Abstract：
Autophagy and Unfolded Protein Response (UPR) can be regarded as the safe keepers of cells exposed to intense stress. Autophagy maintains cellular homeostasis, ensuring the removal of foreign particles and misfolded macromolecules from the cytoplasm and facilitating the return of the building blocks into the system. On the other hand, UPR serves as a shock response to prolonged stress, especially Endoplasmic Reticulum Stress (ERS), which also includes the accumulation of misfolded proteins in the ER. Since one of the many effects of viral infection on the host cell machinery is the hijacking of the host translational system, which leaves in its wake a plethora of misfolded proteins in the ER, it is perhaps not surprising that UPR and autophagy are common occurrences in infected cells, tissues, and patient samples. In this book chapter, we try to emphasize how UPR, and autophagy are significant in infections caused by six major oncolytic viruses-Epstein-Barr (EBV), Human Papilloma Virus (HPV), Human Immunodeficiency Virus (HIV), Human Herpesvirus-8 (HHV-8), Human T-cell Lymphotropic Virus (HTLV-1), and Hepatitis B Virus (HBV). Here, we document how whole-virus infection or overexpression of individual viral proteins in vitro and in vivo models can regulate the different branches of UPR and the various stages of macro autophagy. As is true with other viral infections, the relationship is complicated because the same virus (or the viral protein) exerts different effects on UPR and Autophagy. The nature of this response is determined by the cell types, or in some cases, the presence of diverse extracellular stimuli. The vice versa is equally valid, i.e., UPR and autophagy exhibit both anti-tumor and pro-tumor properties based on the cell type and other factors like concentrations of different metabolites. Thus, we have tried to coherently summarize the existing knowledge, the crux of which can hopefully be harnessed to design vaccines and therapies targeted at viral carcinogenesis.
摘要：
自噬和未折叠蛋白反应（UPR）可以被视为暴露于强烈压力的细胞的安全饲养者。自噬维持细胞稳态，确保从细胞质中去除外来颗粒和错误折叠的大分子，并促进结构单元返回系统。另一方面,普遍定期审议是对长期压力的休克反应，尤其是内质网应激（ERS），这也包括内质网中错误折叠蛋白的积累。由于病毒感染对宿主细胞机制的许多影响之一是劫持宿主翻译系统，它在急诊室留下了大量的错误折叠的蛋白质，UPR和自噬在感染细胞中很常见，这也许并不奇怪，组织，和患者样本。在这本书的章节中，我们试图强调普遍定期审议，自噬在由六种主要溶瘤病毒-Epstein-Barr（EBV）引起的感染中具有重要意义，人乳头瘤病毒(HPV),人类免疫缺陷病毒(HIV),人类疱疹病毒-8（HHV-8），人类T细胞嗜淋巴细胞病毒（HTLV-1），和乙型肝炎病毒（HBV）。这里,我们记录了体外和体内模型中的全病毒感染或单个病毒蛋白的过表达如何调节UPR的不同分支和宏观自噬的各个阶段.与其他病毒感染一样，由于同一病毒（或病毒蛋白）对UPR和自噬的影响不同，因此这种关系很复杂。这种反应的性质由细胞类型决定，或者在某些情况下，不同细胞外刺激的存在。反之亦然同样有效，即，基于细胞类型和其他因素，如不同代谢物的浓度，UPR和自噬表现出抗肿瘤和促肿瘤特性。因此，我们试图连贯地总结现有的知识，其关键有望被用来设计针对病毒致癌作用的疫苗和疗法。
