Potential effects of HMGB1 on viral replication and virus infection-induced inflammatory responses: A promising therapeutic target for virus infection-induced inflammatory diseases

•The released HMGB1 and proinflammatory cytokines form A feed-back loop to enhance the inflammatory response due to virus infection.•The inhibition of HMGB1 release or neutralization of extracellular HMGB1 would suppress inflammatory response and disease severity.•Post-translational modifications (P...

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Published in:Cytokine & growth factor reviews Vol. 62; pp. 54 - 61
Main Authors: Ding, Xiuyan, Li, Shitao, Zhu, Liqian
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-12-2021
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Summary:•The released HMGB1 and proinflammatory cytokines form A feed-back loop to enhance the inflammatory response due to virus infection.•The inhibition of HMGB1 release or neutralization of extracellular HMGB1 would suppress inflammatory response and disease severity.•Post-translational modifications (PTMs), such as acetylation, are critical for the release of HMGB1 following virus infection.•ROS is potentially involved in the regulation of inflammatory response via interaction with HMGB1.•Intracellular HMGB1 regulates viral replication by interacting with viral genomes, viral proteins, or even cellular proteins. Inflammatory responses, characterized by the overproduction of numerous proinflammatory mediators by immune cells, is essential to protect the host against invading pathogens. Excessive production of proinflammatory cytokines is a key pathogenic factor accounting for severe tissue injury and disease progression during the infection of multiple viruses, which are therefore termed as “cytokine storm”. High mobility group box 1 (HMGB1), a ubiquitous DNA-binding protein released either over virus-infected cells or activated immune cells, may act as a proinflammatory cytokine with a robust capacity to potentiate inflammatory response and disease severity. Moreover, HMGB1 is a host factor that potentially participates in the regulation of viral replication cycles with complicated mechanisms. Currently, HMGB1 is regarded as a promising therapeutic target against virus infection. Here, we provide an overview of the updated studies on how HMGB1 is differentially manipulated by distinct viruses to regulate viral diseases.
ISSN:1359-6101
1879-0305
DOI:10.1016/j.cytogfr.2021.08.003