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Of the many viruses screened, adenovirus 36 has been found to be a strong candidate virus that is associated with obesity, based on evidence in various model systems as well as clinical data. The mechanism of how the adenovirus could lead to obesity is not known and this paper proposes some new insights into how oxidative stress could be a possible mechanism of how adenovirus might lead to obesity. This paper reviews the relevant literature of both the effect of adenovirus on cells' anti-oxidant response and the link between obesity and oxidative stress.

"Our results suggest that oxidative stress may be partly responsible for the toxicity of adenovirus transduction."

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"Concordantly, E1A sensitized cells to the cytotoxic effects of oxidative stress and enhanced the accumulation of reactive oxygen species in response to pro-oxidant challenge. These results demonstrate that expression of E1A impedes the cellular response to oxidative stress, including the induction of ferritin."

Research in Alzheimer disease has recently demonstrated compelling evidence on the importance of oxidative processes in its pathogenesis. Cellular changes show that oxidative stress is an event that precedes the appearance of the hallmark pathologies of the disease, neurofibrillary tangles, and senile plaques.

A viral infection that involves virus invasion, protein synthesis, and virion assembly is typically accompanied by sharp fluctuations in the intracellular levels of metabolites. Under certain conditions, dramatic metabolic shifts can result in various types of cell death. Here, we review different types of adenovirus-induced cell death associated with changes in metabolic profiles of the infected cells.

As evidenced by experimental data, in most cases changes in the metabolome precede cell death rather than represent its consequence. In our previous study, the induction of autophagic cell death was observed following adenovirus-mediated lactate production, acetyl-CoA accumulation, and ATP release, while apoptosis was demonstrated to be modulated by alterations in acetate and asparagine metabolism.