FLANIGAN C C, SPRUNT D H
J Exp Med. 1956 Nov 1;104(5):687-706. doi: 10.1084/jem.104.5.687.
The effect of progressive long term dietary protein depletion on viral susceptibility was investigated in 2 host-virus systems: (1) swine influenza in the male CF(1) mouse, and (2) Rous sarcoma virus in the New Hampshire red chicken. Data are presented demonstrating a relationship between host protein nutrition and susceptibility to virus infection. This relationship is shown to be cyclic in character, involving phases of increased and decreased viral susceptibility. The relative resistance of the host on low protein intake is a function of the duration on incomplete diet administration before virus inoculation, and consequently a function of the host's state of depletion. As illustrated in Fig. 6, the cyclic susceptibility change demonstrated by these animals on low protein diet was characterized by an initial phase of increased susceptibility, a secondary phase of increased resistance, and a final phase of increased susceptibility. It is proposed that these alterations in relative viral susceptibility result from metabolic changes occurring within the host during the process of dietary protein depletion. The resistance changes are roughly correlated to periods of depot fat utilization (increased susceptibility), reserve protein utilization (decreased susceptibility), and tissue breakdown subsequent to protein starvation (increased susceptibility). Many previously published concepts of the interplay of viral susceptibility and host nutrition maintained that host malnourishment led to increased host resistance. The cyclic change in resistance, reported herein, is given as evidence that the effect of host deficiency cannot be explained simply on the basis of an inhibition of virus growth due to retarded cellular metabolism in the host. Protein deficiency is shown not to produce an "all-or-none" effect, but a series of reproducible phases of increased and decreased resistance. From the aforementioned results it is proposed that the phases of viral susceptibility seen in the protein-deficient host are demonstrative of the dynamic interrelationship between the physiologic state and the resistance of the host. Dietary influences in the normal host, by producing similar metabolic changes, could have analogous implications on innate resistance. It is believed that the foregoing leads to a more clear and dynamic concept of viral resistance in the normal individual.
在两个宿主 - 病毒系统中研究了长期渐进性膳食蛋白质缺乏对病毒易感性的影响：（1）雄性CF(1)小鼠的猪流感，以及（2）新罕布什尔红鸡的劳斯肉瘤病毒。给出的数据表明宿主蛋白质营养与病毒感染易感性之间存在关系。这种关系表现为周期性，涉及病毒易感性增加和降低的阶段。宿主在低蛋白摄入时的相对抵抗力是病毒接种前不完全饮食给药持续时间的函数，因此也是宿主消耗状态的函数。如图6所示，这些低蛋白饮食动物表现出的周期性易感性变化的特征是：初始阶段易感性增加，第二阶段抵抗力增加，最后阶段易感性增加。有人提出，这些相对病毒易感性的改变是由于膳食蛋白质缺乏过程中宿主内发生的代谢变化所致。抵抗力的变化大致与储存脂肪利用期（易感性增加）、储备蛋白质利用期（易感性降低）以及蛋白质饥饿后的组织分解期（易感性增加）相关。许多先前发表的关于病毒易感性与宿主营养相互作用的概念认为，宿主营养不良会导致宿主抵抗力增加。本文报道的抵抗力的周期性变化证明，宿主缺乏的影响不能简单地基于宿主细胞代谢迟缓导致病毒生长受抑制来解释。蛋白质缺乏并非产生“全或无”效应，而是一系列可重复的抵抗力增加和降低阶段。根据上述结果，有人提出在蛋白质缺乏的宿主中看到的病毒易感性阶段证明了生理状态与宿主抵抗力之间的动态相互关系。正常宿主中的饮食影响通过产生类似的代谢变化，可能对先天抵抗力有类似的影响。据信，上述内容导致对正常个体中病毒抵抗力有更清晰和动态的概念。
