Establishment and maintenance of Kaposi's sarcoma-associated herpesvirus latency in B cells. Export

@article{citeulike:1318015, abstract = {Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the infectious cause of Kaposi's sarcoma and is also associated with two B-cell lymphoproliferative diseases, primary effusion lymphoma and the plasmablastic form of multicentric Castleman's disease. KSHV is also found in the B-cell fraction of peripheral blood mononucleocytes of some KS patients. Despite in vivo infection of B cells and the ability of KSHV to infect many cell types in culture, to date B cells in culture have been resistant to KSHV infection. However, as shown here, the lack of infection is not due to the inability of B cells to support latent KSHV infection. When KSHV DNA is introduced into B cells, the virus is maintained as an episome and can establish and maintain latency over the course of months. As in all primary effusion lymphoma cell lines, there is a low level of spontaneous lytic replication in latently infected BJAB cells. Importantly, viral gene expression is similar to that of primary effusion lymphoma cell lines. Furthermore, the virus can be reactivated to higher levels with specific stimuli and transmitted to other cells, indicating that this is a productive infection. Thus B cells in culture are capable of establishing, maintaining, and reactivating from latency. These studies provide a controlled system to analyze how KSHV alters B cells during KSHV latency and reactivation.}, address = {University of Washington, Department of Microbiology, 1959 N.E. Pacific St., HSB H-310J, Box 357242, Seattle WA 98195, USA.}, author = {Chen, L. and Lagunoff, M.}, citeulike-article-id = {1318015}, citeulike-linkout-0 = {http://dx.doi.org/10.1128/JVI.79.22.14383-14391.2005}, citeulike-linkout-1 = {http://jvi.asm.org/cgi/content/abstract/79/22/14383}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/16254372}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=16254372}, comment = {establishment of kshv infection in Bjabs via direct introduction of viral DNA! B cells in culture are resistant to kshv ks tumors made up primarily of spindle cells which are of endothelial origin that express markers of the lymphatic endothilium electroporation to get viral episome into bjabs tpa induces lytic replication bcbl- primary effusioin lymphoma cell line infected cells (bjabs) slowly lose the viral episome when split regularly}, doi = {10.1128/JVI.79.22.14383-14391.2005}, issn = {0022-538X}, journal = {J Virol}, keywords = {bac, clone, kshv}, month = {November}, number = {22}, pages = {14383--14391}, posted-at = {2007-05-21 17:39:25}, priority = {0}, title = {Establishment and maintenance of Kaposi's sarcoma-associated herpesvirus latency in B cells.}, url = {http://dx.doi.org/10.1128/JVI.79.22.14383-14391.2005}, volume = {79}, year = {2005} }

TY - JOUR ID - citeulike:1318015 L3 - citeulike-article-id:1318015 N2 - Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is the infectious cause of Kaposi's sarcoma and is also associated with two B-cell lymphoproliferative diseases, primary effusion lymphoma and the plasmablastic form of multicentric Castleman's disease. KSHV is also found in the B-cell fraction of peripheral blood mononucleocytes of some KS patients. Despite in vivo infection of B cells and the ability of KSHV to infect many cell types in culture, to date B cells in culture have been resistant to KSHV infection. However, as shown here, the lack of infection is not due to the inability of B cells to support latent KSHV infection. When KSHV DNA is introduced into B cells, the virus is maintained as an episome and can establish and maintain latency over the course of months. As in all primary effusion lymphoma cell lines, there is a low level of spontaneous lytic replication in latently infected BJAB cells. Importantly, viral gene expression is similar to that of primary effusion lymphoma cell lines. Furthermore, the virus can be reactivated to higher levels with specific stimuli and transmitted to other cells, indicating that this is a productive infection. Thus B cells in culture are capable of establishing, maintaining, and reactivating from latency. These studies provide a controlled system to analyze how KSHV alters B cells during KSHV latency and reactivation. IS - 22 JF - J Virol SN - 0022-538X AD - University of Washington, Department of Microbiology, 1959 N.E. Pacific St., HSB H-310J, Box 357242, Seattle WA 98195, USA. EP - 14391 TI - Establishment and maintenance of Kaposi's sarcoma-associated herpesvirus latency in B cells. VL - 79 SP - 14383 KW - bac KW - clone KW - kshv N1 - establishment of kshv infection in Bjabs via direct introduction of viral DNA! B cells in culture are resistant to kshv ks tumors made up primarily of spindle cells which are of endothelial origin that express markers of the lymphatic endothilium electroporation to get viral episome into bjabs tpa induces lytic replication bcbl- primary effusioin lymphoma cell line infected cells (bjabs) slowly lose the viral episome when split regularly AU - Chen, L AU - Lagunoff, M PY - 2005/11// UR - http://dx.doi.org/10.1128/JVI.79.22.14383-14391.2005 ER -