Immunometabolic Links Underlying the Infectobesity with Persistent Viral Infections

Abstract

Obesity and its related comorbidities are prevailing globally. Multiple factors are etiological to cause obesity and relevant metabolic disorders. In this regard, some pathogenic infections including those by viruses have also been associated with obesity (termed especiallky as infectobesity). In this mini-review, I examined recent publications about primary or cofactorial role of viral infections to exacerbate the local and systemic immunometabolic cues that underlie most cofactorial obesity. Major immuno-metabolic pathways involved, including that mediated by interferon (IFN) signaling and peroxisome proliferator activated receptor-γ (PPAR-γ), are discussed. at an inter-systemic level. While excess intake of energy-dense food (such as high-fat diet, HFD) forms a substantial physical factor for adipogenesis, active molecules derived from diet-microbiota interaction in gut, such as short- or long-chain fatty acid (LFA) in HFD, dramatically alter immune and metabolic homeostasis locally and systemically that entails obesity — a globally prevalent disease at the interface of immunity and metabolism involving multiple organs in digestive, endocrine and nervous systems. Major immunological links underlying obesity including local and systemic inflammation, altered cytokine and hormonal regulation, activated immune cells (macrophages, T cells etc.) as briefly listed by each major organ in obesogenesis. From an immunological view, some infections, particularly chronic viral infections as focused here, are associated and even form a reciprocal causality with obesity through their pathogenic intervention with host immune and metabolic systems at various stages of obesity development. Abbreviations: FA, fatty acid; IFN, interferon;