Virus boosts fat in chickens and mice

Sniffling and sneezing, pinkeye, and diarrhea are bad enough. Now, extra body fat? The growing litany of indignities caused by adenoviruses, a set of normally nonlethal but annoying pathogens, appears to be taking an unusual direction.

Researchers at the University of Wisconsin–Madison report in the August International Journal of Obesity that chickens and mice injected with Ad-36, an adenovirus that causes colds in people, have more body fat than uninfected animals.

After 5 weeks, chickens infected with Ad-36 didn’t actually weigh more than uninfected ones. But they had significantly more body fat, less body protein, and lower blood concentrations of cholesterol and triglycerides than control chickens did. Mice receiving an Ad-36 injection were significantly heavier and had 35 percent more body fat than uninfected mice did.

In both chickens and mice, pronounced changes occurred in the amount of abdominal padding known as visceral fat. Compared with controls, there was 67 percent more of this padding in infected mice and more than twice as much in infected chickens. Intriguingly, infected animals didn’t consume more food.

Ethical considerations precluded the scientists from infecting people with adenovirus, but the team examined the blood of obese and nonobese volunteers for the presence of antibodies to Ad-36. These markers of past exposure appeared more frequently in the obese group.

Furthermore, as with the experimental animals, obese people with the antibodies had lower cholesterol and triglyceride concentrations than did obese people without the antibodies. Blood concentrations of antibodies to other adenovirus strains didn’t differ between the two groups.

Anthony Comuzzie of the Southwest Foundation for Biomedical Research in San Antonio calls the study intriguing. “It’s perplexing but interesting,” he says. Too often people dismiss obesity as a matter of food intake, he says, but “we know there are real genetic contributors.”

And genetic expression, he notes, can be affected by pathogens. So, he says, “a viral interaction is completely plausible.”

The viral hypothesis is “radical” but worthy of consideration, says Barbara Corkey, director of the obesity research center at the Boston Medical Center in Massachusetts. Until recently, she says, most scientists considered similarly radical the idea that gastric ulcers are caused by Helicobacter pylori infection rather than an unhealthy lifestyle. Now, the microbe-ulcer link is widely accepted.

Nikhil Dhurandhar, the new paper’s lead author, is currently at Wayne State University in Detroit studying the paradoxical lowering of cholesterol that accompanies Ad-36 infection. He hopes to discover whether the virus decreases production of cholesterol—a health-promoting change—or only moves it from the blood into harmful deposits in the arteries and heart.

Dhurandhar is also searching for the mechanism that parlays viral infection into the observed bodily changes. It’s possible that the virus alters metabolic rate, he says, but his preliminary studies suggest that, instead, Ad-36 increases the rate at which precursor cells mature into fat-storing cells.

In the long term, Dhurandhar says, he’d like to investigate the possibility of using antiviral drugs and vaccines to treat human obesity. He is also exploring whether the other 49 types of human adenovirus promote obesity. Most of these, however, are less likely to play that role than Ad-36 is says Dhurandhar, and “we have our hands full with one virus.”