Anti-Malaria Drug May Help Prevent Zika Infections
Researchers at UC San Diego School of Medicine and Sanford Burnham Prebys Medical Discovery Institute report that a medication long used to prevent and treat malaria may also be effective against Zika.
The medication is chloroquine, discovered in 1934 and used worldwide, particularly in developing countries where malaria is endemic, to prevent or treat the infectious disease.
Researchers studied pregnant mice infected with the Zika virus, treating them with chloroquine (delivered through drinking water) at doses equivalent to acceptable levels used in humans.
“Our research is the first to study Zika infection in a mouse model that transmits the virus in a way similar to humans,” said Alysson R. Muotri, PhD, professor and director of the Stem Cell Program at UC San Diego and co-senior author of the study with Alexey Terskikh at Sanford Burnham Prebys.
Designer DNA drugs approach a potential watershed moment
Next year, Carlsbad’s Ionis Pharmaceuticals is expected to release clinical trial results for Huntington’s and Lou Gehrig’s diseases that use designer DNA drugs to mute the mutant genes responsible for causing patients’ nervous systems to gradually go haywire.
Ionis has been able to previously show success working on the far side of the blood-brain barrier, a protective shield of sorts that automatically filters out most drugs injected into the bloodstream, making targets in the brain and spine extremely difficult to hit, with an FDA approved drug called 'Spinraza'.
If early-phase results, the first of which are expected in January, show that these DNA drugs — formally called “antisense oligonucleotides” — can reduce harmful proteins in nerve cells, it will be a watershed moment toward creating viable long-term treatments.
“We don’t get two hours of efficacy. We don’t get two to three days. We don’t get two or three weeks. We get three or four months. The drug lasts a really long time,” Don Cleveland, PhD, said.
That means that patients could theoretically come in a few times a year, get a shot in the spine, and go home.
“That would be more like going to the dentist. You don’t necessarily look forward to it, but you do it,” Cleveland said.
Frozen in Action: How Cells Repair DNA as it's Being Transcribed
In a paper published November 22 in Nature, Dong Wang, PhD, Andres Leschziner, PhD, and colleagues used cryoEM to get a clear look at how cells repair damaged bits of DNA that hold up the molecular machinery trying to transcribe it into mRNA. This process is called transcription-coupled repair.
Wang and Leschziner’s team solved the first cryoEM structure of the yeast form of the key proteins that initiate transcription-coupled repair, known as the Pol II-CSB complex.
“Our work with the Wang lab is a beautiful example of how structure tells us about function,” said Leschziner, professor in the UC San Diego School of Medicine and division of biological sciences.
Human ‘mini-brains’ make themselves at home in mice
Spheres of brain cells derived from people and implanted into mouse brains recruit blood vessels and integrate with mouse neurons. The work represents a technical leap in the field of brain organoids, also known as ‘mini-brains.’ It also raises ethical questions.
“Several people have injected human fetal cells into rodents and monkeys,” says Alysson Muotri, PhD, associate professor of pediatrics and of cellular and molecular medicine at the University of California, San Diego. “I don’t think this is new territory, because the authors did not show that the organoids are having any sophisticated brain waves or that the animal has changed its behavior.”
How a gene that usually protects against cancer becomes the disease’s aggressor
A study led by a University of California San Diego researcher has found an explanation for one of the biggest causes of cancer, mutations in a gene that normally guards against cancer.
The study, led by Shannon Lauberth and co-authored by UCSD colleagues Hanbin Lu, Sascha Duttke, Christopher Benner and Christopher Glass, PhD, showed that mutations in the gene, called p53, can lead to inflammation, stimulating an immune response that fuels cancer, the study found.