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FUNGUS MAY BE RESPONSIBLE FOR OHIO INFANT DEATHS


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.

         

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

CHICKEN OBESITY VIRUS MAY MAKE HUMANS FAT


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.

           

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.

the Biology Place BIOLOGY PLACE EXCERPTS


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?
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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