Mohamed Abdel-Mohsen, PhD

SARS-CoV-2 infection can cause translocation (leakiness) of bacteria and fungi from the lungs or gut to the blood. This translocation can result in systemic inflammation, dysregulated metabolic processes, and worsen the severity of the disease. This study aims to understand the role of microbial translocation in sustaining inflammation after recovering from acute COVID-19. Our hypothesis is that the infection leads to leakiness in the lungs or gut, which can contribute to long-term COVID-19 by influencing inflammatory and metabolic processes. Understanding how microbial translocation contributes to potential long-term complications will establish the foundation for developing innovative biomarkers and therapeutic interventions for Long COVID, or post-acute sequelae SARS-CoV-2 infection (PASC).

Update:

Throughout the past year, we have made substantial progress across several key areas:

Biomarker Development: We discovered metabolic markers that can be measured before infection to predict the severity of COVID-19 and the risk of developing Long COVID. These biomarkers could help identify at-risk individuals early and allow for preventive measures.

Collaborations and Model Development: Working with a large team experienced in creating animal models for viral infections, we helped develop a model for studying Long COVID. This model is crucial for testing new treatments for the condition.

Longitudinal Studies: We have collected and analyzed over 342 samples from 142 people, studying inflammation, intestinal damage, and microbial changes over time. This research is helping us understand how the microbiome affects Long COVID and will lead to new treatment strategies. We also plan to create 3D organoids from some of these samples for more detailed studies.

Our research has important implications. By exploring the link between the gut microbiome and Long COVID, we are improving our understanding of the condition and helping prepare for future pandemics that affect the lungs.