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A cAMP response element within the latency-associated transcript promoter of HSV-1 facilitates induced ocular reactivation in a mouse hyperthermia model.

Herpes simplex virus type 1 (HSV-1) recombinant strain 17CRE contains a site-directed mutation in the 7-bp CRE consensus sequence located 38 nucleotides upstream of the transcription start site. Scarified mouse corneas received inoculations of 17syn+ (parent), 17CRE, and rescue 17CREr. Slit lamp examination of herpetic lesions and tear film swabs containing infectious virus showed that 17CRE had the same acute phenotype as 17syn+ and 17CREr. At 4 weeks, when the corneas had healed and latency was established, mice received hyperthermic shock. Eye swabs taken 24 h after hyperthermia showed that 17CRE reactivated significantly less than 17syn+ and 17CREr, while no significant differences were found in HSV-1 DNA genome copy numbers and latent virus in the trigeminal ganglia. These results are evidence that this CRE site in the LAT promoter facilitates ocular HSV-1 reactivation in mice.