The Induction of Interferon by Vesicular Stomatitis Virus in Mouse L Cells

The Induction of Interferon by Vesicular Stomatitis Virus in Mouse L Cells
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水泡性口炎病毒在小鼠L细胞中诱导干扰素

DOI:
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发表时间:
1979
影响因子:
2.6
通讯作者:
Y. Kimura
Y. Kimura
中科院分区:
医学4区
文献类型:
--
作者:
Y. Nishiyama;Yasuhiko Ito;K. Shimokata;Y. Kimura

文献摘要

被引文献

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虽然当L细胞感染野生型VSV(VSV-o)时没有可检测到的干扰素产生,但当细胞感染UV照射的VSV-o时,以相当于10 PFU/细胞的多重性产生了相当数量的干扰素。用紫外线处理VSV‐o导致病毒的RNA合成能力和细胞毒性显著降低,并且紫外线照射的病毒对同源病毒既没有感染性也没有干扰活性。UV-VSV-o诱导的干扰素量受感染复数和孵育温度的显著影响。来自持续感染VSV的L细胞的毒性较低的温度敏感突变体(VSV-mp和VSV-sp)在未用紫外线处理的情况下诱导L细胞中的干扰素,但如果感染的细胞在非允许温度下孵育,或者如果细胞以超过10 PFU/细胞的多重性感染,则这些病毒不能诱导干扰素。另一方面,研究表明,用放线菌酮(100 μg/ml)处理细胞延迟了由非辐照VSV-o引起的细胞损伤的表达,并在从培养物中去除放线菌酮时导致干扰素的产生。这些结果表明,VSV在L细胞中具有固有的干扰素诱导能力,并且如果在抑制或延迟VSV引起的细胞损伤的条件下进行诱导,则可以诱导干扰素。此外,还讨论了干扰素预处理细胞和VSV‐o未稀释传代对干扰素诱导的影响与持续感染的关系。
Although no detectable interferon was produced when L cells were infected with wild‐type VSV (VSV‐o), considerable amounts of interferon were produced when cells were infected with UV‐irradiated VSV‐o at a multiplicity equivalent to 10 PFU/cell. Treatment of VSV‐o with UV‐light resulted in the marked reduction of the RNA synthesizing capacity and cytotoxity of the virus, and the UV‐irradiated virus had neither infectivity nor interfering activity against homologous viruses. The amount of interferon induced by UV‐VSV‐o was markedly influenced by multiplicity of infection and incubation temperature. Less‐virulent temperature‐sensitive mutants (VSV‐mp and VSV‐sp) derived from L cells persistently infected with VSV induced interferon in L cells without treatment of the viruses with UV‐light, but these viruses could not induce interferon if the infected cells were incubated at nonpermissive temperature, or if cells were infected at multiplicities of more than 10 PFU/cell. On the other hand, it was shown that treatment of cells with cycloheximide (100 μg/ml) delayed the expression of cell damage caused by non‐irradiated VSV‐o and resulted in the production of interferon when cycloheximide was removed from the cultures. These results indicate that VSV has intrinsically interferon‐inducing capacity in L cells and can induce interferon if the induction is carried out under such condition that cell damage caused by VSV are suppressed or delayed. Furthermore, the effect of pretreatment of cells by interferon and undiluted passage of VSV‐o on interferon induction was discussed in relation to persistent infection.