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致癌病毒对细胞凋亡的调控。

The modulation of apoptosis by oncogenic viruses.

机构信息

Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, México/Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Av. San Fernando 22, col. Sección XVI, Tlalpan, C.P. 14080, Mexico City, Mexico.

出版信息

Virol J. 2013 Jun 6;10:182. doi: 10.1186/1743-422X-10-182.

DOI:10.1186/1743-422X-10-182
PMID:23741982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3691765/
Abstract

Transforming viruses can change a normal cell into a cancer cell during their normal life cycle. Persistent infections with these viruses have been recognized to cause some types of cancer. These viruses have been implicated in the modulation of various biological processes, such as proliferation, differentiation and apoptosis. The study of infections caused by oncogenic viruses had helped in our understanding of several mechanisms that regulate cell growth, as well as the molecular alterations leading to cancer. Therefore, transforming viruses provide models of study that have enabled the advances in cancer research. Viruses with transforming abilities, include different members of the Human Papillomavirus (HPV) family, Hepatitis C virus (HCV), Human T-cell Leukemia virus (HTLV-1), Epstein Barr virus (EBV) and Kaposi's Sarcoma Herpesvirus (KSHV).Apoptosis, or programmed cell death, is a tightly regulated process that plays an important role in development and homeostasis. Additionally, it functions as an antiviral defense mechanism. The deregulation of apoptosis has been implicated in the etiology of diverse diseases, including cancer. Oncogenic viruses employ different mechanisms to inhibit the apoptotic process, allowing the propagation of infected and damaged cells. During this process, some viral proteins are able to evade the immune system, while others can directly interact with the caspases involved in apoptotic signaling. In some instances, viral proteins can also promote apoptosis, which may be necessary for an accurate regulation of the initial stages of infection.

摘要

转化病毒在其正常生命周期中可以将正常细胞转化为癌细胞。这些病毒的持续感染已被认为会导致某些类型的癌症。这些病毒已被牵涉到各种生物学过程的调节,如增殖、分化和凋亡。致癌病毒感染的研究有助于我们理解调节细胞生长的几个机制,以及导致癌症的分子改变。因此,转化病毒为癌症研究提供了可研究的模型。具有转化能力的病毒包括人乳头瘤病毒(HPV)家族的不同成员、丙型肝炎病毒(HCV)、人类 T 细胞白血病病毒(HTLV-1)、爱泼斯坦-巴尔病毒(EBV)和卡波济肉瘤疱疹病毒(KSHV)。凋亡,或程序性细胞死亡,是一个严格调节的过程,在发育和体内平衡中起着重要作用。此外,它还是一种抗病毒防御机制。凋亡的失调与包括癌症在内的多种疾病的病因有关。致癌病毒采用不同的机制来抑制凋亡过程,从而允许受感染和受损细胞的增殖。在这个过程中,一些病毒蛋白能够逃避免疫系统,而另一些则可以直接与参与凋亡信号的半胱天冬酶相互作用。在某些情况下,病毒蛋白也可以促进凋亡,这可能是对感染初始阶段的准确调节所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ab/3691765/738d5efc01c4/1743-422X-10-182-6.jpg
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Kaposi's sarcoma-associated herpesvirus K3 and K5 proteins down regulate both DC-SIGN and DC-SIGNR.卡波济肉瘤相关疱疹病毒 K3 和 K5 蛋白下调 DC-SIGN 和 DC-SIGNR。
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Association of human papillomavirus type 16 long control region mutation and cervical cancer.
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