It has been demonstrated that obese individuals are at a greater risk for complications following SARS-CoV-2 infection [1]. Beyond COVID-19, obesity has been associated with severe complications from a variety of viral infections. Studies on both seasonal and highly pathogenic influenza show a relationship between complications (i.e., hospitalizations and ICU stays) and increased BMI [2, 3]. Numerous studies have demonstrated that obesity elicits a state of low-grade chronic inflammation, in part due to the circulation of mononuclear cells including leukocytes and lymphocytes [4, 5]. Many of the co-morbidities associated with obesity also have shown to alter the immune system, including types 1 and 2 diabetes. Yang and colleagues found that obesity may accelerate thymic involution and a depletion in T-cell repertoire diversity [6]. These effects are typically seen in elderly populations, leading to an increased risk in infection and weakened vaccine efficacy. High fat deposits decrease the level of adiponectin while increasing leptin levels. Adiponectin is an adipocyte hormone, which has shown to decrease macrophage activation and pro-inflammatory cytokine generation, including TNF, IL-6, and NFkB [7]. In contrast, leptin has shown to promote inflammatory reactions in the body as well as its direct action as a pro-inflammatory cytokine [8].