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潜伏性结核分枝杆菌的遗传信息概述

An Overview of Genetic Information of Latent Mycobacterium tuberculosis.

作者信息

Hamidieh Faezeh, Farnia Parissa, Nowroozi Jamileh, Farnia Poopak, Velayati Ali Akbar

机构信息

Departement of Microbiology, Faculty of Biological Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran.

Mycobacteriology Research (MRC), National Research Institute of Tuberculosis and Lung Disease (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Tuberc Respir Dis (Seoul). 2021 Jan;84(1):1-12. doi: 10.4046/trd.2020.0116. Epub 2020 Oct 30.

Abstract

Mycobacterium tuberculosis has infected more than two billion individuals worldwide, of whom 5%-10% have clinically active disease and 90%-95% remain in the latent stage with a reservoir of viable bacteria in the macrophages for extended periods of time. The tubercle bacilli at this stage are usually called dormant, non-viable, and/or non-culturable microorganisms. The patients with latent bacilli will not have clinical pictures and are not infectious. The infections in about 2%-23% of the patients with latent status become reactivated for various reasons such as cancer, human immunodeficiency virus infection, diabetes, and/or aging. Many studies have examined the mechanisms involved in the latent state of Mycobacterium and showed that latency modified the expression of many genes. Therefore, several mechanisms will change in this bacterium. Hence, this study aimed to briefly examine the genes involved in the latent state as well as the changes that are caused by Mycobacterium tuberculosis. The study also evaluated the relationship between the functions of these genes.

摘要

结核分枝杆菌已感染全球超过20亿人,其中5%-10%患有临床活动性疾病,90%-95%仍处于潜伏阶段,巨噬细胞中长期存在有活力的细菌库。此阶段的结核杆菌通常被称为休眠、无活力和/或不可培养的微生物。潜伏有杆菌的患者不会出现临床症状,也不具有传染性。约2%-23%处于潜伏状态的患者因各种原因(如癌症、人类免疫缺陷病毒感染、糖尿病和/或衰老)导致感染复发。许多研究探讨了结核分枝杆菌潜伏状态所涉及的机制,并表明潜伏状态改变了许多基因的表达。因此,该细菌的多种机制将会发生变化。因此,本研究旨在简要研究与潜伏状态相关的基因以及结核分枝杆菌所引起的变化。该研究还评估了这些基因功能之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9365/7801807/4cedd89af7c6/trd-2020-0116f1.jpg

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