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马尔堡病毒的出现:关于致命疫情及临床挑战的全球视角

Emergence of Marburg virus: a global perspective on fatal outbreaks and clinical challenges.

作者信息

Srivastava Shriyansh, Sharma Deepika, Kumar Sachin, Sharma Aditya, Rijal Rishikesh, Asija Ankush, Adhikari Suraj, Rustagi Sarvesh, Sah Sanjit, Al-Qaim Zahraa Haleem, Bashyal Prashant, Mohanty Aroop, Barboza Joshuan J, Rodriguez-Morales Alfonso J, Sah Ranjit

机构信息

Department of Pharmacology, Delhi Pharmaceutical Sciences and Research University (DPSRU), New Delhi, India.

Department of Pharmacy, School of Medical and Allied Sciences, Galgotias University, Greater Noida, India.

出版信息

Front Microbiol. 2023 Sep 13;14:1239079. doi: 10.3389/fmicb.2023.1239079. eCollection 2023.

DOI:10.3389/fmicb.2023.1239079
PMID:37771708
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10526840/
Abstract

The Marburg virus (MV), identified in 1967, has caused deadly outbreaks worldwide, the mortality rate of Marburg virus disease (MVD) varies depending on the outbreak and virus strain, but the average case fatality rate is around 50%. However, case fatality rates have varied from 24 to 88% in past outbreaks depending on virus strain and case management. Designated a priority pathogen by the National Institute of Allergy and Infectious Diseases (NIAID), MV induces hemorrhagic fever, organ failure, and coagulation issues in both humans and non-human primates. This review presents an extensive exploration of MVD outbreak evolution, virus structure, and genome, as well as the sources and transmission routes of MV, including human-to-human spread and involvement of natural hosts such as the Egyptian fruit bat () and other . The disease progression involves early viral replication impacting immune cells like monocytes, macrophages, and dendritic cells, followed by damage to the spleen, liver, and secondary lymphoid organs. Subsequent spread occurs to hepatocytes, endothelial cells, fibroblasts, and epithelial cells. MV can evade host immune response by inhibiting interferon type I (IFN-1) synthesis. This comprehensive investigation aims to enhance understanding of pathophysiology, cellular tropism, and injury sites in the host, aiding insights into MVD causes. Clinical data and treatments are discussed, albeit current methods to halt MVD outbreaks remain elusive. By elucidating MV infection's history and mechanisms, this review seeks to advance MV disease treatment, drug development, and vaccine creation. The World Health Organization (WHO) considers MV a high-concern filovirus causing severe and fatal hemorrhagic fever, with a death rate ranging from 24 to 88%. The virus often spreads through contact with infected individuals, originating from animals. Visitors to bat habitats like caves or mines face higher risk. We tailored this search strategy for four databases: Scopus, Web of Science, Google Scholar, and PubMed. we primarily utilized search terms such as "Marburg virus," "Epidemiology," "Vaccine," "Outbreak," and "Transmission." To enhance comprehension of the virus and associated disease, this summary offers a comprehensive overview of MV outbreaks, pathophysiology, and management strategies. Continued research and learning hold promise for preventing and controlling future MVD outbreaks. GRAPHICAL ABSTRACT.

摘要

马尔堡病毒(MV)于1967年被发现,已在全球引发致命疫情。马尔堡病毒病(MVD)的死亡率因疫情和病毒株而异,但平均病死率约为50%。然而,根据病毒株和病例管理情况,过去疫情中的病死率在24%至88%之间波动。马尔堡病毒被美国国立过敏与传染病研究所(NIAID)指定为优先病原体,它会在人类和非人类灵长类动物中引发出血热、器官衰竭和凝血问题。本综述广泛探讨了MVD疫情的演变、病毒结构和基因组,以及马尔堡病毒的来源和传播途径,包括人际传播以及埃及果蝠等天然宿主的参与情况。疾病进展包括早期病毒复制影响单核细胞、巨噬细胞和树突状细胞等免疫细胞,随后损害脾脏、肝脏和二级淋巴器官。随后病毒会扩散到肝细胞、内皮细胞、成纤维细胞和上皮细胞。马尔堡病毒可通过抑制I型干扰素(IFN-1)合成来逃避宿主免疫反应。这项全面调查旨在增进对宿主病理生理学、细胞嗜性和损伤部位的了解,有助于深入了解MVD的病因。文中讨论了临床数据和治疗方法,尽管目前仍难以找到阻止MVD疫情爆发的方法。通过阐明马尔堡病毒感染的历史和机制,本综述旨在推动马尔堡病毒病的治疗、药物研发和疫苗创制。世界卫生组织(WHO)认为马尔堡病毒是一种令人高度关注的丝状病毒,可导致严重且致命的出血热,死亡率在24%至88%之间。该病毒通常通过与受感染个体接触传播,这些个体最初来自动物。前往洞穴或矿井等蝙蝠栖息地的游客面临更高风险。我们针对四个数据库(Scopus、科学网、谷歌学术和PubMed)制定了此搜索策略。我们主要使用了“马尔堡病毒”“流行病学”“疫苗”“疫情爆发”和“传播”等搜索词。为加强对该病毒及相关疾病的理解,本综述全面概述了马尔堡病毒疫情、病理生理学和管理策略。持续的研究和学习有望预防和控制未来的MVD疫情爆发。图形摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/5d3e4d409958/fmicb-14-1239079-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/502125166592/fmicb-14-1239079-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/fa0887e3308f/fmicb-14-1239079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/9e732c577a55/fmicb-14-1239079-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/53aa40ec414e/fmicb-14-1239079-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/5d3e4d409958/fmicb-14-1239079-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/502125166592/fmicb-14-1239079-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/fa0887e3308f/fmicb-14-1239079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/9e732c577a55/fmicb-14-1239079-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/53aa40ec414e/fmicb-14-1239079-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0022/10526840/5d3e4d409958/fmicb-14-1239079-g004.jpg

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