Abstract
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.
Highlights
Epstein–Barr Virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) are two human γ-herpesviruses; both are maintained extra-chromosomally in proliferating cells and both cause several kinds of cancers in people
We have found that EBV and KSHV replicate and partition as independent replicons in the same cell, that both viruses contribute selective advantages to their host cell, and that KSHV pays a penalty by clustering its genomes
Cantheir theybeing be a disadvantage to the synthesis of genomes per se (a selective disadvantage that acts eliminated by their being a disadvantage to the synthesis of KSHV genomes per se? We modeled the first hypothesis by including a selective disadvantage on the selective disadvantage that acts on plasmids)? We modeled the first hypothesis by probability of replication of a cell proportional to the square of the number of plasmids—a including a selective disadvantage on the probability of replication of a cell proportional function used in [2] to limit extreme plasmid copy numbers
Summary
Epstein–Barr Virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) are two human γ-herpesviruses; both are maintained extra-chromosomally in proliferating cells and both cause several kinds of cancers in people. EBV titers were at a multiplicity generations, these parameters yielded a distribution of the number of plasmids per cell of infection (m.o.i.) of approximately 2, which is the initial condition used in our current that approximates an exponential decay These simulations were developed using conceptually simple forms of selective advantages and disadvantages to achieve an equilibrium in the distributions of EBV and KSHV plasmids in the same cells.
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