Over half of the people carrying HIV experience chronic pain at some point, which is difficult to treat. In a new JNeurosci paper, Hui-Lin Pan, from The University of Texas MD Anderson Cancer Center, and colleagues used mice to explore how HIV leads to chronic pain.
Previous research separately linked a viral protein called glycoprotein 120 (gp120) to increased pain sensitivity and overactive signaling of a type of nerve receptor in the spine to nerve pain. Informed by these findings, the researchers sought to investigate whether gp120 influences signaling of this nerve receptor. Injecting gp120 into the spine of mice increased the nerve receptor's activity through a mechanism that affected a specific neuron population. Using a combination of drug-based and genetic approaches targeting the molecular players involved, the researchers discovered they could reverse the mechanism they identified and reduce pain hypersensitivity in the mice.
According to the researchers, this work shows how an HIV-associated protein amplifies pain signaling in the spinal cord and shows that disrupting this mechanism may lessen pain sensitivity. Pan looks forward to continuing this work, saying, "We are particularly excited about developing therapeutic approaches to disrupt [this mechanism, specifically by targeting protein interactions with the nerve receptor]. These targeted strategies may provide more precise and effective treatments for chronic neuropathic pain, not only in HIV, but potentially in other conditions as well."
