<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Myoung J</submitter><funding>NIDCR NIH HHS</funding><funding>Howard Hughes Medical Institute</funding><pagination>1130-40</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3049404</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(3)</volume><pubmed_abstract>Kaposi sarcoma-associated herpesvirus (KSHV) is a B-lymphotropic virus whose primary site of replication is the oropharynx. KSHV can infect both T and B cells from primary tonsillar explant cultures. However, T cells do not support lytic replication, while B cells spontaneously produce substantial amounts of infectious virus. Here, we provide evidence for a mechanism by which activated T cells may promote or stabilize latency of KSHV infection in B cells. When mixed cultures of B cells and activated T cells were exposed to KSHV, little spontaneous virus production was observed. Removing T cells from the mix or treating the mixed culture with immune suppressants enhanced virus production. Adding back activated T cells to purified infected B cells efficiently suppressed KSHV production, prim</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Active lytic infection of human primary tonsillar B cells by KSHV and its noncytolytic control by activated CD4+ T cells.</pubmed_title><pmcid>PMC3049404</pmcid><funding_grant_id>P01 DE019085</funding_grant_id><funding_grant_id>P01DE019085</funding_grant_id><pubmed_authors>Ganem D</pubmed_authors><pubmed_authors>Myoung J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Active lytic infection of human primary tonsillar B cells by KSHV and its noncytolytic control by activated CD4+ T cells.</name><description>Kaposi sarcoma-associated herpesvirus (KSHV) is a B-lymphotropic virus whose primary site of replication is the oropharynx. KSHV can infect both T and B cells from primary tonsillar explant cultures. However, T cells do not support lytic replication, while B cells spontaneously produce substantial amounts of infectious virus. Here, we provide evidence for a mechanism by which activated T cells may promote or stabilize latency of KSHV infection in B cells. When mixed cultures of B cells and activated T cells were exposed to KSHV, little spontaneous virus production was observed. Removing T cells from the mix or treating the mixed culture with immune suppressants enhanced virus production. Adding back activated T cells to purified infected B cells efficiently suppressed KSHV production, prim</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Mar</publication><modification>2025-04-07T00:15:14.641Z</modification><creation>2019-03-27T00:39:24Z</creation></dates><accession>S-EPMC3049404</accession><cross_references><pubmed>21339648</pubmed><doi>10.1172/JCI43755</doi><doi>10.1172/jci43755</doi></cross_references></HashMap>