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单纯疱疹病毒感染细胞中的钠和钾转运

Sodium and potassium transport in herpes simplex virus-infected cells.

作者信息

Hackstadt T, Mallavia L P

出版信息

J Gen Virol. 1982 Jun;60(Pt 2):199-207. doi: 10.1099/0022-1317-60-2-199.

Abstract

Sodium (Na+) and potassium (K+) flux in African green monkey kidney cells (Vero) was examined following infection by herpes simplex virus type 1 (HSV-1). A decline in the rate of K+ uptake at 5 h post-infection was shown using 86Rb+ as a K+ tracer. In contrast, host protein synthesis was inhibited by 3 h post-infection. The decrease in rate of K+ transport to levels 70 to 90% of that of mock-infected cells did not, however, reflect an inability of HSV-1-infected cells to maintain normal intracellular concentrations of Na+ and K+. At 7 h post-infection, intracellular Na+ and K+ concentrations were determined to be 26.6 +/- 9.4 mM- and 33.3 +/- 10.3 mM-Na+ and 130.1 +/- 4.7 mM- and 137.1 +/- 3.2 mM-K+ in mock-infected and HSV-1-infected cells respectively. Intracellular Na+ did not increase above control levels over at least a 9 h period following HSV-1 infection. The Michaelis constant (Km) of K+ transport in HSV-1-infected or mock-infected Vero cells at 6 h post-infection was determined to be the same with calculated values of 1.38 +/- 0.51 mM and 1.79 +/- 0.42 mM respectively. A virus-induced alteration of intracellular Na+ and K+ concentrations cannot, therefore, account for the HSV-1 induced inhibition of host protein synthesis at 3 h post-infection as has been suggested in other virus systems.

摘要

在非洲绿猴肾细胞(Vero细胞)感染1型单纯疱疹病毒(HSV-1)后,对其钠(Na+)和钾(K+)通量进行了检测。以86Rb+作为K+示踪剂,结果显示感染后5小时K+摄取率下降。相比之下,宿主蛋白合成在感染后3小时受到抑制。然而,K+转运速率降至 mock 感染细胞的70%至90%,这并不反映HSV-1感染细胞无法维持正常的细胞内Na+和K+浓度。在感染后7小时,测定mock感染细胞和HSV-1感染细胞内的Na+和K+浓度分别为26.6±9.4 mM-Na+和33.3±10.3 mM-Na+,以及130.1±4.7 mM-K+和137.1±3.2 mM-K+。在HSV-1感染后的至少9小时内,细胞内Na+并未升高至对照水平以上。在感染后6小时,测定HSV-1感染或mock感染的Vero细胞中K+转运的米氏常数(Km)相同,计算值分别为1.38±0.51 mM和1.79±0.42 mM。因此,病毒诱导的细胞内Na+和K+浓度变化不能像其他病毒系统中所提出的那样,解释HSV-1在感染后3小时对宿主蛋白合成的抑制作用。

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