Obesity and its associated metabolic factors contribute to defective innate immunity and impaired B and T cell responses, enhancing susceptibility to severe SARS-CoV2 infection.
Obesity-induced chronic inflammation and metabolic reprogramming impair immune responses, increasing susceptibility to severe SARS-CoV2 infection.
The risks for complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection are higher in obese individuals. Obesity is a state of chronic low-grade inflammation, with high leptin levels due to leptin resistance, high basal levels of other pro-inflammatory cytokines such as TNF-alpha, MCP-I and IL-6, and low adiponectin levels, thus contributing to a state of defective innate immunity as well as impaired B and T cell responses. Obesity is a risk factor for metabolic syndrome, diabetes, cardiovascular disease and hypertension. It has been observed that pre-existence of these diseases confers a higher risk of severe SARS CoV2 infection as well as the need for intensive care; even below the age of 60 years if their body mass index (BMI) is greater than 30 kg/m2, and even more so if it is 35 kg/m2. The metabolic factors contributing to the changes in altering the immune mechanisms in obese individuals and how this enhances the susceptibility to infection and development of serious SARS-CoV2 infection have been the subject of many debates. Future development of targeted therapy and guidelines will be benefited by greater understanding into these metabolic pathways.
Mehta et al. (Fri,) conducted a review in Obesity and SARS-CoV2. Obesity and its associated metabolic factors contribute to defective innate immunity and impaired B and T cell responses, enhancing susceptibility to severe SARS-CoV2 infection.
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