The COVID-19 Effect on the Immune System and Mitochondrial Dynamics in Diabetes, Obesity, and Dementia

Abstract

The coronavirus disease 2019 (COVID-19) is a pandemic disease, originated in Wuhan City, China. It is caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) and its biology is still poorly understood. Currently, there are no vaccines and drugs/or agents that can reduce severity of this new disease. Recent data suggest that patients with age-related comorbidities, including cardiovascular disease, diabetes, obesity, hypertension, chronic kidney disease, and dementia are highly susceptible to severe respiratory illness due to coronavirus infection. Recent research also revealed that aged individuals with elevated baseline inflammation cause defects in T and B cells, leading to decreased body’s immune response to viral infection. In the current article, we discuss the effects of SARS-CoV-2 on age-related chronic diseases, such as diabetes, obesity, and Alzheimer’s disease. Our article also highlights the interaction between coronavirus and immune cells, and how COVID-19 alters mitochondrial activities in host cells. Based on new and compelling evidence, we propose that mitochondrial fission is inhibited while fusion is promoted, causing mitochondrial elongation and providing a receptive intracellular environment for viral replication in infected cells. Further research is still needed to understand the cross talk between viral replication in mitochondria and disease progression in patients with COVID-19.