Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression

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Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression. / McHugh, Donal; Caduff, Nicole; Barros, Mario Henrique M; Rämer, Patrick C; Raykova, Ana; Murer, Anita; Landtwing, Vanessa; Quast, Isaak; Styles, Christine T; Spohn, Michael; Fowotade, Adeola; Delecluse, Henri-Jacques; Papoudou-Bai, Alexandra; Lee, Yong-Moon; Kim, Jin-Man; Middeldorp, Jaap; Schulz, Thomas F; Cesarman, Ethel; Zbinden, Andrea; Capaul, Riccarda; White, Robert E; Allday, Martin J; Niedobitek, Gerald; Blackbourn, David J; Grundhoff, Adam; Münz, Christian.

In: CELL HOST MICROBE, Vol. 22, No. 1, 12.07.2017, p. 61-73.e7.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

McHugh, D, Caduff, N, Barros, MHM, Rämer, PC, Raykova, A, Murer, A, Landtwing, V, Quast, I, Styles, CT, Spohn, M, Fowotade, A, Delecluse, H-J, Papoudou-Bai, A, Lee, Y-M, Kim, J-M, Middeldorp, J, Schulz, TF, Cesarman, E, Zbinden, A, Capaul, R, White, RE, Allday, MJ, Niedobitek, G, Blackbourn, DJ, Grundhoff, A & Münz, C 2017, 'Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression', CELL HOST MICROBE, vol. 22, no. 1, pp. 61-73.e7. https://doi.org/10.1016/j.chom.2017.06.009

APA

McHugh, D., Caduff, N., Barros, M. H. M., Rämer, P. C., Raykova, A., Murer, A., Landtwing, V., Quast, I., Styles, C. T., Spohn, M., Fowotade, A., Delecluse, H-J., Papoudou-Bai, A., Lee, Y-M., Kim, J-M., Middeldorp, J., Schulz, T. F., Cesarman, E., Zbinden, A., ... Münz, C. (2017). Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression. CELL HOST MICROBE, 22(1), 61-73.e7. https://doi.org/10.1016/j.chom.2017.06.009

Vancouver

Bibtex

@article{fc1461b3bea140cda8232af74711d032,
title = "Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression",
abstract = "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 co-infection 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.",
keywords = "Animals, B-Lymphocytes, Cell Line, Tumor, Coinfection, Cytokines, DNA, Viral, Disease Models, Animal, Epstein-Barr Virus Infections, Gene Expression Regulation, Viral, Genes, Viral, Herpesviridae Infections, Herpesvirus 4, Human, Herpesvirus 8, Human, High-Throughput Nucleotide Sequencing, Humans, Lymphoma, Primary Effusion, Mice, Neoplasms, Spleen, Survival Rate, Virus Replication, Journal Article",
author = "Donal McHugh and Nicole Caduff and Barros, {Mario Henrique M} and R{\"a}mer, {Patrick C} and Ana Raykova and Anita Murer and Vanessa Landtwing and Isaak Quast and Styles, {Christine T} and Michael Spohn and Adeola Fowotade and Henri-Jacques Delecluse and Alexandra Papoudou-Bai and Yong-Moon Lee and Jin-Man Kim and Jaap Middeldorp and Schulz, {Thomas F} and Ethel Cesarman and Andrea Zbinden and Riccarda Capaul and White, {Robert E} and Allday, {Martin J} and Gerald Niedobitek and Blackbourn, {David J} and Adam Grundhoff and Christian M{\"u}nz",
note = "Copyright {\textcopyright} 2017 Elsevier Inc. All rights reserved.",
year = "2017",
month = jul,
day = "12",
doi = "10.1016/j.chom.2017.06.009",
language = "English",
volume = "22",
pages = "61--73.e7",
journal = "CELL HOST MICROBE",
issn = "1931-3128",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - Persistent KSHV Infection Increases EBV-Associated Tumor Formation In Vivo via Enhanced EBV Lytic Gene Expression

AU - McHugh, Donal

AU - Caduff, Nicole

AU - Barros, Mario Henrique M

AU - Rämer, Patrick C

AU - Raykova, Ana

AU - Murer, Anita

AU - Landtwing, Vanessa

AU - Quast, Isaak

AU - Styles, Christine T

AU - Spohn, Michael

AU - Fowotade, Adeola

AU - Delecluse, Henri-Jacques

AU - Papoudou-Bai, Alexandra

AU - Lee, Yong-Moon

AU - Kim, Jin-Man

AU - Middeldorp, Jaap

AU - Schulz, Thomas F

AU - Cesarman, Ethel

AU - Zbinden, Andrea

AU - Capaul, Riccarda

AU - White, Robert E

AU - Allday, Martin J

AU - Niedobitek, Gerald

AU - Blackbourn, David J

AU - Grundhoff, Adam

AU - Münz, Christian

N1 - Copyright © 2017 Elsevier Inc. All rights reserved.

PY - 2017/7/12

Y1 - 2017/7/12

N2 - 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 co-infection 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.

AB - 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 co-infection 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.

KW - Animals

KW - B-Lymphocytes

KW - Cell Line, Tumor

KW - Coinfection

KW - Cytokines

KW - DNA, Viral

KW - Disease Models, Animal

KW - Epstein-Barr Virus Infections

KW - Gene Expression Regulation, Viral

KW - Genes, Viral

KW - Herpesviridae Infections

KW - Herpesvirus 4, Human

KW - Herpesvirus 8, Human

KW - High-Throughput Nucleotide Sequencing

KW - Humans

KW - Lymphoma, Primary Effusion

KW - Mice

KW - Neoplasms

KW - Spleen

KW - Survival Rate

KW - Virus Replication

KW - Journal Article

U2 - 10.1016/j.chom.2017.06.009

DO - 10.1016/j.chom.2017.06.009

M3 - SCORING: Journal article

C2 - 28704654

VL - 22

SP - 61-73.e7

JO - CELL HOST MICROBE

JF - CELL HOST MICROBE

SN - 1931-3128

IS - 1

ER -