How Epstein-Barr Virus and Kaposi's Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell

Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) independently cause human cancers, and both are maintained as plasmids in tumor cells. They differ, however, in their mechanisms of segregation; EBV partitions its genomes quasi-faithfully, while KSHV often clusters its genomes and partitions them randomly. Both viruses can infect the same B-cell to transform it in vitro and to cause primary effusion lymphomas (PELs) in vivo. We have developed simulations based on our measurements of these replicons in B-cells transformed in vitro to elucidate the synthesis and partitioning of these two viral genomes when in the same cell. These simulations successfully capture the biology of EBV and KSHV in PELs. They have revealed that EBV and KSHV replicate and partition independently, that they both contribute selective advantages to their host cell, and that KSHV pays a penalty to cluster its genomes.

Automated summary

EBV and KSHV independently cause human cancers and exist as plasmids in tumor cells. They differ in their mechanisms of segregation, with EBV partitioning its genomes quasi-faithfully and KSHV often clustering its genomes and partitioning them randomly. Both viruses replicate and partition independently in B-cells, providing selective advantages to their host cells. KSHV incurs a penalty for clustering its genomes.