MST-312 inhibits lytic herpes simplex virus-1 replication in neuronal cells
Description
Herpes simplex viruses (HSV) cause disease ranging from cold sores to life-threatening brain infections. HSV typically enters the body through mucosal epithelium, where its initial replication takes place. During this time, HSV enters sensory neurons servicing the site of infection. Most of the infected neurons eventually enter a latent state, however, in cases of HSV encephalitis in neonates, the virus spreads to the central nervous system and undergoes lytic replication without entering latency. Unfortunately, approximately 23% of the most severe neonatal HSV infections are fatal, even with current antiviral treatment. Thus, identifying an antiviral that could block or reduce HSV replication in neurons would greatly reduce the disease burden of this virus. We previously determined that MST-312 suppresses HSV infection in epithelial cells. The aim of this research is to determine the effect of MST-312 on HSV-1 infection in neuronal cells. We used Lund human mesencephalic (LUHMES) cells, which are human embryonic neuronal precursor cells that can be differentiated into post-mitotic neuronal cells as our model for neuronal infection. Initially, we used an MTT assay to determine the toxicity of MST-312 treatment of LUHMES cells. Concentrations between 20-100 μM did not lead to increased cell toxicity compared to controls. Next, we infected differentiated LUHMES cells with HSV-1 in the presence and absence of 20-100 μM MST-312. When virus production was quantified via plaque assays, we found that MST-312 treatment significantly reduced the production of HSV-1. Together, this shows that MST-312 can inhibit the replication of HSV-1 in neuronal cells.
Citation Information
Patil, Samiksha; Liles, Kayli; Pradhan, Prajakta; and Nguyen, Marie, "MST-312 inhibits lytic herpes simplex virus-1 replication in neuronal cells" (2026). Office of Research DMU Research Symposium. 89.
https://digitalcommons.dmu.edu/researchsymposium/2025rs/2025abstracts/89
MST-312 inhibits lytic herpes simplex virus-1 replication in neuronal cells
Herpes simplex viruses (HSV) cause disease ranging from cold sores to life-threatening brain infections. HSV typically enters the body through mucosal epithelium, where its initial replication takes place. During this time, HSV enters sensory neurons servicing the site of infection. Most of the infected neurons eventually enter a latent state, however, in cases of HSV encephalitis in neonates, the virus spreads to the central nervous system and undergoes lytic replication without entering latency. Unfortunately, approximately 23% of the most severe neonatal HSV infections are fatal, even with current antiviral treatment. Thus, identifying an antiviral that could block or reduce HSV replication in neurons would greatly reduce the disease burden of this virus. We previously determined that MST-312 suppresses HSV infection in epithelial cells. The aim of this research is to determine the effect of MST-312 on HSV-1 infection in neuronal cells. We used Lund human mesencephalic (LUHMES) cells, which are human embryonic neuronal precursor cells that can be differentiated into post-mitotic neuronal cells as our model for neuronal infection. Initially, we used an MTT assay to determine the toxicity of MST-312 treatment of LUHMES cells. Concentrations between 20-100 μM did not lead to increased cell toxicity compared to controls. Next, we infected differentiated LUHMES cells with HSV-1 in the presence and absence of 20-100 μM MST-312. When virus production was quantified via plaque assays, we found that MST-312 treatment significantly reduced the production of HSV-1. Together, this shows that MST-312 can inhibit the replication of HSV-1 in neuronal cells.
