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Vol. LXVII, No. 6
March 13, 2015
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Digest

Peanut Consumption in Infancy Prevents Peanut Allergy

Introduction of peanut products into the diets of infants at high risk of developing peanut allergy was safe and led to an 81 percent reduction in the subsequent development of the allergy, a clinical trial has found.

Introduction of peanut products into the diets of infants at high risk of developing peanut allergy was safe and led to an 81 percent reduction in the subsequent development of the allergy, a clinical trial has found.

Introduction of peanut products into the diets of infants at high risk of developing peanut allergy was safe and led to an 81 percent reduction in the subsequent development of the allergy, a clinical trial has found. The study was supported by the National Institute of Allergy and Infectious Diseases and conducted by the Immune Tolerance Network. The results appeared last month in the New England Journal of Medicine.

Researchers led by Dr. Gideon Lack of King’s College London designed their study based on observations that Israeli children have lower rates of peanut allergy compared to Jewish children of similar ancestry residing in the United Kingdom. Unlike children in the U.K., Israeli children begin consuming peanut-containing foods early in life. The study tested the hypothesis that the very low rates of peanut allergy in Israeli children were a result of high levels of peanut consumption beginning in infancy.

“Food allergies are a growing concern, not just in the United States but around the world,” said NIAID director Dr. Anthony Fauci. “For a study to show a benefit of this magnitude in the prevention of peanut allergy is without precedent. The results have the potential to transform how we approach food allergy prevention.”

NIH-Funded Scientists Create Potential Long-Acting HIV Therapeutic

Scientists have created a new molecule that shows promise for controlling HIV without daily antiretroviral drugs. The molecule foils a wider range of HIV strains in the laboratory than any known broadly neutralizing HIV antibody and is more powerful than some of the most potent of these antibodies. In addition, the molecule safely protected monkeys from infection with an HIV-like virus during a 40-week study period. Together, the data suggest that the molecule could, with further research, be used to subdue HIV in humans. The authors note that the molecule potentially could be used as both a preventive drug and as a treatment. The findings appeared in the Feb. 18 issue of Nature.

“This innovative research holds promise for moving us toward two important goals: achieving long-term protection from HIV infection and putting HIV into sustained remission in chronically infected people,” said NIAID director Dr. Anthony Fauci.

The new molecule is called eCD4-Ig and works by tightly binding to two unchanging sites on the surface of HIV that the virus uses to attach to receptors on cells called CD4 and CCR5. Typically, when HIV attaches to these receptors, it unlocks a door to the cell and gets inside. However, when eCD4-Ig binds to HIV, it effectively takes away the virus’s key, locking it out of the cell and preventing it from multiplying.

Molecule Hijacks Enzyme to Boost Alcohol Metabolism

An experimental compound empowers an enzyme to help process acetaldehyde, a toxic metabolite of alcohol, according to research supported by the National Institute on Alcohol Abuse and Alcoholism. The findings, published in the Proceedings of the National Academy of Sciences, might lead to new treatments to help people with impaired ability to metabolize acetaldehyde and other toxic substances.

“This intriguing finding could have important implications,” said NIAAA director Dr. George Koob. “Developing pharmacologic agents that alter an enzyme’s substrate specificity is a unique approach that may have wide clinical application in treating patients with impaired ability to detoxify toxic substances. We look forward to further research aimed at translating these laboratory discoveries into possible treatments for people.”

After alcohol is consumed, it is first metabolized into acetaldehyde, a toxic chemical that can cause DNA damage and cancer. In the liver, aldehyde dehydrogenase 2 (ALDH2) is the main enzyme responsible for breaking down acetaldehyde into acetate, a nontoxic metabolite. It also removes other toxic aldehydes that can accumulate in the body. An estimated 560 million people in East Asia, and many people of East Asian descent, carry a genetic mutation that produces an inactive form of ALDH2. When individuals with the ALDH2 mutation drink alcohol, acetaldehyde accumulates in the body, resulting in facial flushing, nausea and rapid heartbeat. People with the ALDH2 mutation are also at increased risk for cancers of the mouth, esophagus and other areas of the upper aerodigestive tract.


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