Lbachir BenMohamed, PhD, Receives $3.2 Million NIH Grant to Develop Immunotherapy Against Recurrent Ocular Herpes

“Our goal is to develop a safe and durable immunotherapy that can reduce potentially blinding recurrent herpetic disease, limit transmission and ultimately improve the lives of millions of people worldwide,” says Lbachir BenMohamed, PhD.

Irvine, Calif., Sept. 22, 2026 — University of California, Irvine immunologist Lbachir BenMohamed, PhD, has been awarded a National Institutes of Health grant of more than $3.2 million to develop a novel immunotherapy aimed at preventing recurrent ocular herpes, a leading infectious cause of blindness.

“Despite decades of research, people living with potentially recurrent ocular herpes still have no therapeutic T cell-targeted immunotherapy option,” says BenMohamed, professor of immunology and director of the Laboratory of Cellular and Molecular Immunology in the UC Irvine School of Medicine. “This award allows us to advance an innovative immunotherapy that not only boosts protective T cells but directs them to the tissues where the virus hides and reactivates.”

This award comes on the heels of a $3.9 million grant BenMohamed received in June 2026 to advance a therapeutic vaccine to help end genital herpes.

Boosting Protective Tissue-Resident T Cells to Clear the Virus

The project targets herpes simplex virus type 1 (HSV-1), which establishes lifelong latent infection in the trigeminal ganglia. Most infected people periodically shed the virus without ever developing eye disease. Still, a smaller group suffers repeated bouts of recurrent ocular herpes — episodes often accompanied by stress, anxiety, social withdrawal and cognitive decline — which can lead to permanent vision loss.

BenMohamed’s team developed a human leukocyte antigen (HLA) transgenic mouse model that reproduces the virus reactivation, recurrent ocular disease, and associated stress and behavioral changes seen in symptomatic patients. Their prior work found that a viral gene active during latency, the latency-associated transcript (LAT), promotes disease by driving exhaustion in the CD4+ and CD8+ tissue-resident memory T cells that would otherwise keep the virus in check. Mice with abundant, functional populations of these T cells showed less recurrent disease, less stress, and better cognitive performance, and an early T cell-based immunotherapy reduced both disease and stress-related behavior in the model.

Reducing Viral Reactivation and Recurrent Ocular Herpetic Disease

Building on these findings, the newly funded research will confirm that protective immunity in asymptomatic individuals relies on effector-memory and tissue-resident T cell subsets, while symptomatic disease reflects a shift toward central-memory T cells.

The team will then test whether an immunotherapy that selectively expands the protective subsets can reduce viral reactivation, decrease recurrent ocular herpes and ease the accompanying stress and cognitive effects.

“Our goal is to develop a safe and durable immunotherapy that can reduce potentially blinding recurrent herpetic disease, limit transmission and ultimately improve the lives of millions of people worldwide,” says BenMohamed.

The multidisciplinary project brings together immunologists and clinicians from the UC Irvine School of Medicine to translate these findings into a therapeutic strategy that could spare patients the blindness and psychological toll caused by recurrent ocular herpes.

About the UC Irvine School of Medicine: Each year, the UC Irvine School of Medicine educates more than 500 medical students and over 180 PhD and MS students. Nearly 900 residents and fellows are trained at the UCI Medical Center and affiliated institutions. The School of Medicine offers multiple MD, PhD, and MS degrees, and students are encouraged to pursue an expansive range of interests and options. The UC Irvine School of Medicine is accredited by the Liaison Committee on Medical Education and ranks among the top 50 nationwide for research. For more information, visit medschool.uci.edu.