Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV) is the
causative agent of two B cell lymphoproliferative diseases,
namely primary effusion lymphoma (PEL) and multicentric
Castleman’s disease (MCD). KSHV infection of B cell lymphoma
in vitro has been a long-standing battle in advancing
human KSHV biology. In this study, a modified form of
KSHV BAC36 named BAC36A significantly increased the
fidelity of gene-targeted site-directed mutagenesis in the
KSHV genome. This modification eliminates tedious screening
steps required to obtain mutant clones when a KSHV
BAC36 reverse genetic system is used. Coculturing B-cell
lymphoma BJAB cells with KSHV BAC36A stably transfected
293T cells enabled us to infect BJAB cells with a
KSHV virion derived from the KSHV BAC36A. The coculture
system produced substantial amounts of KSHV infection
to BJAB, meaning that KSHV virions were released
from 293T cells and then infected neighboring BJAB cells.
Owing to our success with the KSHV BAC36A and coculture
system, we propose a new genetic system for the study of
KSHV gene expression and regulation in B-cell lymphoma.
Citations
Citations to this article as recorded by

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