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Article: Virus-like vesicles of Kaposi's sarcoma-associated herpesvirus activate lytic replication by triggering differentiation signaling

TitleVirus-like vesicles of Kaposi's sarcoma-associated herpesvirus activate lytic replication by triggering differentiation signaling
Authors
KeywordsEnvelope protein
Extracellular vesicle
Herpesvirus
KSHV
MicroRNA
PRDM1
RTA
Tegument protein
Virus-like vesicle
EBV
Issue Date2017
Citation
Journal of Virology, 2017, v. 91, n. 15, article no. e00362-17 How to Cite?
Abstract© 2017 American Society for Microbiology. Virus-like vesicles (VLVs) are membrane-enclosed vesicles that resemble native enveloped viruses in organization but lack the viral capsid and genome. During the productive infection of tumor-associated gammaherpesviruses, both virions and VLVs are produced and are released into the extracellular space. However, studies of gammaherpesvirus-associated VLVs have been largely restricted by the technical difficulty of separating VLVs from mature virions. Here we report a strategy of selectively isolating VLVs by using a Kaposi's sarcoma-associated herpesvirus (KSHV) mutant that is defective in small capsid protein and is unable to produce mature virions. Using mass spectrometry analysis, we found that VLVs contained viral glycoproteins required for cellular entry, as well as tegument proteins involved in regulating lytic replication, but lacked capsid proteins. Functional analysis showed that VLVs induced the expression of the viral lytic activator RTA, initiating KSHV lytic gene expression. Furthermore, employing RNA sequencing, we performed a genomewide analysis of cellular responses triggered by VLVs and found that PRDM1, a master regulator in cell differentiation, was significantly upregulated. In the context of KSHV replication, we demonstrated that VLV-induced upregulation of PRDM1 was necessary and sufficient to reactivate KSHV by activating its RTA promoter. In sum, our study systematically examined the composition of VLVs and demonstrated their biological roles in manipulating host cell responses and facilitating KSHV lytic replication.
Persistent Identifierhttp://hdl.handle.net/10722/285792
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGong, Danyang-
dc.contributor.authorDai, Xinghong-
dc.contributor.authorXiao, Yuchen-
dc.contributor.authorDu, Yushen-
dc.contributor.authorChapa, Travis J.-
dc.contributor.authorJohnson, Jeffrey R.-
dc.contributor.authorLi, Xinmin-
dc.contributor.authorKrogan, Nevan J.-
dc.contributor.authorDeng, Hongyu-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:39Z-
dc.date.available2020-08-18T04:56:39Z-
dc.date.issued2017-
dc.identifier.citationJournal of Virology, 2017, v. 91, n. 15, article no. e00362-17-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285792-
dc.description.abstract© 2017 American Society for Microbiology. Virus-like vesicles (VLVs) are membrane-enclosed vesicles that resemble native enveloped viruses in organization but lack the viral capsid and genome. During the productive infection of tumor-associated gammaherpesviruses, both virions and VLVs are produced and are released into the extracellular space. However, studies of gammaherpesvirus-associated VLVs have been largely restricted by the technical difficulty of separating VLVs from mature virions. Here we report a strategy of selectively isolating VLVs by using a Kaposi's sarcoma-associated herpesvirus (KSHV) mutant that is defective in small capsid protein and is unable to produce mature virions. Using mass spectrometry analysis, we found that VLVs contained viral glycoproteins required for cellular entry, as well as tegument proteins involved in regulating lytic replication, but lacked capsid proteins. Functional analysis showed that VLVs induced the expression of the viral lytic activator RTA, initiating KSHV lytic gene expression. Furthermore, employing RNA sequencing, we performed a genomewide analysis of cellular responses triggered by VLVs and found that PRDM1, a master regulator in cell differentiation, was significantly upregulated. In the context of KSHV replication, we demonstrated that VLV-induced upregulation of PRDM1 was necessary and sufficient to reactivate KSHV by activating its RTA promoter. In sum, our study systematically examined the composition of VLVs and demonstrated their biological roles in manipulating host cell responses and facilitating KSHV lytic replication.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.subjectEnvelope protein-
dc.subjectExtracellular vesicle-
dc.subjectHerpesvirus-
dc.subjectKSHV-
dc.subjectMicroRNA-
dc.subjectPRDM1-
dc.subjectRTA-
dc.subjectTegument protein-
dc.subjectVirus-like vesicle-
dc.subjectEBV-
dc.titleVirus-like vesicles of Kaposi's sarcoma-associated herpesvirus activate lytic replication by triggering differentiation signaling-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.00362-17-
dc.identifier.pmid28515293-
dc.identifier.pmcidPMC5651724-
dc.identifier.scopuseid_2-s2.0-85023175514-
dc.identifier.volume91-
dc.identifier.issue15-
dc.identifier.spagearticle no. e00362-17-
dc.identifier.epagearticle no. e00362-17-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000405866600012-
dc.identifier.issnl0022-538X-

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