The Campbell Foundation, which funds nontraditional HIV/AIDS research, has awarded two more grants this summer. One focuses on looking at the hidden reservoirs of HIV and another on developing drugs to target the “viral budding” of HIV.
Researcher Susana Valente, PhD, at Scripps Research Institute in Florida, received a $79,151 grant. She and her team are targeting latent HIV, the virus that hides in reservoirs throughout the body and isn’t affected by HIV meds.
For latent HIV to be killed, it has to be activated—at least, that is the common perception among researchers. The goal at Valente’s lab is to “deep freeze” the HIV in the genome to eradicate it. She and her team hope to accomplish this with a molecule called didehydro-Cortistatin A (dCA) that may be able to reduce the HIV reservoir by blocking viral replication, reactivation and replenishment.
“One interesting feature of this molecule,” said Valente in a Campbell Foundation press release, “is that even when dCA treatment is halted, virus production does not rebound, as usually happens with other antiretroviral drugs, because viral RNA production is shut off or driven into a state of deep latency.”
Another Campbell grant went to Jonathan Leis, PhD, and his team at Northwestern University in Chicago. They received $80,000 to further develop “viral budding inhibitors” (VBIs), drugs that could stop HIV from exiting a host cell, a process called viral budding.
People with HIV would be less likely to develop resistance to VBIs, Leis explained in a press release, which makes VBIs different from the current crop of available HIV meds.
“The need for a new class of inhibitors is essential to control the spread of AIDS until a cure is possible,” said The Campbell Foundation’s executive director, Ken Rapkin. “This new class of inhibitors, which HIV has not developed resistance to, could prolong existing therapies until a cure is found.”
“VBIs are expected to prevent the release of virus particles from cells and thus will slow down the spread of HIV infection to uninfected cells,” Leis said. “Controlling the spread of virus at any time will help protect the immune system and enhance defenses to the infection.”