<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gong D</submitter><funding>NIDCR NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>11369-82</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4178812</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>88(19)</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>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 chromoso</pubmed_abstract><journal>Journal of virology</journal><pubmed_title>Kaposi's sarcoma-associated herpesvirus ORF18 and ORF30 are essential for late gene expression during lytic replication.</pubmed_title><pmcid>PMC4178812</pmcid><funding_grant_id>P01 CA180779</funding_grant_id><funding_grant_id>P30 CA016042</funding_grant_id><funding_grant_id>AI078133</funding_grant_id><funding_grant_id>R01 CA115284</funding_grant_id><funding_grant_id>R01 DE015752</funding_grant_id><funding_grant_id>R01 CA091791</funding_grant_id><funding_grant_id>R21 AI078133</funding_grant_id><funding_grant_id>DE15752</funding_grant_id><funding_grant_id>CA91791</funding_grant_id><pubmed_authors>Park NH</pubmed_authors><pubmed_authors>Xie Y</pubmed_authors><pubmed_authors>Tong L</pubmed_authors><pubmed_authors>Wu NC</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>Brulois KF</pubmed_authors><pubmed_authors>Luan H</pubmed_authors><pubmed_authors>Gong D</pubmed_authors><pubmed_authors>Wang CY</pubmed_authors><pubmed_authors>Feng J</pubmed_authors><pubmed_authors>Jung JU</pubmed_authors><pubmed_authors>Sun R</pubmed_authors><pubmed_authors>Kang MK</pubmed_authors><pubmed_authors>Wu TT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Kaposi's sarcoma-associated herpesvirus ORF18 and ORF30 are essential for late gene expression during lytic replication.</name><description>&lt;h4>Unlabelled&lt;/h4>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 chromoso</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Oct</publication><modification>2025-04-22T20:42:05.775Z</modification><creation>2019-03-27T01:36:41Z</creation></dates><accession>S-EPMC4178812</accession><cross_references><pubmed>25056896</pubmed><doi>10.1128/jvi.00793-14</doi><doi>10.1128/JVI.00793-14</doi></cross_references></HashMap>