SIMILARITIES IN REGULATION OF THE HSV-1-LAT PROMOTER IN CORNEAL AND NEURONAL CELLS

Purpose. To address the possibility of neuronal-like herpes simplex vi rus type 1 (HSV-1) latency in the cornea by determining if regulation of the HSV-1 LAT promoter in stromal keratocytes is similar to LAT pro moter regulation in neurons. Methods. Transient chloramphenicol acetyl transferase (CAT) assays were used to measure the relative promoter ac tivity of various HSV-1 LAT promoter fragments in primary human cornea l cells versus neuronal and nonneuronal cells. Results. The authors fo und that the LAT promoter, whose location they previously mapped in ne urons using transient CAT assays, functioned in stromal keratocytes us ing the same assay System and that two regions between -283 and -1932 nucleotides relative (upstream) to the start of LAT transcription slig htly increased the LAT promoter activity in stromal keratocytes. They previously showed a similar increase in neuronal cells, and a large de crease in nonneuronal cells. In addition, they found that a neuronal s pecific enhancer region they previously defined between -162 and -283 nucleotides upstream of the start of LAT transcription also enhanced p romoter activity in stromal keratocytes. Using gel-shift assays, they detected a nu clear factor specific to neurons and stromal keratocytes that binds to the LAT promoter and that may be a LAT regulatory facto r. Conclusions. Recently, it has been suggested that the cornea might serve as an alternative site of latent herpes simplex virus type 1 (HS V-1) infection. However, this remains controversial. The authors' find ings suggest that corneal and neuronal cells regulate the LAT promoter similarly and that this regulation differs from that seen in nonneuro nal cells. Thus, the possibility of neuronal-like latency in the corne a remains plausible.