Researchers discover a potential mechanism to prevent development of herpes stromal keratitis
The study compared the quantity and quality of tissue-resident memory T cells in HSV-1 infected corneas that did or did not develop herpes stromal keratitis.
Susmit Suvas, PhD Image credit: Wayne State University
Researchers at the Wayne State University School of Medicine have discovered a potential mechanism that could prevent patients from developing herpes stromal keratitis (HSK), a vision condition that occurs in response to a herpes infection in the eye.1 Conducted in the lab of Professor of Ophthalmology, Visual and Anatomical Sciences Susmit Suvas, PhD, who is also the principal investigator of the study, the goal of the research was to find new prophylactic and therapeutic approaches in manage the development of HSK, according to a news release.
“For long time, it was unclear why some eyes that shed infectious HSV-1 (herpes simplex virus) at the ocular surface do not develop herpes stromal keratitis, whereas the other infected eyes develop HSK. Our study for the first time showed that HSV-1 infected corneas that do not develop HSK exhibit a large pool of protective tissue-resident memory T cells, or TRM, whereas the corneas that develop HSK have poor quantity and quality of tissue-resident memory T cells,” Suvas said in the release. “The function of tissue-resident memory T cells is to clear the infectious virus before it can initiate tissue damage. Having a good quantity and quality of Trm cells in HSV-1 infected cornea protect them from the development of HSK.”
The study “Herpes stromal keratitis erodes the establishment of tissue-resident memory T cell pool in HSV-1 infected corneas” was published in Mucosal Immunology and is comprised of research that was conducted over 2 years. The study compared the quantity and quality of tissue-resident memory T cells in HSV-1 infected corneas that did or did not develop HSK. According to the study, not all HSV-1 infected corneas that shed infectious virus at the ocular surface develop HSK, which suggests that corneal HSV-1 infection may cause an establishment of protective immunity in HSV-1 infected corneas.1
“Our results showed the predominance of TRM cell in the epithelium than in stroma of HSV-1 infected corneas. Furthermore, HSV-1 infected non-HSK corneas exhibited more CD4 and CD8 TRM cells than HSK corneas,” first author Mizumi Setia et al. stated. “The TRM cells in non-HSK than in HSK corneas were more effective in clearing the infectious virus upon secondary corneal HSV-1 infection. Our results demonstrate the differential quantity and quality of TRM cells in HSV-1 infected corneas that did or did not develop HSK.”
The 2 major outcomes of corneal HSV-1 infection are the development of herps epithelial keratitis (HEK) and HSK.1
“HEK is a self-resolving condition, whereas the development of HSK can cause vision loss. Our study showed that strategies to augment the quantity and quality of tissue-resident memory T cells in HSV-1 infected corneas can reduce the incidence of the development of HSK,” Suvas said in the release.
References:
Suvas lab finds potential mechanism to protect against infection-induced vision impairment. News release. Wayne State University. January 16, 2025. Accessed March 26, 2025. https://today.wayne.edu/medicine/news/2025/01/16/suvas-lab-finds-potential-mechanism-to-protect-against-infection-induced-vision-impairment-65281
Setia M, Suvas PK, Rana M, Chakraborty A, Suvas S. Herpes stromal keratitis erodes the establishment of tissue-resident memory T cell pool in HSV-1 infected corneas. Mucosal Immunol. 2025;18(1):188-204. doi:10.1016/j.mucimm.2024.11.003
