Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiological agent contributing to development of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman desease. During latency, only a few viral genes are expressed, and these include the three genes of the so-called latency transcript (LT) cluster: v-FLIP (open reading frame 71 [ORF71]), v-cyclin (ORF72), and latency-associated nuclear antigen (ORF73). HHV-6 established latency in the macrophage, kept a fairly stable intermediate stage between latency and reactivation, and the viral reactivation was induced by two or more factors. The review briefly focuses on herpes infections in the horse and cat where some progress has already been achieved in the veterinary antiviral field. By changing the origin architecture, LANA may help to assemble a specific nucleoprotein structure important for the initiation of DNA replication. As in all primary effusion lymphoma cell lines, there is a low level of spontaneous lytic replication in latently infected BJAB cells. Inhibiting MEK/ERK signalling by using MEK-specific inhibitors decreased expression of the TPA-induced KSHV lytic-cycle gene ORF8.
In gel filtration chromatography analyses of BC-3 cell lysates, ANG coeluted with LANA-1, p53, and Mdm2 in high-molecular-weight fractions, and LANA-1, p53, and Mdm2 also coimmunoprecipitated with ANG. We propose that RNAPII interactions and nucleosome displacement serve as a biochemical basis for programming RNAPII in the KSHV transcriptional control region. LTC, but not parental TIVE cells, formed tumors in nude mice. These results also suggest that the KSHV latent origin of replication is a unique chromatin environment containing histone H3 hyperacetylation within heterochromatic tandem repeats.