Impact of obesity and SARS-CoV-2 infection: implications for host defence - a living review

Abstract

The role of obesity in the pathophysiology of respiratory virus infections has become particularly apparent during the current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, where obese patients are twice as likely to suffer from severe coronavirus disease 2019 (COVID-19) than healthy weight individuals. Obesity results in disruption of systemic lipid metabolism promoting a state of chronic low-grade inflammation. However, it remains unclear how these underlying metabolic and cellular processes promote severe SARS-CoV-2 infection. Emerging SARS-CoV-2 data and studies of influenza A virus (IAV) show that viruses can further subvert the host’s altered lipid metabolism and exploit obesity-induced alterations in immune cell metabolism and function to promote chronic inflammation and viral propagation. In this review, we outline the systemic metabolic and immune alterations underlying obesity and discuss how these baseline alterations impact the immune response and disease pathophysiology. A better understanding of the immuno-metabolic landscape of obese patients may aid better therapies and future vaccine design.

Does abdominal obesity influence immunological response to SARS-CoV-2 infection?

“…Enhanced abdominal visceral adipose tissue deposition in the obese represents the “soil” for chronic low-grade systemic inflammation by activated immune cells in response to over-nutrition [ 17 ]. Abnormal secretion of cytokines and other immune mediators, such as interferon, tumor necrosis factor-alpha from abdominal adipocytes, is partly responsible for a chronic low-grade inflammation, thus reducing immune system activity and adversely affecting lung function [ 18 ].…”

COVID-19 in People With Schizophrenia: Potential Mechanisms Linking Schizophrenia to Poor Prognosis

“…First, as mentioned earlier, obesity is highly prevalent in people with chronic schizophrenia (8), and ACE2 gene expression has been reported to be higher in visceral and subcutaneous adipose tissue than in lung tissues (59). ACE2 is the principal cellular entry receptor for SARS-CoV-2 (77), and this mechanism may suggest a high viral propagation in people with schizophrenia who are obese (78). The adipose tissue may, therefore act as a viral reservoir, contributing to prolonged viral shedding (79), and a more contagious state in people with schizophrenia.…”

CD8+ T Cells in SARS-CoV-2 Induced Disease and Cancer—Clinical Perspectives

“…Obesity is among preexisting conditions that cause patients to be prone to a more severe SARS-CoV-2 disease (154). A possibility of experiencing a severe disease is twice in obese individuals compared with normal-weight SARS-CoV-2 patients (155). Obesity alters the balance between innate and adaptive immunity.…”