病毒诱导肿瘤和其他致病性单细胞实体的裂解及其治疗利什曼病的潜力。

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Janaina Fernandes
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引用次数: 0

摘要

本文主要介绍了病毒感染和裂解单细胞真核生物的主要途径,这些单细胞真核生物被描述为多细胞生物的致病性。根据最近关于肿瘤细胞如何表现单细胞行为的讨论,高度恶性细胞可以被认为是另一种单细胞致病实体,但具有内源性起源。因此,一个比较面板的病毒裂解外源性致病性单细胞真核生物,如棘阿米巴sp.,酵母和肿瘤提出。重要的细胞内寄生虫利什曼原虫sp也提出,相比之下,它的毒力提高了病毒感染。讨论了利用病毒介导的真核细胞裂解来克服利什曼原虫感染的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Virus-Induced Lysis of Tumor and Other Pathogenic Unicellular Entities and Its Potential to Treat Leishmaniasis.

This article is focused on the main pathways used by viruses to achieve infection and lysis of unicellular eukaryotes described as pathogenic for multicellular organisms. In light of the recent discussions on how tumor cells exhibit unicellular behavior, highly malignant cells can be considered as another unicellular pathogenic entity, but with endogenous origin. Thus, a comparative panel of viral lysis of exogenous pathogenic unicellular eukaryotes such as Acanthamoeba sp., yeast, and tumors is presented. The important intracellular parasite Leishmania sp is also presented, which, in contrast, has its virulence improved by viral infections. The possible exploitation of viral-mediated eukaryotic cell lysis to overcome infections of Leishmania sp is discussed.

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来源期刊
DNA and cell biology
DNA and cell biology 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
93
审稿时长
1.5 months
期刊介绍: DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward. DNA and Cell Biology coverage includes: Gene Structure, Function, and Regulation Gene regulation Molecular mechanisms of cell activation Mechanisms of transcriptional, translational, or epigenetic control of gene expression Molecular Medicine Molecular pathogenesis Genetic approaches to cancer and autoimmune diseases Translational studies in cell and molecular biology Cellular Organelles Autophagy Apoptosis P bodies Peroxisosomes Protein Biosynthesis and Degradation Regulation of protein synthesis Post-translational modifications Control of degradation Cell-Autonomous Inflammation and Host Cell Response to Infection Responses to cytokines and other physiological mediators Evasive pathways of pathogens.
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