The American Board of Obesity Medicine requires a thorough knowledge of secondary etiologies of obesity, including epigenetics, disordered eating, iatrogenic (obesogenic medications), genetic causes, and hormonal dysregulation, just to name a few. One of the oddities that also falls into this category is viral associations. Unlike the ABOM exam, and more like the viral genome, this blog will be short. However, this topic does show up in the ABOM blueprint, and thus, the small amount of time to read it may provide an easy point or two come test day.

As our understanding of the complexities of obesity comes to light, so do associations that may play a role in increased weight. Some of these associations may be preventable, while others are not. Human adenovirus-36 (Adv-36) is one of these. This specific serotype has been found in multiple studies to have a correlation with obesity. In fact, it has been the only virus that correlates with obesity in experimental animals and naturally infected humans. In animals (chickens, monkeys, and rats), post-infection led to an increase in weight of approximately 10-30%. In humans, 30% of those with obesity had antibodies against Adv-36, whereas only 11% of those with a BMI in a normal range had antibodies; those infected were an average of 25 kg heavier. A meta-analysis confirmed an increased risk of obesity with exposure to this virus, which was especially prominent in children.

The mechanism behind excess weight gain physiologically makes sense. Adv-36 seems to inhibit leptin gene expression. Recall that leptin is made from adipose tissue and is one of the few good adipokines, as it increases both satiety and energy expenditure by activating the POMC/CART pathway and inhibiting the NPY/AgRP pathway. Therefore, with decreased leptin expression, there is decreased POMC/CART activation, and thus, satiety and energy expenditure are subsequently decreased. In addition, the virus increases genetic expression affecting the regulation of fatty acid synthase, ultimately leading to enhanced fat accumulation. Other cellular pathways are disrupted leading to adipogenesis. Although these other pathways are likely beyond the scope of boards, they provide research opportunities into targeted therapies that may eventually lead to pharmacological treatments.

What complicates this topic is that although Adv-36 increases adipogenic accumulation, it has some seemingly positive metabolic effects. Those infected with Adv-36 had increased skeletal glucose uptake independent of insulin signaling. In addition, another modulated pathway proved positive regarding circulating cholesterol and triglyceride levels as a result of increased cholesterol storage, thus reducing circulating levels. All these pathways are being studied for potential treatment targets.

It is too simplistic to say that Adv-36 is the sole cause of the rising levels of obesity, but it makes sense to consider this viral serotype as one of the many hypotheses for why the relatively recent sharp rise in worldwide obesity has occurred. Obesity is a complex, multifaceted disease, but Adv-36 may be a cofactor in this process and, if nothing else, has provided research pathways for future targeted therapies. Although there are numerous other potential viral and infectious correlations with obesity, Adv-36 is the most well-studied and, thus, the most likely culprit to show up on test day. A relatively superficial knowledge of this immensely complex topic is all that is needed on test day.

For a more in-depth reading on this virus (beyond the level for boards) and the specific pathways involved, check out the NCBI review here.

Sample Question

A research grant is approved to study individuals with seropositivity to an adenovirus strain that has been linked with obesity. Per the study protocol, 200 individuals exposed to this virus with confirmed immunoassays are compared to 200 matched seronegative cohorts. Numerous laboratory and anthropometric measurements are obtained in both groups. The seropositive group, when compared to the seronegative group, will likely be found to have higher ratios of which of the following?

A. Glucose resistance

B. Triglyceride levels

C. Leptin-mediated POMC/CART activation

D. Energy expenditure

E. Stored cholesterol

Next Week: Metabolic-associated steatohepatitis

Following Week: Monthly Knowledge Check. This is a review checklist of must-know items for ABOM exams based on the previous four blog topics (Weight gain in pregnancy, measuring dietary intake, viral etiology of obesity, metabolic-associated steatohepatitis). In addition, this will include a brief explanation of the correct answers to previous sample questions.

Upcoming: Single anastomosis gastric bypass, Alstrom’s disease, ketogenic diet, and everything to know about metformin

For more practice questions, check out the following:

  • Obesity Medicine Board Review Questions (2026): Q 55.
  • Obesity Medicine Practice Tests (2026): Q 281.

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