Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production
Abstract Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. KSHV establishes a life-long infection in its host and alternates between a latent and lytic infection state. During lytic infection, l...
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doaj-7edb23e7d1dd45b89d061a74f4b215382020-12-08T02:11:26ZengNature Publishing GroupScientific Reports2045-23222017-03-017111210.1038/s41598-017-00401-7Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus productionMayu Nishimura0Tadashi Watanabe1Syota Yagi2Takahiro YamanakaMasahiro Fujimuro3Department of Cell Biology, Kyoto Pharmaceutical UniversityDepartment of Cell Biology, Kyoto Pharmaceutical UniversityDepartment of Cell Biology, Kyoto Pharmaceutical UniversityDepartment of Cell Biology, Kyoto Pharmaceutical UniversityAbstract Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. KSHV establishes a life-long infection in its host and alternates between a latent and lytic infection state. During lytic infection, lytic-related genes are expressed in a temporal manner and categorized as immediate early, early, and late gene transcripts. ORF34 is an early-late gene that interacts with several viral transcription-associated factors, however its physiological importance remains poorly understood. Here, we investigated the role of ORF34 during KSHV infection by generating ORF34-deficient KSHV, using a bacterial artificial chromosome system. Our results reveal that ORF34-deficient KSHV exhibited significantly attenuated late gene expression and viral production but did not affect viral DNA replication. ORF34 interacted with transcription factors ORF18, ORF24, ORF31, and ORF66, and a novel ORF34-interaction partner, ORF23. The C-terminal region of ORF34 was important for interaction with ORF24 and viral production. Our data support a model, in which ORF34 serves as a hub for recruiting a viral transcription complex to ORF24 to promote late viral gene expression.https://doi.org/10.1038/s41598-017-00401-7 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mayu Nishimura Tadashi Watanabe Syota Yagi Takahiro Yamanaka Masahiro Fujimuro |
spellingShingle |
Mayu Nishimura Tadashi Watanabe Syota Yagi Takahiro Yamanaka Masahiro Fujimuro Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production Scientific Reports |
author_facet |
Mayu Nishimura Tadashi Watanabe Syota Yagi Takahiro Yamanaka Masahiro Fujimuro |
author_sort |
Mayu Nishimura |
title |
Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production |
title_short |
Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production |
title_full |
Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production |
title_fullStr |
Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production |
title_full_unstemmed |
Kaposi’s sarcoma-associated herpesvirus ORF34 is essential for late gene expression and virus production |
title_sort |
kaposi’s sarcoma-associated herpesvirus orf34 is essential for late gene expression and virus production |
publisher |
Nature Publishing Group |
series |
Scientific Reports |
issn |
2045-2322 |
publishDate |
2017-03-01 |
description |
Abstract Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. KSHV establishes a life-long infection in its host and alternates between a latent and lytic infection state. During lytic infection, lytic-related genes are expressed in a temporal manner and categorized as immediate early, early, and late gene transcripts. ORF34 is an early-late gene that interacts with several viral transcription-associated factors, however its physiological importance remains poorly understood. Here, we investigated the role of ORF34 during KSHV infection by generating ORF34-deficient KSHV, using a bacterial artificial chromosome system. Our results reveal that ORF34-deficient KSHV exhibited significantly attenuated late gene expression and viral production but did not affect viral DNA replication. ORF34 interacted with transcription factors ORF18, ORF24, ORF31, and ORF66, and a novel ORF34-interaction partner, ORF23. The C-terminal region of ORF34 was important for interaction with ORF24 and viral production. Our data support a model, in which ORF34 serves as a hub for recruiting a viral transcription complex to ORF24 to promote late viral gene expression. |
url |
https://doi.org/10.1038/s41598-017-00401-7 |
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