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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Clin Infect Dis. Sep 8, 2026; 15(1): 124175
Published online Sep 8, 2026. doi: 10.5495/wjcid.124175
Post-acute COVID-19 gastrointestinal sequelae: Mechanisms of persistent dysbiosis, intestinal barrier dysfunction, and emerging long-COVID phenotypes
Ahmed Salman
Ahmed Salman, Department of Internal Medicine, Kasr Alainy School of Medicine, Cairo 11562, Egypt
Author contributions: Salman A contributed to the study conception, manuscript drafting, critical revision, and final approval of the manuscript.
AI contribution statement: Claude (Anthropic) was used in a limited manner solely for language refinement, including grammar, clarity, and readability. All scientific content, interpretations, and conclusions were independently reviewed and verified by the authors, who take full responsibility for the integrity and accuracy of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Ahmed Salman, FRACP, FRCP, MRCP, Department of Internal Medicine, Kasr Alainy School of Medicine, 1 Al-Saray Street, Al-Manial, Cairo 11562, Egypt. awea844@gmail.com
Received: June 9, 2026
Revised: July 1, 2026
Accepted: July 14, 2026
Published online: September 8, 2026
Processing time: 91 Days and 5.3 Hours
Core Tip

Core Tip: Long-coronavirus disease gastrointestinal manifestations affect 10%-30% of survivors, but remain overlooked. Persistent dysbiosis-the loss of beneficial bacteria and pathogenic enrichment-drives symptoms through barrier dysfunction, immune dysregulation, and endotoxemia. Dysbiosis has been implicated as a potential contributor to short-chain fatty acid depletion and impaired tryptophan metabolism; however, current human evidence is largely observational, and causality remains unproven. Clinical biomarkers (zonulin, I-FABP, and dysbiotic signatures) enable patient stratification. Microbiota-targeted interventions (probiotics, synbiotics, fecal microbiota transplantation, and postbiotics) offer rational therapeutic approaches. This review establishes dysbiosis as a central therapeutic target and provides an evidence-based framework for its clinical management.

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