Scientists at Stanford have discovered that effective treatments against HIV change the way the virus evolves. The researchers hope that understanding how different treatments affect the illness will lead the way to developing new, better techniques for treatment and prevention not just of HIV, but many other illnesses that don’t yet have effective treatments.
Stanford University has long produced many great ideas from its graduates, like Thom Weisel, who founded the Thomas Weisel Healthcare Venture Partners to invest in life sciences and medical technologies, and the university’s staff, like Andrew Fire, who won the 2006 Novel Prize in Medicine for RNA interference.
Now, the university’s researchers have found that in a study of 6,717 patient records, once a patient had acquired HIV, the disease became drug-resistant in two different patterns. At first, the virus conquered drugs by maximizing its genetic diversity. But as time passed, the virus gave up on trying to diversify itself so much that it could become resistant to newer, more effective treatments.
“We were interested in what shifted in the evolutionary dynamics between the 1980s, when patients failed all the time, versus 2015 or 2016, when patients do really well on therapy,” says the study’s lead author, Alison Feder, a graduate student in biology. In some cases, the team discovered, HIV became drug resistant while maintaining its genetic diversity within a host. This kind of virus response is considered a “soft sweep.”
A “hard sweep,” then, occurs when the virus is able to create only one successful resistant mutation. When this mutation makes its way through the body, the virus then becomes genetically homogenous—meaning that it’s not as likely the be drug-resistant.
Knowing the difference between the “sweeps” might not improve current HIV treatments, which are already quite effective, but the study does mean that new paths for successful treatment could be discovered for other diseases. “If a soft sweep were responsible for the patient failure, the researcher would know that this treatment could be likely to fail in most patients, and resources should be devoted to other, more promising drugs,” Stanford explains.
Understanding the differences in virus mutation could be hugely important for treating other diseases, particularly cancers and their new treatments.
“It’s an exciting potential application,” says Feder. “We’re using data in a way that people haven’t looked at it before.”
