REVIEW article
Front. Immunol.
Sec. Viral Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1647517
This article is part of the Research TopicLiver Diseases – From Pathophysiology to New Treatment OptionsView all 7 articles
Characteristics and Mechanisms of Liver Injury Caused by Emerging Infectious Diseases
Provisionally accepted
- Huazhong University of Science and Technology Tongji Medical College Union Hospital, Wuhan, China
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Abnormal liver function has become a common phenomenon in emerging infectious diseases caused by viruses, with incidence rates ranging from 2.5% to 98.6% across different pathogens. This review summarized the characteristics of liver injury caused by SARS-CoV-2, MERS-CoV, H7N9, SFTSV, DENV, and EBOV viruses. Viral infection initiates liver injury through direct attack, ischemia, and microthrombosis, triggering an exaggerated immune response often exacerbated by drug toxicity. Core mechanisms involve interconnected mitochondrial dysfunction (causing energy failure, ROS/mt-DNA release), endoplasmic reticulum stress (with dual roles in adaptation and apoptosis), and aberrant inflammation. These pathways form a vicious cycle, culminating in hepatocyte death, metabolic disruption, and severe hepatic damage. An in-depth exploration of the causes and mechanisms of liver injury also provides diversified strategies for treating and preventing these infectious diseases.
Keywords: liver injury, COVID-19, Dengue, SFTS, Ebola, Mitochondrial damage, Endoplasmic Reticulum Stress, Apoptosis
Received: 15 Jun 2025; Accepted: 24 Sep 2025.
Copyright: © 2025 Cheng and Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Xin Zheng, xinz@hust.edu.cn
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