大的抑郁症的细胞色素P-450。这些数据是一致的假设，一些IFN-依赖性机制可能有助于MCMV感染的影响，细胞色素P-450水平和PEN-ST;然而，时间关系的各种反应后测得的病毒感染表明，IFN反应的影响可能是间接的，由于其他宿主防御机制的调制。使用抗-IFN抗血清来确定IFN在此处观察到的作用中的作用被证明是不成功的。对PEN-ST和cyt P-450水平的影响似乎与肝脏感染的程度无关。（250字处删节）
The purpose of this study was to determine the relative roles of viral-induced interferon (IFN) and viral infection of the liver in mouse cytomegalovirus (MCMV)-induced depression of cytochrome P-450 (cyt P-450) levels and enhancement of pentobarbital-induced sleeping time (PEN-ST). This was done by establishing the temporal relationship among the IFN response, viral infection of the liver, suppression of cyt P-450 levels, and enhancement of PEN-ST, by determining the effect of anti-IFN antibody treatment on all of these responses, and by manipulating factors known to influence viral pathogenesis and host response to virus such as animal age, virulence of the virus, and dose of virus. In general, manipulation of these factors toward increased stimulation of host immune responses resulted in greater depression of cyt P-450. The data are consistent with the hypothesis that some IFN-dependent mechanism may have contributed to the effects of MCMV infection on both cyt P-450 levels and PEN-ST; however, the temporal relationship among the various responses measured following viral infection suggested that the effect of the IFN response may be indirect and due to modulation of other host defense mechanisms. Use of anti-IFN antisera to definitively establish a role for IFN in the effects observed here proved unsuccessful. Effects on PEN-ST and cyt P-450 levels did not appear to be related to the magnitude of infection in the liver.(ABSTRACT TRUNCATED AT 250 WORDS)