bySociety for Neuroscience

Credit: Kindel Media from Pexels

Over half of the people carrying HIV experience chronic pain at some point, which is difficult to treat. In a newJNeuroscipaper, 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 ofdrug-based and genetic approachestargeting 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 anHIV-associated proteinamplifies 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."

Publication details HIV-1 gp120 Induces Nociceptive Hypersensitivity via α2δ-1–bound NMDA Receptors at Primary Afferent-Excitatory Neuron Synapses, JNeurosci (2026). DOI: 10.1523/JNEUROSCI.0368-26.2026 Journal information: Journal of Neuroscience