Study Finds Drug Effective at Disrupting Latent HIV

Some patients struggle with latent immune cells infected with HIV even after successful antiretroviral therapy.

April 20, 2026

2 min read

Key Highlights

Citarinostat selectively inhibits histone decrotonylation, a process that helps HIV evade immune detection.
The drug was tested on human white blood cells and microglial cells, showing promising results in reactivating latent HIV.
By forcing dormant HIV-infected cells to become active, citarinostat may enhance the effectiveness of immune responses and future HIV cures.
This research offers a new approach to targeting HIV reservoirs that persist despite antiretroviral therapy.
Further studies are needed to evaluate the safety and efficacy of citarinostat in clinical settings for HIV treatment.

A new study led by researchers at UNC found that a drug named citarinostat is effective at disrupting latent HIV reservoirs.

Even when effective antiretroviral therapy happens, “immune cells infected with HIV can hide and lie inactive in certain areas of the body called latent reservoirs. If treatment is discontinued, these reservoirs may become active again, causing patients to face renewed challenges with symptoms of” AIDS. This drug is a promising candidate in the quest for agitating and forcing HIV-infected immune cells to “come out of latency and be attacked by the immune system.”

Antiretroviral therapy (ART) stops the virus from reproducing, but it is not effective against latent reservoirs. Medications that can re-active and coerce HIV-infected immune cells to “crawl out of latent reservoirs in a controlled manner” have been tested. The drug in this study “selectively stops histone decrotonylation (HDCR), a genetic process that allows HIV to successfully fly under the immune system’s radar.”

The research team “introduced the drug to human white blood cells collected from study participants at UNC-Chapel Hill, as well as microglial cells derived from brain tissue.” The drug “effectively increases histone crotonylation, disrupts latent HIV in immune cells, and induces HIV transcription to successfully agitate and force the HIV-infected immune cells to re-awaken.”