tetano
Editor, Senior Moderator
Front Immunol
. 2024 Aug 12:15:1433531.
doi: 10.3389/fimmu.2024.1433531. eCollection 2024. Obesity-compromised immunity in post-COVID-19 condition: a critical control point of chronicity
Soonwoo Jang[SUP] 1 2 3 [/SUP], Wooyoung Hong[SUP] 4 [/SUP], Yuseok Moon[SUP] 1 2 3 5 [/SUP]
Affiliations
Post-COVID-19 condition is recognized as a multifactorial disorder, with persistent presence of viral antigens, discordant immunity, delayed viral clearance, and chronic inflammation. Obesity has emerged as an independent risk factor for both SARS-CoV-2 infection and its subsequent sequelae. In this study, we aimed to predict the molecular mechanisms linking obesity and post-COVID-19 distress. Viral antigen-exposed adipose tissues display remarkable levels of viral receptors, facilitating viral entry, deposition, and chronic release of inflammatory mediators and cells in patients. Subsequently, obesity-associated inflammatory insults are predicted to disturb cellular and humoral immunity by triggering abnormal cell differentiation and lymphocyte exhaustion. In particular, the decline in SARS-CoV-2 antibody titers and T-cell exhaustion due to chronic inflammation may account for delayed virus clearance and persistent activation of inflammatory responses. Taken together, obesity-associated defective immunity is a critical control point of intervention against post-COVID-19 progression, particularly in subjects with chronic metabolic distress.
Keywords: ACE2; COVID-19; SARS-CoV-2; adipose tissue; immunity; long COVID; obesity; post COVID-19 condition.
. 2024 Aug 12:15:1433531.
doi: 10.3389/fimmu.2024.1433531. eCollection 2024. Obesity-compromised immunity in post-COVID-19 condition: a critical control point of chronicity
Soonwoo Jang[SUP] 1 2 3 [/SUP], Wooyoung Hong[SUP] 4 [/SUP], Yuseok Moon[SUP] 1 2 3 5 [/SUP]
Affiliations
- PMID: 39188722
- PMCID: PMC11345197
- DOI: 10.3389/fimmu.2024.1433531
Post-COVID-19 condition is recognized as a multifactorial disorder, with persistent presence of viral antigens, discordant immunity, delayed viral clearance, and chronic inflammation. Obesity has emerged as an independent risk factor for both SARS-CoV-2 infection and its subsequent sequelae. In this study, we aimed to predict the molecular mechanisms linking obesity and post-COVID-19 distress. Viral antigen-exposed adipose tissues display remarkable levels of viral receptors, facilitating viral entry, deposition, and chronic release of inflammatory mediators and cells in patients. Subsequently, obesity-associated inflammatory insults are predicted to disturb cellular and humoral immunity by triggering abnormal cell differentiation and lymphocyte exhaustion. In particular, the decline in SARS-CoV-2 antibody titers and T-cell exhaustion due to chronic inflammation may account for delayed virus clearance and persistent activation of inflammatory responses. Taken together, obesity-associated defective immunity is a critical control point of intervention against post-COVID-19 progression, particularly in subjects with chronic metabolic distress.
Keywords: ACE2; COVID-19; SARS-CoV-2; adipose tissue; immunity; long COVID; obesity; post COVID-19 condition.