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 geno...
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doaj-ca229d89db054eb784722d5958f4e69c2021-08-26T14:26:36ZengMDPI AGViruses1999-49152021-07-01131478147810.3390/v13081478How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-CellArthur U. Sugden0Mitch Hayes1Bill Sugden2McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53705, USAMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53705, USAMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53705, USAEpstein–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.https://www.mdpi.com/1999-4915/13/8/1478KSHVEBVmodeldual-infection |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Arthur U. Sugden Mitch Hayes Bill Sugden |
spellingShingle |
Arthur U. Sugden Mitch Hayes Bill Sugden How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell Viruses KSHV EBV model dual-infection |
author_facet |
Arthur U. Sugden Mitch Hayes Bill Sugden |
author_sort |
Arthur U. Sugden |
title |
How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell |
title_short |
How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell |
title_full |
How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell |
title_fullStr |
How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell |
title_full_unstemmed |
How Epstein–Barr Virus and Kaposi’s Sarcoma-Associated Herpesvirus Are Maintained Together to Transform the Same B-Cell |
title_sort |
how epstein–barr virus and kaposi’s sarcoma-associated herpesvirus are maintained together to transform the same b-cell |
publisher |
MDPI AG |
series |
Viruses |
issn |
1999-4915 |
publishDate |
2021-07-01 |
description |
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. |
topic |
KSHV EBV model dual-infection |
url |
https://www.mdpi.com/1999-4915/13/8/1478 |
work_keys_str_mv |
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