Full Text Available
Note: Clicking the button above will open the full text document at the original institutional repository in a new window.
Persistent KSHV infection increases EBV-associated tumor formation in Vivo via enhanced EBV Lytic Gene expression
The human tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persistent infections in B cells. KSHV is linked to primary effusion lymphoma (PEL), and 90% of PELs also contain EBV. Studies on persistent KSHV infection in vivo and the role of EBV coinfect...
Saved in:
| Format: | Article |
|---|---|
| Published: |
2017
|
| Tags: |
No Tags, Be the first to tag this record!
|
MARC
| LEADER | 00000njm a2000000a 4500 | ||
|---|---|---|---|
| 001 | oai:repository.ui.edu.ng:123456789/12721 | ||
| 042 | |a dc | ||
| 720 | |a McHugh, D. |e author | ||
| 720 | |a Caduff, N. |e author | ||
| 720 | |a Barros, M. H. M. |e author | ||
| 720 | |a Rämer, P. C. |e author | ||
| 720 | |a Raykova, A. |e author | ||
| 720 | |a Murer, A. |e author | ||
| 720 | |a Landtwing, V. |e author | ||
| 720 | |a Quast, I. |e author | ||
| 720 | |a Styles, C. T. |e author | ||
| 720 | |a Spohn, M. |e author | ||
| 720 | |a Fowotade, A. |e author | ||
| 720 | |a Delecluse, H. J. |e author | ||
| 720 | |a Papoudou-Bai, A. |e author | ||
| 720 | |a Lee, Y.-M. |e author | ||
| 720 | |a Kim, J.-M. |e author | ||
| 720 | |a Middeldorp, J. |e author | ||
| 720 | |a Schulz, T. F. |e author | ||
| 720 | |a Cesarman, E. |e author | ||
| 720 | |a Zbinden, A. |e author | ||
| 720 | |a Capaul, R. |e author | ||
| 720 | |a White, R. E. |e author | ||
| 720 | |a Allday, M. J. |e author | ||
| 720 | |a Niedobitek, G. |e author | ||
| 720 | |a Blackbourn, D. J. |e author | ||
| 720 | |a Grundhoff, A. |e author | ||
| 720 | |a Münz, C. |e author | ||
| 260 | |c 2017 | ||
| 520 | |a The human tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persistent infections in B cells. KSHV is linked to primary effusion lymphoma (PEL), and 90% of PELs also contain EBV. Studies on persistent KSHV infection in vivo and the role of EBV coinfection in PEL development have been hampered by the absence of small animal models. We developed mice reconstituted with human immune system components as a model for KSHV infection and find that EBV/KSHV dual infection enhanced KSHV persistence and tumorigenesis. Dual-infected cells displayed a plasma cell-like gene expression pattern similar to PELs. KSHV persisted in EBV-transformed B cells and was associated with lytic EBV gene expression, resulting in increased tumor formation. Evidence of elevated lytic EBV replication was also found in EBV/KSHV dually infected lymphoproliferative disorders in humans. Our data suggest that KSHV augments EBV-associated tumorigenesis via stimulation of lytic EBV replication. | ||
| 024 | 8 | |a 1931-3128 | |
| 024 | 8 | |a 1934-6069 | |
| 024 | 8 | |a ui_art_mchugh_persistent_2017 | |
| 024 | 8 | |a Cell Host & Microbe 22, pp. 61-73 | |
| 024 | 8 | |a https://repository.ui.edu.ng/handle/123456789/12721 | |
| 245 | 0 | 0 | |a Persistent KSHV infection increases EBV-associated tumor formation in Vivo via enhanced EBV Lytic Gene expression |