Infectobesity and Lifestyle Responsiveness: Infectious Modifiers of Adiposity with Implications for Nutrition and Exercise Science: An Integrated Review

Abstract

Obesity is a chronic, relapsing, and multifactorial condition with rising global prevalence and substantial cardiometabolic and functional consequences. Although diet and physical activity remain foundational therapies, large inter-individual variability in weight loss and health responses suggests that biological modifiers influence lifestyle responsiveness. The infectobesity hypothesis proposes that specific pathogens can promote adiposity and remodel metabolic phenotypes through effects on adipogenesis, insulin signaling, inflammation, and host–microbiome interactions. Notably, the earliest empirical roots of infectobesity research emerged from avian models, where infection-related adiposity was first documented in chickens. Six pathogens have been reported to cause obesity in animals. The first was an avian retrovirus, which has been shown to cause stunting, obesity, and hyperlipidemia in chickens. The obesity-promoting effect of Borna disease virus was next demonstrated in rats. Scrapie agents were reported to induce obesity in mice and hamsters. The final two reports were of SMAM-1, an avian adenovirus, and Ad-36, a human adenovirus that caused obesity in animals. Additionally, an association with human obesity is a unique feature of SMAM-1 and Ad-36. Human adenovirus 36 (HAdV-36) is the most studied adipogenic pathogen, supported by mechanistic evidence in cell and animal models and by human sero-epidemiological findings, although there are heterogeneous and method-dependent null results. From a sports- and exercise-science perspective, the infection–obesity interface is clinically relevant because training load, energy availability, and dietary patterns can alter immune competence, susceptibility to infection, recovery, and inflammatory tone—factors that may interact with metabolic adaptation and weight-regain biology. This review synthesizes contemporary evidence on infectobesity, highlights methodological pitfalls (diagnostics, temporality, confounding, and publication bias), and proposes an integrated "infection–lifestyle" framework for precision obesity management in clinical and athletic contexts