Effect of fatty acids on arenavirus replication:: inhibition of virus production by lauric acid
Effect of fatty acids on arenavirus replication:: inhibition of virus production by lauric acid
复制标题
DOI：
10.1007/s007050170146
复制
发表时间：
2001-01-01
影响因子：
2.7
通讯作者：
Damonte, EB
中科院分区：
文献类型：
--
作者：
Bartolotta, S;García, CC;Damonte, EB
为了研究细胞膜特性对沙粒病毒感染的功能参与，研究了可变链长饱和脂肪酸（C10-C18）对朱宁病毒（JUNV）增殖的抑制作用。最有效的抑制剂是月桂酸（C12），它能以剂量依赖的方式降低几种JUNV减毒株和致病性株的病毒产量，而不影响细胞活力。链长或链短的脂肪酸抗junv活性降低或可忽略。月桂酸既不能灭活病毒粒子的感染性，也不能与细胞相互作用以诱导对病毒感染不耐受的状态。从机理研究来看，月桂酸抑制了JUNV繁殖周期中的一个后期成熟阶段。该化合物不影响病毒蛋白的合成，但降低了质膜中糖蛋白的表达。抑制JUNV的产生和刺激三酰甘油细胞含量之间存在直接关系，并且月桂酸诱导的两种效应都依赖于脂肪酸的持续存在。因此，病毒糖蛋白插入质膜的减少，显然是由于三酰基甘油掺入的增加，似乎导致JUNV成熟和释放的抑制。
To study the functional involvement of cellular membrane properties on arenavirus infection, saturated fatty acids of variable chain length (C10-C18) were evaluated for their inhibitory activity against the multiplication of Junin virus (JUNV). The most active inhibitor was lauric acid (C12), which reduced virus yields of several attenuated and pathogenic strains of JUNV in a dose dependent manner, without affecting cell viability. Fatty acids with shorter or longer chain length had a reduced or negligible anti-JUNV activity. Lauric acid did not inactivate virion infectivity neither interacted with the cell to induce a state refractory to virus infection. From mechanistic studies, it can be concluded that lauric acid inhibited a late maturation stage in the replicative cycle of JUNV. Viral protein synthesis was not affected by the compound, but the expression of glycoproteins in the plasma membrane was diminished. A direct correlation between the inhibition of JUNV production and the stimulation of triacylglycerol cell content was demonstrated, and both lauric-acid induced effects were dependent on the continued presence of the fatty acid. Thus, the decreased insertion of viral glycoproteins into the plasma membrane, apparently due to the increased incorporation of triacylglycerols, seems to cause an inhibition of JUNV maturation and release.