[en] A previous study identified a 348-bp region at the 5' end of the 8.5-kb latency-associated transcript (LAT) of HSV-1 strain 17Syn+ that is necessary for maximum adrenergically induced reactivation following transcorneal iontophoresis of epinephrine , J. Virol. 70, 2449-2459). In that study, the construct with complete deletion of the 348-bp region, 17Δ348, failed to achieve the high reactivation frequency demonstrated by the parent (17Syn+) and rescued (17Δ348R) viruses. To further characterize the function of the 348-bp region, we analyzed two genetic constructs with partial deletions in the same 348-bp region, 17Δ201 and 17Δ207, in the rabbit model. Both constructs exhibited the same high reactivation frequencies demonstrated by the parent 17Syn+ and the rescued 17Δ348R viruses. These results suggest that the control of reactivation is distributed over a large portion of the 348-bp region, rather than being confined within a smaller, more discrete region. To assess whether the low reactivation phenotype of the 17Δ348 construct was caused by a requirement for proper spacing of elements outside the 348-bp region, we constructed a virus (17Δ348St) that contained a 360-bp stuffer fragment of heterologous DNA (lacZ) to maintain the proper spacing. The 17Δ348St construct also displayed a low reactivation phenotype, similar to that of 17Δ348, suggesting that the effect of deleting this segment of the 5' exon of LAT is obtained through a mechanism other than the disruption of spacing