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Article: Kaposi's sarcoma-associated herpesvirus ORF18 and ORF30 are essential for late gene expression during lytic replication

TitleKaposi's sarcoma-associated herpesvirus ORF18 and ORF30 are essential for late gene expression during lytic replication
Authors
Issue Date2014
Citation
Journal of Virology, 2014, v. 88, n. 19, p. 11369-11382 How to Cite?
Abstract© 2014, American Society for Microbiology. Kaposi's sarcoma-associated herpesvirus (KSHV) is associated with several human malignances. As saliva is likely the major vehicle for KSHV transmission, we studied in vitro KSHV infection of oral epithelial cells. Through infection of two types of oral epithelial cells, normal human oral keratinocytes (NHOKs) and papilloma-immortalized human oral keratinocyte (HOK16B) cells, we found that KSHV can undergo robust lytic replication in oral epithelial cells. By employing de novo lytic infection of HOK16B cells, we studied the functions of two previously uncharacterized genes, ORF18 and ORF30, during the KSHV lytic cycle. For this purpose, an ORF18-deficient virus and an ORF30-deficient virus were generated using a mutagenesis strategy based on bacterial artificial chromosome (BAC) technology. We found that neither ORF18 nor ORF30 is required for immediately early or early gene expression or viral DNA replication, but each is essential for late gene expression during both de novo lytic replication and reactivation. This critical role of ORF18 and ORF30 in late gene expression was also observed during KSHV reactivation. In addition, global analysis of viral transcripts by RNA sequencing indicated that ORF18 and ORF30 control the same set of viral genes. Therefore, we suggest that these two viral ORFs are involved in the same mechanism or pathway that coregulates the viral late genes as a group.
Persistent Identifierhttp://hdl.handle.net/10722/285947
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.authorWu, Nicholas C.-
dc.contributor.authorXie, Yafang-
dc.contributor.authorFeng, Jun-
dc.contributor.authorTong, Leming-
dc.contributor.authorBrulois, Kevin F.-
dc.contributor.authorLuan, Harding-
dc.contributor.authorDu, Yushen-
dc.contributor.authorJung, Jae U.-
dc.contributor.authorWang, Cun Yu-
dc.contributor.authorKang, Mo Kwan-
dc.contributor.authorPark, No Hee-
dc.contributor.authorSun, Ren-
dc.contributor.authorWu, Ting Ting-
dc.date.accessioned2020-08-18T04:57:03Z-
dc.date.available2020-08-18T04:57:03Z-
dc.date.issued2014-
dc.identifier.citationJournal of Virology, 2014, v. 88, n. 19, p. 11369-11382-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285947-
dc.description.abstract© 2014, American Society for Microbiology. Kaposi's sarcoma-associated herpesvirus (KSHV) is associated with several human malignances. As saliva is likely the major vehicle for KSHV transmission, we studied in vitro KSHV infection of oral epithelial cells. Through infection of two types of oral epithelial cells, normal human oral keratinocytes (NHOKs) and papilloma-immortalized human oral keratinocyte (HOK16B) cells, we found that KSHV can undergo robust lytic replication in oral epithelial cells. By employing de novo lytic infection of HOK16B cells, we studied the functions of two previously uncharacterized genes, ORF18 and ORF30, during the KSHV lytic cycle. For this purpose, an ORF18-deficient virus and an ORF30-deficient virus were generated using a mutagenesis strategy based on bacterial artificial chromosome (BAC) technology. We found that neither ORF18 nor ORF30 is required for immediately early or early gene expression or viral DNA replication, but each is essential for late gene expression during both de novo lytic replication and reactivation. This critical role of ORF18 and ORF30 in late gene expression was also observed during KSHV reactivation. In addition, global analysis of viral transcripts by RNA sequencing indicated that ORF18 and ORF30 control the same set of viral genes. Therefore, we suggest that these two viral ORFs are involved in the same mechanism or pathway that coregulates the viral late genes as a group.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleKaposi's sarcoma-associated herpesvirus ORF18 and ORF30 are essential for late gene expression during lytic replication-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.00793-14-
dc.identifier.pmid25056896-
dc.identifier.pmcidPMC4178812-
dc.identifier.scopuseid_2-s2.0-84906985212-
dc.identifier.volume88-
dc.identifier.issue19-
dc.identifier.spage11369-
dc.identifier.epage11382-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000341872700032-
dc.identifier.issnl0022-538X-

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