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International Journal of Obesity
and related metabolic disorders

IS OBESITY CONTAGIOUS?

Most doctors have heard their obese patients blame their condition on their glands, or their metabolism, or their genes, but they might soon be hearing a different excuse. This time it could be that they “caught” their obesity from their spouse or a close colleague, in much the same way as they might catch a cold.

In a paper published in this month’s International Journal of Obesity (“Increased adiposity in animals due to a human virus”; Dhurandhar et al, IJO 24(8): 989-996), a group from the University of Wisconsin have shown that inoculating chickens and mice with a human adenovirus (Ad-36) causes them to gain excessive amounts of fat. Not only did they gain more than the controls, they also gained more than a group of chickens inoculated with another virus, an avian adenovirus called CELO. This indicates that the excessive fat deposition was not a non-specific effect in response to any viral infection. The mechanism causing the obesity is not known, but does not appear to be due to increased food intake and would implicate a decrease in energy expenditure as the cause. In chickens, there was no evidence of the AD-36 virus causing damage to those parts of the brain (hypothalamus) that control energy balance. However, one would like to see more of these studies carried out in those mammals (e.g. mice and rats) where much more is known about the physiological control of energy balance, as well as being more applicable to humans.

Virus-induced obesity is not a new phenomenon, with at least four different animal models having been described, but this is the first time that a human virus has been used to produce adiposity in animals. This raises the obvious question – if human viruses can cause obesity in animals, perhaps animal viruses can do the same in humans? The answer to this is to be found in an earlier study by the main author, who found that out of 52 obese subjects, the 10 subjects with antibodies to a chicken adenovirus (SMAM-1) were the most obese. This, however, is too small a sample on which to build a convincing case for an infective agent in the aetiology of obesity, and much larger epidemiological surveys linking animal and/or human adenoviruses to obesity are required. Collecting this sort of circumstantial evidence is necessary since, although Ad-36 is a human virus, ethical considerations prevent the experimental infection of volunteers to test its effects on adiposity.

So, how seriously should one take this latest theory? As the authors point out, very little is known about the incidence of Ad-36 in humans and whether it is linked to a predisposition to obesity, and most experts will reserve judgement until such data are available. Even then, it could turn out that obesity predisposes to the infection, rather than vice versa. However, it would be unwise to dismiss the idea completely out of hand since this is not the first chronic disease that has been linked to infection. It is now known that the stomach organism, Helicobacter pylori, is a major cause of ulcers, and evidence is now accumulating to indicate that heart disease may be associated with infection by another infective agent, Chlamydia pneumoniae. Also, even if the association between obesity and viral infection is weak, this could be enhanced if accompanied by other predisposing factors, such as one or more of the genes linked to obesity, plus a high-fat diet and a sedentary lifestyle. In other words, there could be a synergistic potentiation between a viral infection and these other genetic and environmental factors. Unfortunately, there is not much one can do about the genes linked to obesity (at least at present), and it is easier said than done to change eating habits and activity patterns. However, it might be relatively easy to formulate some form of anti-viral therapy for the treatment of “infectious obesity” – that’s if such a disease really does exist in humans.


Further information may be obtained from Dr N V Dhurandhar (Fax: +1 313 577 8616; email: ndhurand@sun.science.wayne.edu). For additional information on this and other articles appearing in the International Journal of Obesity, contact the Executive Editor, Prof Mike Stock (Fax: +44 (0)208 725 2993; email: m.stock@sghms.ac.uk).

Visit the IJO website at www.nature.com/ijo

Click here to view the full text of this paper FREE.

If you would like a full printed copy of this paper (the abstract follows here), please contact Michael Osuch on m.osuch@nature.com or by fax on + 44 (0) 1256 354018.

ABSTRACT:

International Journal of Obesity

Volume 24, Issue 8, 989-996pp

Abstract from the paper, Adiposity in Animals due to a Human Virus by Dhurandhar, Israel, Kolesar, Mayhew, Cook and Atkinson.

Background
Four animal models of virus-induced obesity including adiposity induced by avian adenovirus have been described previously. This is the first report of adiposity induced in animals by a human virus.

Objective
We investigated the adiposity promoting effect of a human adenovirus (Ad-36) in two different animal models

Design
Due to the novel nature of the findings we replicated the experiments using a chicken model three times and a mammal model once. In four separate experiments, chickens and mice were inoculated with human adenovirus Ad-36. Weight matched groups inoculated with tissue culture media were used as non-infected controls in each experiment. Ad-36 inoculated and uninfected control groups were housed in separate rooms under biosafety level 2 containment. The first experiment included additional weight matched groups of chickens that was inoculated with CELO (chick embryo lethal orphan virus), an avian adenovirus. Food intakes and body weights were measured weekly. At the time of sacrifice blood drawn and visceral fat was carefully separated and weighed. Total body fat was determined by chemical extraction of carcass fat.

Results
Animals inoculated with Ad-36 developed a syndrome of increased adipose tissue and paradoxically low levels of serum cholesterol and triglycerides. This syndrome was not seen in chickens inoculated with CELO virus. Sections of the brain and hypothalamus of Ad-36 DNA could be detected in adipose tissue, but not skeletal muscles of randomly selected animals for as long as 16 weeks after Ad-36 inoculation.

Conclusions
Data from these animal models suggest that the role of viral diseases in the etiology of human obesity must be considered

Keywords
Serum cholesterol, serum triglycerides, body fat, weight, obesity, visceral fat

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© Macmillan Publishers Ltd 2001

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