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通过基因组可塑性和表观遗传学理解利什曼原虫寄生虫体内寄生虫生存和耐药性的范例：认知和未来展望。

The paradigm of intracellular parasite survival and drug resistance in leishmanial parasite through genome plasticity and epigenetics: Perception and future perspective.

机构信息

Infectious Diseases and Immunology Division, Indian Institute of Chemical Biology, Kolkata, West Bengal, India.

出版信息

Front Cell Infect Microbiol. 2023 Feb 6;13:1001973. doi: 10.3389/fcimb.2023.1001973. eCollection 2023.

DOI:10.3389/fcimb.2023.1001973
PMID:36814446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9939536/
Abstract

is an intracellular, zoonotic, kinetoplastid eukaryote with more than 1.2 million cases all over the world. The leishmanial chromosomes are divided into polymorphic chromosomal ends, conserved central domains, and antigen-encoding genes found in telomere-proximal regions. The genome flexibility of chromosomal ends of the leishmanial parasite is known to cause drug resistance and intracellular survival through the evasion of host defense mechanisms. Therefore, in this review, we discuss the plasticity of genome organization which is the primary cause of drug resistance and parasite survival. Moreover, we have not only elucidated the causes of such genome plasticity which includes aneuploidy, epigenetic factors, copy number variation (CNV), and post-translation modification (PTM) but also highlighted their impact on drug resistance and parasite survival.

摘要

利什曼原虫是一种细胞内、人畜共患的动质体原生动物，全世界有超过 120 万例病例。利什曼原虫染色体分为多态性染色体末端、保守的中央结构域和位于端粒近端区域的抗原编码基因。已知利什曼原虫染色体末端的基因组灵活性会导致药物耐药性，并通过逃避宿主防御机制来实现细胞内生存。因此，在这篇综述中，我们讨论了导致药物耐药性和寄生虫生存的基因组组织可塑性的主要原因。此外，我们不仅阐明了导致这种基因组可塑性的原因，包括非整倍体、表观遗传因素、拷贝数变异（CNV）和翻译后修饰（PTM），还强调了它们对药物耐药性和寄生虫生存的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c69e/9939536/11740a5d0a05/fcimb-13-1001973-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c69e/9939536/88b6296175b4/fcimb-13-1001973-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c69e/9939536/11740a5d0a05/fcimb-13-1001973-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c69e/9939536/88b6296175b4/fcimb-13-1001973-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c69e/9939536/11740a5d0a05/fcimb-13-1001973-g002.jpg

相似文献

[1]
The paradigm of intracellular parasite survival and drug resistance in leishmanial parasite through genome plasticity and epigenetics: Perception and future perspective.

Front Cell Infect Microbiol. 2023

[2]
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[3]
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引用本文的文献

[1]
Unravelling drug resistance in leishmaniasis: genomic adaptations and emerging therapies.

Front Mol Biosci. 2025-5-26

[2]
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Med Microbiol Immunol. 2025-4-9

[3]
Molecular Mechanisms of Drug Resistance in spp.

Pathogens. 2024-9-27

[4]
Targeting and activation of macrophages in leishmaniasis. A focus on iron oxide nanoparticles.

Front Immunol. 2024

本文引用的文献

[1]
Bromodomain factor 5 is an essential regulator of transcription in Leishmania.

Nat Commun. 2022-7-13

[2]
The pathogenicity and virulence of Leishmania - interplay of virulence factors with host defenses.

Virulence. 2022-12

[3]
Revealing a Novel Antigen Repressor of Differentiation Kinase 2 for Diagnosis of Human Visceral Leishmaniasis in India.

Pathogens. 2022-1-20

[4]
Going ballistic: Leishmania nuclear subversion of host cell plasticity.

Trends Parasitol. 2022-3

[5]
Super enhancer-mediated transcription of miR146a-5p drives M2 polarization during Leishmania donovani infection.

PLoS Pathog. 2021-2-25

[6]
: Responding to environmental signals and challenges without regulated transcription.

Comput Struct Biotechnol J. 2020-12-7

[7]
Casein kinase 1.2 over expression restores stress resistance to Leishmania donovani HSP23 null mutants.

Sci Rep. 2020-9-29

[8]
Subverts Host Immune Response by Epigenetic Reprogramming of Macrophage M(Lipopolysaccharides + IFN-γ)/M(IL-10) Polarization.

J Immunol. 2020-5-15

[9]
A BONCAT-iTRAQ method enables temporally resolved quantitative profiling of newly synthesised proteins in Leishmania mexicana parasites during starvation.

PLoS Negl Trop Dis. 2019-12-19

[10]
Tracking of quiescence in Leishmania by quantifying the expression of GFP in the ribosomal DNA locus.

Sci Rep. 2019-12-12

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