VITAMIN-E-DEFICIENCY INTENSIFIES THE MYOCARDIAL INJURY OF COXSACKIEVIRUS B3 INFECTION OF MICE
VITAMIN-E-DEFICIENCY INTENSIFIES THE MYOCARDIAL INJURY OF COXSACKIEVIRUS B3 INFECTION OF MICE
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DOI：
10.1093/jn/124.3.345
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发表时间：
1994-03-01
影响因子：
4.2
通讯作者：
LEVANDER, OA
中科院分区：
文献类型：
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作者：
BECK, MA;KOLBECK, PC;LEVANDER, OA
喂养缺乏维生素E的饮食会增加感染心肌炎性柯萨奇病毒B3（CVB 3/20）的小鼠心脏的病理学。从被感染的小鼠的心脏喂养的维生素E缺乏的饮食富含高度不饱和脂肪（鲱鱼油）表现出更严重的病理比心脏从被感染的小鼠喂养的维生素E缺乏的饮食主要是基于饱和脂肪（猪油）。此外，克隆和测序的心肌肌萎缩性柯萨奇病毒B3（CVB 3/0），引起很少或没有病理在维生素E补充小鼠的心脏，诱导广泛的心脏病理在维生素E缺乏的小鼠。在受感染的小鼠中，维生素E缺乏抑制了有丝分裂原和抗原反应，尽管中和抗体反应不受影响。自然杀伤细胞的反应是相当的感染小鼠喂养猪油为基础的饮食补充或不补充维生素E。然而，与以猪油为基础的饮食相比，以鲱鱼油为基础的饮食，无论是否补充维生素E，都显着抑制了感染小鼠的自然杀伤细胞活性。柯萨奇病毒B3/0从缺乏维生素E的供体小鼠的心脏中回收，在HeLa细胞上传代一次，当传递回补充维生素E的受体小鼠时，引起显著的心脏损伤，表明心肌炎性CVB 3/0已变为毒性表型。在维生素E缺乏的供体中同样传代的CVB 3/20病毒也观察到增强的毒力。我们的工作证明了宿主营养抗氧化状态在决定某些病毒感染的严重程度方面的重要作用。
Feeding a vitamin E-deficient diet increases pathology in hearts of mice infected with a myocarditic coxsackievirus B3 (CVB3/20). Hearts from infected mice fed a vitamin E-deficient diet rich in highly unsaturated fat (menhaden oil) exhibited more severe pathology than hearts from infected mice fed a vitamin E-deficient diet based largely on saturated fat (lard). Furthermore, a cloned and sequenced amyocarditic coxsackievirus B3 (CVB3/0), which caused little or no pathology in the hearts of vitamin E-supplemented mice, induced extensive cardiac pathology in vitamin E-deficient mice. In infected mice, both mitogen and antigen responses were depressed by vitamin E deficiency, although neutralizing antibody responses were unaffected. Natural killer cell responses were comparable in infected mice fed a lard-based diet with or without supplemented vitamin E. However, a menhaden oil-based diet, whether supplemented with vitamin E or not, significantly depressed natural killer cell activity in infected mice compared with mice fed the lard-based diet. Coxsackievirus B3/0 recovered from the heart of a vitamin E-deficient donor mouse, passaged one time onto HeLa cells, caused significant heart damage when passed back into vitamin E-supplemented recipient mice, demonstrating that the amyocarditic CVB3/0 had changed to a virulent phenotype. Enhanced virulence was also seen with CVB3/20 virus similarly passaged in a vitamin E-deficient donor. Our work demonstrates the important role of host nutritional antioxidant status in determining the severity of certain viral infections.