Background: The etiology of obesity has been associated with genetic and epigenetic factors, hormonal changes, unhealthy lifestyle habits, and infectious agents such as human adenovirus-36 (HAdV-36). Viral infections induce reactive oxygen species, and the imbalance between oxidative stress/antioxidant results in fat accumulation. In the Mexican population, little is known about the frequency of HAdV-36 and its effect on the balance between antioxidants and oxidants, inflammation, and metabolic markers. The purpose of our study was to evaluate the frequency of HAdV-36 seroprevalence and its relation to body mass index (BMI), lipid profiles, glucose levels, inflammation, and levels of antioxidants and oxidative stress in a representative sample. A cross-sectional study was carried out on 112 healthy adults between 18 and 28 years old, who were divided into four groups according to their BMI: underweight (BMI < 18.5); normal weight (BMI 18.5–24.9); overweight (BMI ≥ 25); and obese (BMI ≥ 30). Blood samples were taken to evaluate lipid and glucose profiles, as well as antioxidant and oxidative stress status, using colorimetric techniques. Seropositivity for HAdV-36 and levels of TNF-α, IL-6, and cortisol were determined using an enzyme-linked immunosorbent assay. The HAdV-36 frequency was 15.6% in underweight subjects, 18.7% in the normal-weight subjects, 34.37% in the overweight subjects, and 31.24% in the obese subjects. The subjects who were positive for HAdV-36 seroprevalence had increased levels of IL-6, cortisol, and oxidative stress, independently of BMI. The HAdV-36-positive subjects had reduced LDL-C and HDL-C levels only in the low-weight groups. Glutathione and SOD levels increased in the underweight and normal-weight subjects with positive HAdV-36 seroprevalence, while catalase levels decreased in the normal-weight, overweight, and obese subjects. In conclusion, for the first time, an HAdV-36 seroprevalence in the adult Mexican population is reported which was higher and had a relation with the presence of inflammation, alterations in the lipid profile, and imbalance between oxidative stress and antioxidant status, regardless of BMI. The oxidative stress/antioxidant imbalance could be participating in the stimulation of white adipose tissue deposition.