赛氏疱疹病毒导致细胞转化的机制。

Mechanisms of cell transformation by Herpesvirus saimiri.

作者信息

Tsygankov A Y, Romano G

机构信息

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA.

出版信息

Anticancer Res. 1999 Mar-Apr;19(2A):973-83.

Abstract

Herpesvirus saimiri is a virus capable of inducing oncogenic transformation of T lymphocytes of New World primates and immortalizing human T cells in vitro. T lymphocytes immortalized by H. saimiri demonstrate functional biological responses to their antigens. Therefore, H saimiri-induced transformation of T cells emerges as a very powerful tool of T-cell biology. The mechanism of this transformation remains to be elucidated. However, it is apparent that H. saimiri proteins Tip and StpC are crucial for T-cell transformation. Potential mechanisms mediating the effects of Tip and StpC, as well as the possible role of other H. saimiri proteins, are discussed in this review.

摘要

赛米利疱疹病毒是一种能够诱导新大陆灵长类动物T淋巴细胞发生致癌转化并在体外使人类T细胞永生化的病毒。被赛米利疱疹病毒永生化的T淋巴细胞对其抗原表现出功能性生物学反应。因此，赛米利疱疹病毒诱导的T细胞转化成为T细胞生物学中一种非常强大的工具。这种转化的机制仍有待阐明。然而，很明显赛米利疱疹病毒蛋白Tip和StpC对T细胞转化至关重要。本综述讨论了介导Tip和StpC作用的潜在机制，以及其他赛米利疱疹病毒蛋白可能发挥的作用。

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Mechanisms of cell transformation by Herpesvirus saimiri.赛氏疱疹病毒导致细胞转化的机制。

Anticancer Res. 1999 Mar-Apr;19(2A):973-83.

2

Human T cells transduced by a retroviral vector to express Herpesvirus saimiri proteins TIP and STPC.通过逆转录病毒载体转导以表达猴疱疹病毒蛋白TIP和STPC的人T细胞。

Anticancer Res. 1998 Jul-Aug;18(4A):2389-96.

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Tip, an Lck-interacting protein of Herpesvirus saimiri, causes Fas- and Lck-dependent apoptosis of T lymphocytes.Tip是猴疱疹病毒的一种与Lck相互作用的蛋白，可引起T淋巴细胞的Fas和Lck依赖性凋亡。

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Growth transformation of human T cells by herpesvirus saimiri requires multiple Tip-Lck interaction motifs.猴疱疹病毒导致人类T细胞的生长转化需要多个Tip-Lck相互作用基序。

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Herpesvirus saimiri oncoproteins Tip and StpC synergistically stimulate NF-kappaB activity and interleukin-2 gene expression.猴疱疹病毒癌蛋白Tip和StpC协同刺激核因子κB活性和白细胞介素-2基因表达。

Virology. 2001 Jan 5;279(1):325-38. doi: 10.1006/viro.2000.0714.

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Downregulation of p56(lck) tyrosine kinase activity in T cells of squirrel monkeys (Saimiri sciureus) correlates with the nontransforming and apathogenic properties of herpesvirus saimiri in its natural host.松鼠猴（Saimiri sciureus）T细胞中p56(lck)酪氨酸激酶活性的下调与其自然宿主中疱疹病毒Saimiri的非转化和无致病性相关。

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Herpesvirus saimiri.赛米利疱疹病毒

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H. saimiri tyrosine-kinase interacting protein inhibits Tat function: a prototypic strategy for restricting HIV-1-induced cytopathic effects in immune cells.赛氏松鼠猴酪氨酸激酶相互作用蛋白抑制Tat功能：一种限制HIV-1诱导免疫细胞产生细胞病变效应的原型策略。

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Cell transformation by Herpesvirus saimiri.猴疱疹病毒引起的细胞转化

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Altered replication of human immunodeficiency virus type 1 (HIV-1) in T cell lines retrovirally transduced to express Herpesvirus saimiri proteins StpC and/or Tip.在通过逆转录病毒转导以表达猴疱疹病毒蛋白StpC和/或Tip的T细胞系中，1型人类免疫缺陷病毒（HIV-1）复制的改变

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引用本文的文献

1

The Herpesvirus saimiri small nuclear RNAs recruit AU-rich element-binding proteins but do not alter host AU-rich element-containing mRNA levels in virally transformed T cells.赛米利疱疹病毒小核RNA招募富含AU元件结合蛋白，但不改变病毒转化的T细胞中宿主含富含AU元件的mRNA水平。

Mol Cell Biol. 2004 May;24(10):4522-33. doi: 10.1128/MCB.24.10.4522-4533.2004.

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