An NIAID-funded study has
found that spraying malaria-transmitting
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.
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.”