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结核病和 COVID-19:合并感染的特征和相关并发症探讨。

TB and COVID-19: An Exploration of the Characteristics and Resulting Complications of Co-infection.

机构信息

College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766-1854, USA.

出版信息

Front Biosci (Schol Ed). 2022 Mar 1;14(1):6. doi: 10.31083/j.fbs1401006.

DOI:10.31083/j.fbs1401006
PMID:35320917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9005765/
Abstract

Tuberculosis (TB) and Coronavirus Disease-19 (COVID-19) infection are two respiratory diseases that are of particular concern epidemiologically. Tuberculosis is one of the oldest diseases recorded in the history of mankind dating back thousands of years. It is estimated that approximately one quarter of the world's population is infected with latent Mycobacterium tuberculosis (LTBI). This contrasts with COVID-19, which emerged in late 2019. Data continues to accumulate and become available on this pathogen, but the long-term side effect of fibrotic damage in COVID-19 patients evokes parallels between this novel coronavirus and its ancient bacterial affiliate. This similarity as well as several others may incite inquiries on whether coinfection of individuals with latent TB and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) lead to excessive fibrosis in the lungs and thus the emergence of an active TB infection. While it is well understood how TB leads to structural and immunological lung complications including granuloma formation, fibrosis, and T cell exhaustion, less is known about the disease course when coinfection with SARS-CoV-2 is present. Past and present research demonstrate that IL-10, TNF-α, IFN class I-III, TGF-β, IL-35, and Regulatory T cells (T-regs) are all important contributors of the characteristics of host response to mycobacterium tuberculosis. It has also been noted with current research that IL-10, TNF-α, IFN class I, II, and III, TGF-β, ACE-2, and T-regs are also important contributors to the host response to the SARS-CoV-2 virus in different ways than they are to the TB pathogen. Both pathogens may lead to an unbalanced inflammatory immune response, and together a shared dysregulation of immune response suggests an increased risk of severity and progression of both diseases. We have reviewed 72 different manuscripts between the years 1992 and 2021. The manuscripts pertaining to the SARS-COV-2 virus specifically are from the years 2020 and 2021. Our literature review aims to explore the biomolecular effects of these contributors to pathogenicity of both diseases along with current publications on TB/COVID-19 coinfection, focusing on the pathogenicity of SARS-CoV-2 infection with both latent and active TB, as well as the challenges in treating TB during the COVID-19 pandemic. The compiled material will then aid the latticework foundation of knowledge for future research leading to a hopeful improved system of therapeutic strategies for coinfection.

摘要

结核病 (TB) 和 2019 年冠状病毒病 (COVID-19) 感染是两种在流行病学上特别令人关注的呼吸道疾病。结核病是人类历史上记载的最古老的疾病之一,可追溯到几千年前。据估计,全世界约有四分之一的人口感染了潜伏性结核分枝杆菌 (LTBI)。这与 2019 年底出现的 COVID-19 形成鲜明对比。关于这种病原体的数据不断积累并可用,但 COVID-19 患者纤维化损害的长期副作用使这种新型冠状病毒与其古老的细菌分支之间存在相似之处。这种相似性以及其他一些相似性可能会引发人们的疑问,即潜伏性结核病和严重急性呼吸系统综合征冠状病毒 2 (SARS-CoV-2) 感染的个体是否会导致肺部过度纤维化,从而导致活动性结核病感染。虽然人们很清楚结核病如何导致结构和免疫肺部并发症,包括肉芽肿形成、纤维化和 T 细胞衰竭,但当与 SARS-CoV-2 同时感染时,对疾病的过程知之甚少。过去和现在的研究表明,IL-10、TNF-α、IFN Ⅰ-Ⅲ 类、TGF-β、IL-35 和调节性 T 细胞 (T-reg) 都是宿主对结核分枝杆菌反应特征的重要贡献者。目前的研究还注意到,IL-10、TNF-α、IFN Ⅰ、Ⅱ和Ⅲ类、TGF-β、ACE-2 和 T-reg 也是宿主对 SARS-CoV-2 病毒反应的重要贡献者,但它们对结核病病原体的作用方式不同。两种病原体都可能导致炎症免疫反应失衡,共同的免疫反应失调表明这两种疾病的严重程度和进展风险增加。我们回顾了 1992 年至 2021 年期间的 72 篇不同的论文。专门针对 SARS-COV-2 病毒的论文来自 2020 年和 2021 年。我们的文献综述旨在探讨这些生物分子对两种疾病致病性的影响,以及当前关于结核病/COVID-19 合并感染的出版物,重点是 SARS-CoV-2 感染与潜伏性和活动性结核病的致病性,以及在 COVID-19 大流行期间治疗结核病的挑战。然后,汇编的材料将为未来的研究提供知识基础,有望为合并感染带来更好的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13f1/9005765/37fa10489362/nihms-1793425-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13f1/9005765/e0c7a8385ec3/nihms-1793425-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13f1/9005765/37fa10489362/nihms-1793425-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13f1/9005765/e0c7a8385ec3/nihms-1793425-f0001.jpg
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