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对单纯疱疹病毒感染的天然抵抗力。人淋巴细胞和单核细胞对病毒复制的抑制作用。

Innate resistance to herpes simplex virus infection. Human lymphocyte and monocyte inhibition of viral replication.

作者信息

Sarmiento M, Kleinerman E S

机构信息

Department of Veterinary Medicine, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

J Immunol. 1990 Mar 1;144(5):1942-53.

PMID:2155270
Abstract

Peripheral blood monocytes and lymphocytes isolated from most humans are resistant to HSV infection in vitro. Viral replication is inhibited very early in the cycle, prior to the onset of alpha-protein synthesis; no viral protein or DNA synthesis is detectable even up to 1 week later. The enhanced expression of two 62-kDa and 57-kDa cellular proteins, however, is induced in the lymphocyte population within 3 to 5 h after infection. A 30-kDa protein is induced in the monocyte population immediately after infection. The induced expression of 62-kDa and 57-kDa lymphocyte proteins appears to be virus-mediated because: a) HSV and pseudorabies virus (although not vaccinia virus) induce the expression of 62-kDa and 57-kDa proteins, b) heat shock or exposure of lymphocytes to uninfected cell extracts does not induce expression of either protein, c) 62-kDa protein is not induced in lymphocytes stimulated with a mitogenic concentration of PHA. UV-inactivated HSV induces expression of 62-kDa and 57-kDa proteins in a manner similar to that observed with untreated virus. In contrast, expression of 30-kDa monocyte protein is induced nonspecifically by either uninfected cell extracts or cell extracts containing virus. Sixty-two-kilodalton and 57-kDa protein induction appears to be a marker for human lymphocytes that express profound intracellular resistance to infection with HSV. Induced expression of these proteins occurs only in lymphocytes that inhibit viral replication very early in the growth cycle, prior to the onset of alpha-protein synthesis. Expression of 62-kDa and 57-kDa proteins is not induced in lymphocytes that are permissive or partially permissive to infection with HSV.

摘要

从大多数人身上分离出的外周血单核细胞和淋巴细胞在体外对单纯疱疹病毒(HSV)感染具有抗性。病毒复制在周期的极早期就受到抑制,早于α蛋白合成开始之前;甚至在1周后都检测不到病毒蛋白或DNA合成。然而,在感染后3至5小时内,淋巴细胞群体中会诱导两种62 kDa和57 kDa细胞蛋白的表达增强。感染后单核细胞群体中立即诱导出一种30 kDa的蛋白。62 kDa和57 kDa淋巴细胞蛋白的诱导表达似乎是由病毒介导的,原因如下:a)HSV和伪狂犬病病毒(尽管痘苗病毒不是)诱导62 kDa和57 kDa蛋白的表达;b)热休克或淋巴细胞暴露于未感染细胞提取物中不会诱导这两种蛋白的表达;c)用促有丝分裂浓度的PHA刺激淋巴细胞不会诱导62 kDa蛋白的表达。紫外线灭活的HSV以与未处理病毒类似的方式诱导62 kDa和57 kDa蛋白的表达。相比之下,30 kDa单核细胞蛋白的表达可由未感染细胞提取物或含有病毒的细胞提取物非特异性诱导。62 kDa和57 kDa蛋白的诱导似乎是人类淋巴细胞对HSV感染表现出深刻细胞内抗性的一个标志。这些蛋白的诱导表达仅发生在生长周期极早期抑制病毒复制的淋巴细胞中,早于α蛋白合成开始之前。在对HSV感染允许或部分允许的淋巴细胞中不会诱导62 kDa和57 kDa蛋白的表达。

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