INHIBITION OF VESICULAR STOMATITIS-VIRUS INFECTION BY NITRIC-OXIDE
INHIBITION OF VESICULAR STOMATITIS-VIRUS INFECTION BY NITRIC-OXIDE
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DOI：
10.1128/jvi.69.4.2208-2213.1995
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发表时间：
1995-04-01
影响因子：
5.4
通讯作者：
REISS, CS
中科院分区：
文献类型：
--
作者：
BI, ZB;REISS, CS
使用 VSV 敏感的小鼠神经母细胞瘤细胞系 NB41A3 研究了一氧化氮 (NO) 对水泡性口炎病毒 (VSV) 感染的抑制作用。 NB41A3 细胞的生产性 VSV 感染被有机 NO 供体 S-硝基-N-乙酰青霉胺 (SNAP) 显着抑制，而对照化合物 N-乙酰青霉胺 (NAP) 则没有效果。 SNAP处理大大提高了VSV感染细胞的存活率，而NAP处理则没有任何效果。当使用低感染复数 (MOI) 时，在感染前 30 分钟添加 SNAP 会导致病毒产生的完全抑制。在感染前 6 小时以较高 MOI 处理细胞也能显着抑制病毒产生。通过用 N-甲基-D-天冬氨酸 (NMDA) 处理细胞来激活神经元 NO 合酶，可显着抑制受三种病毒测试剂量（MOI 分别为 0.1、1 和 5）感染的细胞的病毒产生。 NMDA对病毒感染的抑制作用被NO合酶抑制剂N-甲基-L-精氨酸完全阻断。然而，添加血红蛋白（一种强NO结合蛋白，因此是NO活性的灭活剂）并不能逆转NMDA诱导的病毒产生抑制，这表明NO可能在产生NO的细胞内发挥其抗病毒作用。总的来说，这些数据支持NO的抗VSV作用，这可能是控制中枢神经系统VSV感染初始阶段的自然免疫的重要因素之一。
Inhibitory effects of nitric oxide (NO) on vesicular stomatitis virus (VSV) infection were investigated by using a VSV-susceptible mouse neuroblastoma cell line, NB41A3. Productive VSV infection of NB41A3 cells was significantly inhibited by an organic NO donor, S-nitro-N-acetylpenicillamine (SNAP), while the control compound N-acetylpenicillamine (NAP) had no effect. Survival rate of VSV-infected cells was greatly increased by the treatment with SNAP, while the NAP treatment did not have any effect. Adding SNAP 30 min prior to infection resulted in complete inhibition of viral production when a low multiplicity of infection (MOI) was used. Substantial inhibition of viral production was also obtained with treating cells 6 h earlier before infection with a higher MOI. Activating the neuronal NO synthase by treating cells with N-methyl-D-aspartate (NMDA) led to significant inhibition of viral production by cells infected at the three doses of virus tested (MOIs of 0.1, 1, and 5). The inhibitory effect of NMDA on viral infection was totally blocked by the NO synthase inhibitor N-methyl-L-arginine. However, adding hemoglobin, a strong NO-binding protein and thus an inactivator of NO activity, did not reverse the NMDA-induced inhibition of viral production, suggesting that NO might exert its antiviral effects inside the NO-producing cells. Collectively, these data support the anti-VSV effects of NO, which might be one of the important factors of natural immunity in controlling the initial stages of VSV infection in the central nervous system.