Based on seroepidemiological studies, human herpes simplex virus types 1 and 2 (HSV-1, HSV-2) are put in relation with a number of cancer diseases; however, they do not appear to play a direct role, being only considered cofactors. Their ability to transform the cells in vitro could be demonstrated experimentally by removing their high lytic ability by a certain dose of UV radiation or by photoinactivation in the presence of photosensitizers, such as neutral red or methylene blue, or culturing under conditions suppressing their lytic activity. However, recent studies indicate that UV irradiated or photoinactivated HSV-1 and HSV-2, able to transform non-transformed cells, behave differently in transformed cells suppressing their transformed phenotype. Furthermore, both transforming and transformed phenotype suppressing activities are pertaining only to non-syncytial virus strains. There are some proposed mechanisms explaining their transforming activity. According to the "hit and run" mechanism, viral DNA induces only initiation of transformation by interacting with cellular DNA bringing about mutations and epigenetic changes and is no longer involved in other processes of neoplastic progression. According to the "hijacking" mechanism, virus products in infected cells may activate signalling pathways and thus induce uncontrolled proliferation. Such a product is e.g. a product of HSV-2 gene designated ICP10 that encodes an oncoprotein RR1PK that activates the Ras pathway. In two cases of cancer, in the case of serous ovarian carcinoma and in some prostate tumours, virus-encoded microRNAs (miRNAs) were detected as a possible cofactor in tumorigenesis. And, recently described herpes virus-associated growth factors with transforming and transformation repressing activity might be considered important factors playing a role in tumour formation. And finally, there is a number of evidence that HSV-2 may increase the risk of cervical cancer after infection with human papillomaviruses. A similar situation is with human cytomegalovirus; however, here, a novel mechanism named oncomodulation has been proposed. Oncomodulation means that HCMV infects tumour cells and modulates their malignant properties without having a direct effect on cell transformation.

中文翻译：

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人类甲型和乙型疱疹病毒和癌症：乘客还是敌人？

根据血清流行病学研究，将人类1型和2型单纯疱疹病毒（HSV-1，HSV-2）与多种癌症疾病相关联；但是，它们似乎没有直接作用，仅被认为是辅助因子。通过在一定剂量的紫外线照射下去除其高裂解能力或在光敏剂（例如中性红或亚甲基蓝）存在下进行光灭活，或在抑制其裂解活性的条件下培养，可以通过实验证明其在体外转化细胞的能力。 。然而，最近的研究表明，能够转化未转化细胞的紫外线照射或光灭活的HSV-1和HSV-2在抑制其转化表型的转化细胞中表现不同。此外，转化和转化表型抑制活性均仅与非合胞体病毒株有关。有一些提出的机制解释了它们的转化活动。根据“即动即跑”机制，病毒DNA通过与细胞DNA相互作用仅诱导转化的启动，从而引起突变和表观遗传学变化，并且不再参与其他肿瘤进展过程。根据“劫持”机制，受感染细胞中的病毒产物可能会激活信号传导途径，从而诱导不受控制的增殖。这样的产物是例如称为ICP10的HSV-2基因的产物，其编码激活Ras途径的癌蛋白RR1PK。在两个癌症病例中，在浆液性卵巢癌和某些前列腺肿瘤中，病毒编码的microRNA（miRNA）被检测为肿瘤发生的可能辅助因子。并且，最近描述的具有转化和转化抑制活性的疱疹病毒相关生长因子可能被认为是在肿瘤形成中起作用的重要因子。最后，有许多证据表明HSV-2可能会增加人类乳头瘤病毒感染后患子宫颈癌的风险。人类巨细胞病毒也有类似情况。但是，这里提出了一种新的机制，称为oncomodulation。Oncomodulation意味着HCMV感染肿瘤细胞并调节其恶性特性，而对细胞转化没有直接影响。最近描述的具有转化和转化抑制活性的疱疹病毒相关生长因子可能被认为是在肿瘤形成中起作用的重要因子。最后，有许多证据表明HSV-2可能会增加人类乳头瘤病毒感染后患子宫颈癌的风险。人类巨细胞病毒也有类似情况。但是，这里提出了一种新的机制，称为oncomodulation。Oncomodulation意味着HCMV感染肿瘤细胞并调节其恶性特性，而对细胞转化没有直接影响。最近描述的具有转化和转化抑制活性的疱疹病毒相关生长因子可能被认为是在肿瘤形成中起作用的重要因子。最后，有许多证据表明HSV-2可能会增加人类乳头瘤病毒感染后患子宫颈癌的风险。人类巨细胞病毒也有类似情况。但是，这里提出了一种新的机制，称为oncomodulation。Oncomodulation意味着HCMV感染肿瘤细胞并调节其恶性特性，而对细胞转化没有直接影响。人类巨细胞病毒也有类似情况。但是，这里提出了一种新的机制，称为oncomodulation。Oncomodulation意味着HCMV感染肿瘤细胞并调节其恶性特性，而对细胞转化没有直接影响。人类巨细胞病毒也有类似情况。但是，这里提出了一种新的机制，称为oncomodulation。Oncomodulation意味着HCMV感染肿瘤细胞并调节其恶性特性，而对细胞转化没有直接影响。