Mini Chromosome Maintenance proteins (MCMs) play an important role in DNA replication by binding to the origins as helicase and recruiting polymerases for DNA synthesis. During the S phase, MCM complex is loaded once to limit DNA replication once per cell-cycle. We identified MCMs as ORF59 binding partners in our protein pull down assays, which led us to hypothesize that this interaction may influence DNA replication. ORF59's interactions with MCMs were confirmed in both endogenous and overexpression systems, which showed its association with MCM 3, 4, 5 and 6. Interestingly, MCM6 interacted with both the N and C terminal domains of ORF59 and its depletion in BCBL-1 and BC3 cells led to an increase in viral genome copies, viral late gene transcripts and virion production compared to the control cells following reactivation. MCMs perform its function by loading onto the replication competent DNA and one means of regulating chromatin loading/unloading, in addition to enzymatic activity of the MCM complex, is by post-translational modifications including phosphorylation of these factors. Interestingly, a hypo-phosphorylated form of MCM3, which is associated with reduced loading onto the chromatin, was detected during lytic reactivation and correlated with its inability to associate with histones in reactivated cells. Additionally, chromatin immunoprecipitation showed lower levels of MCM3 and MCM4 association at cellular origins of replication and decreased levels of cellular DNA synthesis in cells undergoing reactivation. Taken together, this suggests a mechanism in which KSHV ORF59 disrupts the assembly and functions of MCM complex to stall cellular DNA replication and promote viral replication.