结核和COVID-19:合并感染的特点及并发症探讨。

Erica Luke, Kimberly Swafford, Gabriella Shirazi, Vishwanath Venketaraman
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引用次数: 17

摘要

结核病(TB)和冠状病毒病-19 (COVID-19)感染是流行病学上特别令人关注的两种呼吸道疾病。结核病是人类历史上记载的最古老的疾病之一,可以追溯到几千年前。据估计,世界上大约四分之一的人口感染了潜伏结核分枝杆菌(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和可用,但COVID-19患者纤维化损伤的长期副作用令人联想起这种新型冠状病毒与其古老的细菌附属体之间的相似之处。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综合征冠状病毒2 (SARS-CoV-2)患者的共同感染是否会导致肺部过度纤维化,从而出现活动性结核病感染。虽然人们很清楚结核病如何导致包括肉芽肿形成、纤维化和T细胞衰竭在内的结构性和免疫性肺部并发症,但对合并感染SARS-CoV-2时的病程知之甚少。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-regs)都是宿主对结核分枝杆菌反应特征的重要贡献者。目前的研究也注意到,IL-10、TNF-α、IFN I类、II类和III类、TGF-β、ACE-2和T-regs也是宿主对SARS-CoV-2病毒反应的重要贡献者,其方式不同于对TB病原体的反应。这两种病原体都可能导致不平衡的炎症免疫反应,共同的免疫反应失调表明这两种疾病的严重程度和进展的风险增加。我们审查了1992年至2021年间的72份不同的手稿。具体来说,与SARS-COV-2病毒有关的手稿来自2020年和2021年。我们的文献综述旨在探讨这些致病因子对两种疾病致病性的生物分子作用,以及目前关于TB/COVID-19共感染的出版物,重点关注SARS-CoV-2感染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。汇编的材料将有助于为未来的研究奠定知识基础,从而有希望改进合并感染的治疗策略系统。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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.

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