Mary Wilson
Well-known member
Posted: 11 Sep 2024
http://dx.doi.org/10.2139/ssrn.4950019
Silverstein, Ana and Wan, Junxiang and Yen, Kelvin and Mehta, Hemal and Kumagai, Hiroshi and Flores, Melanie and Goodrich, Jesse and Hu, Howard and Klausner, Jeffrey D. and Akbari, Omid and Korlanik, Igor and Cohen, Pinchas
Abstract
Long COVID, affecting an estimated 200 million individuals worldwide, is a poorly understood multisystem disorder following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, with unclear causative factors. However, given common symptoms such as brain fog and chronic fatigue, we suggest that long COVID is partially regulated by changes to mitochondrial genes and energy homeostasis. We explore this here by assessing the differences in acute mitochondrial signatures between retrospectively diagnosed COVID convalescent and long COVID patients using two cohorts. For transcriptomic analyses, whole-blood RNA-seq results from publicly accessible data were extracted, assigned long-COVID or convalescent diagnosis retrospectively at 6-months post infection, and compared against non-symptomatic controls to assess for changes in mitochondrial specific gene signatures at 0-3 weeks post infection; revealing distinct mitochondrial gene expression patterns in those with and without long COVID manifestation. For proteomic analyses, plasma samples from 20 long COVID and 20 age- and sex matched COVID-convalescent participants were selected from the Southern California Clinical and Translational Science Institute COVID biorepository, and correlations between levels of 37 inflammatory biomarkers and three mitochondrial-derived peptides (MDPs) were assessed, revealing unique biomarker clustering between patients with and without long COVID. Combined, these findings suggest that successful COVID recovery is mediated in part by efficient mitochondrial repair and reduced oxidative stress, while mitochondrial dysfunction and continued dysregulation of mitochondrial gene expression contributes to chronic inflammation and long COVID onset.
https://elsevier-ssrn-document-stor...8535c28fe22abf315e950b87ef9ad4ab283e49748dd91
http://dx.doi.org/10.2139/ssrn.4950019
Silverstein, Ana and Wan, Junxiang and Yen, Kelvin and Mehta, Hemal and Kumagai, Hiroshi and Flores, Melanie and Goodrich, Jesse and Hu, Howard and Klausner, Jeffrey D. and Akbari, Omid and Korlanik, Igor and Cohen, Pinchas
Abstract
Long COVID, affecting an estimated 200 million individuals worldwide, is a poorly understood multisystem disorder following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, with unclear causative factors. However, given common symptoms such as brain fog and chronic fatigue, we suggest that long COVID is partially regulated by changes to mitochondrial genes and energy homeostasis. We explore this here by assessing the differences in acute mitochondrial signatures between retrospectively diagnosed COVID convalescent and long COVID patients using two cohorts. For transcriptomic analyses, whole-blood RNA-seq results from publicly accessible data were extracted, assigned long-COVID or convalescent diagnosis retrospectively at 6-months post infection, and compared against non-symptomatic controls to assess for changes in mitochondrial specific gene signatures at 0-3 weeks post infection; revealing distinct mitochondrial gene expression patterns in those with and without long COVID manifestation. For proteomic analyses, plasma samples from 20 long COVID and 20 age- and sex matched COVID-convalescent participants were selected from the Southern California Clinical and Translational Science Institute COVID biorepository, and correlations between levels of 37 inflammatory biomarkers and three mitochondrial-derived peptides (MDPs) were assessed, revealing unique biomarker clustering between patients with and without long COVID. Combined, these findings suggest that successful COVID recovery is mediated in part by efficient mitochondrial repair and reduced oxidative stress, while mitochondrial dysfunction and continued dysregulation of mitochondrial gene expression contributes to chronic inflammation and long COVID onset.
https://elsevier-ssrn-document-stor...8535c28fe22abf315e950b87ef9ad4ab283e49748dd91