Decreased mitochondrial metabolism in activated T cells in post-acute phase after SARS-CoV-2 infection

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B505
Abstract ID: 6297

Presenting Author:
Lavanya Visvabharathy , Research Assistant Professor at Northwestern Univ. Feinberg Sch. of Med., Univ. of Chicago

Abstract:

Since the inception of the COVID-19 pandemic in 2020, it has been evident that SARS-CoV-2 causes multi-system dysfunction and immune perturbations long after clearance of acute infection. Common post-viral sequelae include post-exertional malaise, fatigue, and heart palpitations which are linked to mitochondrial dysfunction even after mild SARS-CoV-2 infection. Severe acute COVID-19 has also been linked to low mitochondrial membrane potential, mitochondrial apoptosis, and decreased mitochondrial respiration in T cells. However, it is unknown whether decreased mitochondrial metabolism persists after conclusion of acute COVID-19 disease, and whether this occurs even in the absence of post-viral sequelae.

We have collected blood samples from healthy donors throughout the course of the COVID-19 pandemic. Using matched PBMC samples from the same subjects pre- and post-SARS-CoV-2 infection, we found decreased mitochondrial metabolism in post-infection T cells after activation. In particular, T cell activation led to decreased mitochondrial mass, decreased mitochondrial reactive oxygen production, and decreased mitochondrial membrane potential in post-COVID compared to pre-COVID samples. This phenotype was most pronounced in CD8 memory T cells. Together, these data suggest that mild SARS-CoV-2 infection can result in decreased mitochondrial metabolism in T cells, providing insight into how SARS-CoV-2 may reprogram T cell function even in the absence of persistent symptoms.