New human virus linked to obesity in animals

NEW YORK (Reuters Health) - Researchers have identified a new human virus that increases fat deposits and, paradoxically, reduces triglyceride levels in animals, according to a report in the American Journal of Physiology -- Regulatory, Integrative, and Comparative Physiology.

These findings could have important clinical implications for understanding and preventing obesity in humans, the authors suggest.

In earlier studies, Dr. Richard L. Atkinson, and his colleagues from the University of Wisconsin at Madison, had shown that inoculation with adenovirus-36 increases fat levels and decreases cholesterol and triglycerides levels in chickens, mice and nonhuman primates. Last year, a different research group reported that adenovirus-5 promotes obesity in mice.

In the present study, Atkinson's team looked at the effect on fat of adenovirus -2, -31, and -37 in chickens. Of the three viruses, only adenovirus-37 had a pronounced effect on fat.

Like adenovirus-36, adenovirus-37 produced a drop in triglyceride levels, the investigators note. By contrast, adenovirus-37 increased cholesterol levels, just the opposite of what had been seen with adenovirus-36.

Increased fat cell differentiation and triglyceride accumulation were seen with both adenovirus-31 and -37, but not with adenovirus-2, the report indicates.

"The nearly simultaneous increase in the prevalence of obesity in most countries of the world is difficult to explain by changes in food intake and exercise alone, and suggests that adenoviruses could have contributed," the authors state.

"The role of adenoviruses in the worldwide epidemic of obesity is a critical question that demands additional research."

All adenoviruses are transmitted through direct contact and most frequently result in respiratory illness. Depending on the type, they may also cause gastrointestinal illness, eye infections, bladder infections or rashes. Some types of adenovirus also cause persistent, asymptomatic respiratory or gastrointestinal infections.

SOURCE: American Journal of Physiology -- Regulatory, Integrative, and Comparative Physiology, January 2006.