Common Virus May Contribute to
    Obesity in Some People
    There is new evidence that infection with a common virus may be a
    contributing factor to the obesity epidemic sweeping through many
    countries.

    In laboratory experiments, scientists showed that infection with
    human adenovirus-36 (Ad-36), long recognized as a cause of
    respiratory and eye infections in humans, transforms adult stem cells
    obtained from fat tissue into fat cells. Stem cells not exposed to the
    virus, in contrast, were unchanged.

    In addition, the study reported identification of a specific gene in the
    virus that appears to be involved in this obesity-promoting effect.

    The findings, which could lead to a vaccine or antiviral medication to
    help fight viral obesity in the future, were presented at the 234th
    national meeting of the American Chemical Society.

    “We’re not saying that a virus is the only cause of obesity, but this
    study provides stronger evidence that some obesity cases may
    involve viral infections,” said study presenter Magdalena Pasarica.

    “Not all infected people will develop obesity,” she said. “We would
    ultimately like to identify the underlying factors that predispose some
    obese people to develop this virus and eventually find a way to treat it.”

    Pasarica was part of the original research group which demonstrated
    that the Ad-36 virus was capable of causing animals infected with it  to
    accumulate fat.

    The group also conducted an epidemiologic study — the first to
    associate a virus with human obesity — showing 30 percent of obese
    people were infected with the Ad-36 virus in comparison to 11 percent
    of lean individuals.

    But evidence that the virus could actually cause fat levels to increase
    in human cells was lacking until now, Pasarica said.

    In the current study, Pasarica and her associates obtained adult stem
    cells from fatty tissue from a broad cross-section of patients who had
    undergone liposuction. Half of the stem cells were exposed to the
    virus.

    After about a week of growth in tissue culture, most of the virus-
    infected adult stem cells developed into fat cells, whereas the stem
    cells which were not exposed to the virus did not, the researchers say.

    Researchers recently  identified a gene in the Ad-36 virus that
    appears to be involved in causing fat accumulation observed in
    infected animals. That gene, called E4Orfl, is now emerging as a
    promising target for future human therapies, such as vaccines and
    anti-viral medicines, aimed at preventing or inhibiting the obesity
    virus, Pasarica said.

    The exact mechanism by which the virus might cause obesity in
    people is currently unknown. Researchers also do not know how long
    the virus remains in the body of obese individuals or how long its fat-
    enhancing effect lasts once the virus is gone.

    However, a recent study demonstrated that animals that developed
    the virus remained obese up to six months after their infection was
    gone. More studies are needed, especially in humans, she adds.

    The researchers are not ruling out the possibility that other human
    viruses may also contribute to obesity.  

    (Source: American Chemical Society)

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