In contrast to these data, we have also reported that HSV-1 recombinants deficient for LAT expression (due to deletion of the core latency-associated promoter, or LAP) established latency in ~33 % more neurons per TG relative to revertant virus (following infection of mouse whisker pads with 106 p.f.u.; Nicoll et al., 2012), suggesting that LAT expression may repress the replication and spread of HSV-1 within the TG. Here, LAT is linked to infection.