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Vol. LXIII, No. 6
March 18, 2011
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An NIAID-funded study has found that spraying malaria-transmitting mosquitoes with a genetically modified fungus can kill the malaria parasite without harming the mosquito, potentially reducing malaria transmission to humans.

Genetically Modified Fungi Kill Malaria- Causing Parasites in Mosquitoes

Spraying malaria-transmitting mosquitoes with a genetically modified fungus can kill the malaria parasite without harming the mosquito, potentially reducing malaria transmission to humans, according to a study in Feb. 25’s Science. Funded by NIAID, the study was led by Dr. Raymond J. St. Leger of the University of Maryland.

An estimated 225 million malaria cases occur worldwide annually, resulting in about 781,000 deaths each year, according to the World Health Organization. Although the disease is present in 106 countries around the world, most cases occur in sub-Saharan Africa. Treating bed nets and indoor walls with insecticides is the main prevention strategy in developing countries, but the Anopheles mosquitoes that transmit malaria are slowly becoming resistant to these insecticides, rendering them less effective.

“Because mosquitoes increasingly are evolving to evade the malaria control methods currently in use, NIAID-supported scientists are testing new, innovative ways to prevent malaria that we hope can be developed into tools that will be effective for years to come,” said NIAID director Dr. Anthony Fauci.

One of these new strategies is killing Anopheles mosquitoes by spraying them with the naturally occurring fungus, Metarhizium anisopliae. Previous studies have found that this method nearly eliminates disease transmission when mosquitoes are sprayed soon after acquiring the malaria parasite. However, this strategy is not sustainable in the long term. If treating mosquitoes with the fungus kills them before they have a chance to reproduce and pass on their susceptibility to the spray, mosquitoes resistant to the fungus, which would reproduce normally, will soon become predominant and the spray will no longer be effective.

Because of this, St. Leger and colleagues tried a different approach. Rather than developing fungi that rapidly kill the mosquito, they genetically modified M. anisopliae to block the development of the malaria parasite in the mosquito.

Study Finds Nitric Oxide Does Not Help Sickle Cell Pain Crisis

Inhaling nitric oxide gas does not reduce pain crises or shorten hospital stays in people living with sickle cell disease, according to the results of a study sponsored by NHLBI. “Nitric Oxide for Inhalation in the Acute Treatment of Sickle Cell Pain Crisis,” was published in the Mar. 2 issue of the Journal of the American Medical Association.

Sickle cell disease is an inherited disorder affecting between 70,000 and 100,000 Americans. The disease causes red blood cells, which are normally disc-shaped and pliable, to become misshapen, stiff and sticky. Severe pain crises occur periodically in people living with sickle cell disease when these sickled red blood cells hinder proper blood flow.

Nitric oxide dilates and expands blood vessels and enhances blood flow. Levels are lower in persons with sickle cell disease than in those without the disease. Previous trials with smaller numbers of patients had suggested that administration of nitric oxide might shorten sickle cell pain crises.

The study involved 150 sickle cell disease patients who were hospitalized for severe pain crises. Each participant was given nitric oxide gas or a placebo gas during treatment. Though the nitric oxide was well-tolerated, it failed to improve outcomes.

Gene Glitch May Hold Clues for Schizophrenia

Scientists are eyeing a rare genetic glitch for clues to improved treatments for some people with schizophrenia, even though they found the mutation in only one-third of 1 percent of patients.

In the study, funded in part by NIH, schizophrenia patients were 14 times more likely than controls to harbor multiple copies of a gene on chromosome 7. The mutations were in the gene for VIPR2, the receptor for vasoactive intestinal peptide (VIP)— a chemical messenger known to play a role in brain development. An examination of patients’ blood confirmed that they had overactive VIP activity.

Discovery of the same genetic abnormality in even a small group of patients buoys hopes for progress in a field humbled by daunting complexity in recent years. The researchers’ previous studies had suggested that the brain disorder that affects about 1 percent of adults might, in many cases, be rooted in different genetic causes in each affected individual, complicating prospects for cures.

“Genetic testing for duplications of the VIP receptor could enable early detection of a subtype of patients with schizophrenia, and the receptor could also potentially become a target for development of new treatments,” said Dr. Jonathan Sebat, an NIMH grantee at the University of California, San Diego, who led the research team. “The growing number of such rare duplications and deletions found in schizophrenia suggests that what we have been calling a single disorder may turn out, in part, to be a constellation of multiple rare diseases.”


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