Herpes Simplex Virus 1 (HSV-1) affects 50-80% of the general population in the United States. Symptoms typically present as cold sores or fever blisters but can also cause genital herpes and more severe effects such as keratitis leading to blindness or encephalitis. Multiple viral and cellular proteins act on the viral genome during viral infection. Previous studies found that human RECQ Like Helicase (RECQL) associates with the HSV-1 genome during viral DNA replication. RECQL is a DNA helicase enzyme that helps repair DNA damage and maintain a stable genome. The function of RECQL during viral replication has yet to be defined. Prior research in the lab found that RECQL knockdown resulted in a slight increase in viral yield. Therefore, it is hypothesized that RECQL is inhibitory during HSV-1 replication and that overexpression of RECQL will result in less efficient HSV-1 DNA replication. To test this, RECQL was successfully cloned into the pLEX305-c-dTAG vector and transfected into HEK293 cells. Proteins were collected, and a western blot was run, indicating that RECQL was successfully overexpressed in the cells. The HEK293 cells were also infected with the HSV-1 laboratory strain KOS to determine how RECQL expression affects viral yield. Virus was collected from infected cells, and a plaque assay will be completed. Fewer plaque-forming units are expected to be present with the overexpression of RECQL, indicating less viral replication. If the expected results occur, the hypothesis will be accepted that RECQL acts as an inhibitory protein during HSV-1 replication, and further research must be done to define the pathways or mechanisms of the inhibitory effects.