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THE ARCHIVES
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FUNGUS MAY BE RESPONSIBLE FOR OHIO
INFANT DEATHS
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In November 1994, Ohio pediatrician Dr. Dorr Dearborn gave
Dr. Ruth Etzel a wake-up call at 7:30 A.M.--eight infants had
been hospitalized with bleeding in their lungs in recent months,
all from a specific area of Cleveland. Dr. Etzel, a researcher
at the Centers for Disease Control and Prevention, was in Ohio
less than 12 hours later. When investigators looked at homes
of these infants to try and find a common trend, they found a
slimy black fungus called Stachybotrys atra growing in
the basements.
In the three years since that November morning, 26 more infants
have been hospitalized with bleeding lungs in Ohio, 10 of whom
died. Nationwide, there have been 84 reports from 1993 to 1997
of cases similar to the original eight infants. On July 30, 1997,
Dr. Dearborn received a grant of $76,000 from the CDC and the
National Institute of Environmental Health Sciences to investigate
his hypothesis--that the spores of Stachybotrys produce
a toxin that weakens the vulnerable lungs of infants.
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Dearborn suspects that a secondary stress, such as cigarette
smoke, is necessary to trigger the problems. He plans to expose
newborn mice to the fungus--preliminary experiments with infant
mice show that spore exposure causes internal bleeding.
Here are some additional sources of information:
- A fact sheet
about the possible link between Stachybotrys and lung
bleeding in infants, including instructions on how to clean the
fungus from your home
- U.S.
infant mortality information from the Centers for Disease Control
and Prevention
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CHICKEN OBESITY VIRUS MAY MAKE HUMANS
FAT
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Several years ago, Nikhil Dhurandhar was in Bombay studying
a chicken virus that caused chickens to become fat. On April
7, 1997, Dhurandar and fellow University of Wisconsin researcher
Richard Atkinson announced findings indicating that a similar
virus may be responsible for weight gain in some obese people.
The virus in question is called Ad-36, an adenovirus that
causes coughing, sneezing, and other cold-like symptoms, and
is a relative of the chicken virus Dhurandhar studied in India.
Fifteen percent of the 154 obese patients studied showed evidence
of past infection by Ad-36. However, none of the 45 lean volunteers
showed evidence of this virus. Even more striking was the difference
in cholesterol levels in the infected and non-infected obese
patients; while high cholesterol was expected and found in the
non-infected obese patients, the obese patients that had been
infected with Ad-36 showed normal cholesterol levels.
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Admittedly, say the researchers, the findings do not prove
that Ad-36 causes humans to grow fat. To show this link more
persuasively, they would have to inject humans with the virus
and see if they got fat, an ethically impossible experiment and
one that few would volunteer for. However, they have demonstrated
that chicken and mice injected with Ad-36 grow fat without a
rise in cholesterol level. Though they have yet to demonstrate
conclusively that Ad-36 causes obesity in humans, the researchers
are working on a test for the virus, as well as a possible vaccine.
Here are some additional sources of information:
- This
page lists the names of all virus families, including the adenoviruses
- An article from Nature Science Update on the cold-like virus and obesity.
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BIOLOGY PLACE EXCERPTS
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OCTOBER
6, 1997
A TROJAN HORSE AGAINST AIDS: USING A COW VIRUS TO KILL HIV-INFECTED
CELLS
While the current AIDS drugs offer real hope to patients, they
are not problem-free: They do kill cells infected with HIV, the
agent that causes AIDS, but they also harm a patient's healthy
cells to some degree. American and German researchers now report
an important step toward improving AIDS drugs--the bioengineering
of animal viruses so they will enter and kill only cells infected
with HIV. Will the approach work safely in human patients, as
well? |
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OCTOBER
13, 1997
COMMON FUNGUS, CANDIDA ALBICANS, MUST BE IN FILAMENTOUS FORM
TO INVADE HOST
Candida albicans is a common fungal pathogen of humans. Being
dimorphic, it can grow either as single-celled budding yeast
or as long, slender filaments. Researchers from Massachusetts
Institute of Technology have now engineered a mutant strain of
C. albicans defective for two genes that control the shift from
yeast form to filaments. In the process, they discovered that
the fungus must be in filamentous form to elude its host's defenses
and invade tissues. This finding may someday lead to better drug
treatments and a deeper understanding of the potentially dangerous
fungal infections called candidiasis. |
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Biology Place.
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