Nair C N
J Gen Virol. 1987 Apr;68 ( Pt 4):1195-8. doi: 10.1099/0022-1317-68-4-1195.
An earlier suggestion that guanidine may inhibit picornavirus replication by interfering with a monovalent cation-mediated event was tested by determining the effect of varying monovalent cation concentration in isotonic medium on the sensitivity of poliovirus replication in HeLa cells to 0.2 mM-guanidine. Lowering [Na+] in the medium to 50 mM had no effect on virus replication. It was found that the degree of inhibition of virus replication by 0.2 mM-guanidine was inversely related to [Na+] in the medium: 99.8%, 99.1%, 38% and 0% inhibition in the presence of 50, 75, 100 and 145 mM-Na+ respectively. Likewise, guanidine uptake by HeLa cells was also inversely related to [Na+] in the medium. On the other hand, lowering medium [Na+] to 50 or 75 mM resulted in reduced intracellular [Na+] and [K+]. The increased sensitivity of virus replication to guanidine in the presence of low Na+ medium could be abolished with excess K+ in such medium. Excess K+ in low Na+ medium restored intracellular [Na+] and reduced guanidine uptake. Thus, the increased sensitivity of poliovirus replication to guanidine in the presence of low Na+ medium correlated with reduced intracellular [Na+] and [K+] and elevated guanidine uptake.
先前有观点认为胍可能通过干扰单价阳离子介导的事件来抑制小核糖核酸病毒复制,为此进行了一项试验,即测定等渗培养基中不同单价阳离子浓度对脊髓灰质炎病毒在HeLa细胞中复制时对0.2 mM胍敏感性的影响。将培养基中的[Na⁺]降至50 mM对病毒复制没有影响。结果发现,0.2 mM胍对病毒复制的抑制程度与培养基中的[Na⁺]呈负相关:在50、75、100和145 mM - Na⁺存在时,抑制率分别为99.8%、99.1%、38%和0%。同样,HeLa细胞对胍的摄取也与培养基中的[Na⁺]呈负相关。另一方面,将培养基中的[Na⁺]降至50或75 mM会导致细胞内[Na⁺]和[K⁺]减少。在低Na⁺培养基中病毒复制对胍的敏感性增加可通过在这种培养基中加入过量K⁺来消除。低Na⁺培养基中的过量K⁺恢复了细胞内[Na⁺]并减少了胍的摄取。因此,在低Na⁺培养基中脊髓灰质炎病毒复制对胍的敏感性增加与细胞内[Na⁺]和[K⁺]减少以及胍摄取增加相关。