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携带SV40肿瘤特异性移植抗原(SV40-TSTA)的水泡性口炎病毒诱导的SV40肿瘤排斥反应。I.免疫保护的特异性及酶处理对TSTA活性的影响。

SV40 tumor rejection induced by vesicular stomatitis virus bearing SV40 tumor-specific transplantation antigen (SV40-TSTA). I. Specificity of immunoprotection and effect of enzyme treatment on TSTA activity.

作者信息

Ansel S, Huet C, Tournier P

出版信息

Int J Cancer. 1977 Jul 15;20(1):51-60. doi: 10.1002/ijc.2910200110.

Abstract

Highly purified vesicular stomatitis virus (VSV) was obtained from VSV-infected SV40-transformed hamster cell lines. Immunization with this virus protected hamsters against challenge with SV40-transformed cells (TSV5-cl2). This protection was obtained regardless of the source of the SV40-transformed cells (e.g. cat, rat, hamster) used to produce VSV, and was therefore associated with the SV40 tumor-specific transplantation antigen (SV40-TSTA). Furthermore, when grown on spontaneously transformed cell lines or on cells transformed by a different oncogenic DNA virus, such as polyoma virus, the VSV failed to protect against the SV40-induced tumor. It was concluded that the SV40-TSTA activity of purified VSV is due to the incorporation of SV40-TSTA within the viral envelope. When VSV was treated with proteolytic enzymes (bromelain, trypsin) no loss of TSTA-induced tumor rejection was observed, although VSV had lost its ability to induce virus-neutralizing antibody. This clearly demonstrates that the TSTA activity is not related to the viral spikes. Phospholipase C suppressed the TSTA activity but neutralizing activity was still detectable in the anti-VSV sera. The results presented here demonstrate that the protection afforded by VSV is highly specific. It is particularly interesting that SV40-TSTA activity may be conveyed by the lipid core of the viral envelope.

摘要

高纯度水泡性口炎病毒(VSV)是从感染VSV的SV40转化仓鼠细胞系中获得的。用这种病毒免疫可保护仓鼠免受SV40转化细胞(TSV5-cl2)的攻击。无论用于生产VSV的SV40转化细胞(如猫、大鼠、仓鼠)的来源如何,均可获得这种保护,因此其与SV40肿瘤特异性移植抗原(SV40-TSTA)相关。此外,当VSV在自发转化细胞系或由不同致癌DNA病毒(如多瘤病毒)转化的细胞上生长时,它无法预防SV40诱导的肿瘤。得出的结论是,纯化的VSV的SV40-TSTA活性是由于SV40-TSTA掺入病毒包膜内。当用蛋白水解酶(菠萝蛋白酶、胰蛋白酶)处理VSV时,虽然VSV失去了诱导病毒中和抗体的能力,但未观察到TSTA诱导的肿瘤排斥反应丧失。这清楚地表明TSTA活性与病毒刺突无关。磷脂酶C抑制了TSTA活性,但在抗VSV血清中仍可检测到中和活性。此处给出的结果表明VSV提供的保护具有高度特异性。特别有趣的是,SV40-TSTA活性可能由病毒包膜的脂质核心传递。

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