Investigating replication of viruses can be a challenging task, particularly if the replication is limited or not causing obvious cytopathic effects (CPEs). Integration of a gene encoding fluorescent protein within the virus genome is a frequently used approach to overcome such issues. However, mutagenesis of large DNA genomes, such as herpesviruses, was until recently very cumbersome. Cloning of large DNA fragments as bacterial artificial chromosomes (BAC) and development of techniques for the site directed and random mutagenesis have enabled a new and highly efficient approach to study biology of large DNA viruses. The main goal of this study was to intensify the green signal in an in vitro system for the visualization of herpes simplex virus type 1 (HSV-1) during active stage of infection, relying on a recombinant virus genome cloned as a bacterial artificial chromosome, expressing reporter gene for the enhanced green fluorescent protein (EGFP). Since the human cytomegalovirus (CMV) promoter is one of the most potent and therefore one of the most commonly used promoters in research for driving the transcription of genes of interest, we wanted to see to what extent it affects the transcription of EGFP upon transfection of Vero cells compared to the original mutant. To optimize the expression of the green protein, another goal was to generate a second HSV-1 recombinant, additionally containing polyadenylation (polyA) termination signal situated downstream of the EGFP sequence in order to evaluate its necessity for stabile gene expression. For genome editing, a KOS viral strain, plasmid vector suitable for the mutagenesis of most of the HSV-1 strains and an “En passant” Lambda Red recombination technique in Escherichia Coli was used. The sequences of interest (CMVp-EGFP and CMVp-EGFP-polyA) were supposed to be inserted into an intergenic region UL3-UL4 and the successful integration of the green protein was supposed to be confirmed using fluorescent microscopy and Western blot. Unfortunately, the construction of viral recombinants failed due to the unsuccessful integration of sequences inside the genome in the first step of the “En passant” recombination.   Still, the collected data is provided, with the discussion section explaining possible reasons of failure, as well as future efforts in resolving the problem.