Influence of intestinal permeability on the manifestations of long COVID-19

SARS-CoV-2 infection causes acute respiratory and systemic disease COVID-19 and leads to cytokine storm. In addition to the lung, damages to the gut and gastrointestinal have also been reported during acute COVID-19. Long lasting symptoms after acute COVID-19 led to description of long-COVID, a syndrome encompassing a protracted course of physical and neurological symptoms that may persist up to 6 months. To date, only few biomarkers of long-COVID have been described. Previous studies showed that high circulating levels of beta-glucan (BDG) are associated with long-COVID and immune activation via NFKB pathway, suggesting a pivotal role of mucosal damage and microbial translocation in persistence of immune activation and disease progressing during COVID-19. We and others showed that acute human immunodeficiency virus (HIV) infection is associated with a decrease epithelial gut integrity, allowing translocation of microbial products in the blood. Moreover, we have shown that gut damage persists in PLWH even after years of antiviral therapy (ART). Cytomegalovirus (CMV) is known directly foster gut damage and inflammation and linked disease severity in COVID-19. Moreover, it is hypothesized that CMV could impair immune response. Currently, the influence of microbial translocation on inflammation and function of the immune system during acute and long-COVID-19 remains unknown. This project will characterize the immune response induced by microbial products during acute and long COVID-19. We hypothesized that acute and long COVID-19 will be associated with gut damage, microbial translocation, inflammation and immune dysfunction. We hope this project will pave the way toward new strategies to decrease the burden of long-COIVD syndrome.