Two studies led by UCLA researchers have shed new light on the development and treatment of HIV/AIDS, 29 years after UCLA doctors recorded the first cases of the epidemic.
Much of the university’s AIDS research takes place through the UCLA AIDS Institute, which supports AIDS research in multiple disciplines through grants from organizations such as the National Institutes of Health.
While the institute alone consists of roughly 200 investigators who come from backgrounds as diverse as ophthamology and social science, not all AIDS research takes place under its umbrella. AIDS Institute member Sally Blower worked outside the institute to follow the transformation of the HIV infection in urban settings.
By tracking the epidemic in San Francisco for the past 20 years, the Semel Institute for Neuroscience and Human Behavior at UCLA and UC San Francisco’s HIV AIDS Program saw how drug-resistant variations of HIV have grown over time. Learning how drug resistance grows is another step in learning how to prevent it, according to Blower, the study’s senior author and director of UCLA’s Center for Biomedical Modeling.
“Drug-resistant strains (of HIV) have emerged because individuals in the model became infected with HIV, went on treatment, somehow developed drug resistance and transmitted these strains to other individuals through sex,” Blower said.
Blower and her associates based their findings on a unique mathematical model that allowed them to predict where the epidemic was headed over the next five years based on its history and found that HIV is continuing to transform.
“This was definitely a big public health problem that was emerging at the time 20 years ago,” said Blower, who was living in San Francisco when AIDS was becoming an national issue. “Everyone is used to living with it now, but 20 years ago it was very amazing for this infectious pathogen to become an epidemic.”
Though it may be too late to save the U.S. from these drug-resistant strains of HIV, Blower said the new findings can be applied to places where HIV treatment is beginning.
By expanding her research this summer to look at AIDS in Denmark, a country with comparatively low levels of drug resistance, Blower said she hopes to see what causes low levels of resistance. This information can be used in areas like Africa to improve HIV treatment in a way that would limit the growth of drug-resistant strains.
“Because the level of drug resistance is really quite high (in the U.S.), it’s causing lots of clinical problems,” Blower said. “It’s harder and more expensive to treat people.”
Another group of 26 researchers, led by Benhur Lee, associate professor of microbiology, immunology and molecular genetics at UCLA’s David Geffen School of Medicine, has stumbled upon a compound that may allow for further treatment of HIV/AIDS. Lee worked in association with Harvard University, Cornell University, University of Texas at Galveston and the United States Army Medical Research Institute of Infectious Diseases. The study was funded by more than $3 million from the National Institutes of Health.
This particular antiviral works by attacking the membrane of a virus, causing irreparable damage, and can therefore be used against a number of viruses. Although the compound was discovered four years ago, it took a while for the researchers to accumulate evidence to support their theories of what the compound could do, according to Lee.
“It took us a long time to figure this out,” Lee said. “We didn’t look out for a broad spectrum antiviral. … It was very confusing for a while because there is no precedent for such a compound with broad spectrum activity.”
Still ahead is a plan to test this antiviral on actual animal models instead of in controlled environments. However, Lee said it may be several years before this antiviral will be made available as a form of treatment. As of now, only the feasibility of the antiviral has been tested.
“Once we get across the pharmacological problem of activating (the antiviral), we will see if it lives up to its promise of what it can do in the test tube,” Lee said. “It may be 10 years for (the antiviral) to get into clinics, but it won’t be 10 years to see its viability. I don’t see a dead end yet.”
The news of this antiviral comes about a month after another Geffen school assistant professor published a study describing how human blood cells could be redesigned to target HIV-infected cells. That finding, by lead investigator Scott G. Kitchen, was also a proof-of-principle study and remains to be tested in human subjects.