KSHV infects B lymphocytes and establishes a predominantly latent infection. The detailed process and the mechanism underlying the establishment of latent infection remain elusive. After a KSHV particle enters a host cell, the virus undergoes D N A replication which results in accumulation of the viral genome to 50-100 copies per cell prior to establishment of latency. Little is known regarding the mode of the abortive viral replication and the regulation mechanism. ORF K8 encodes a nuclear protein of the bZip family. Gur study using K8-null recombinant virus demonstrated a role of KS in initial viral DNA replication following de novo KSHV Infection. K8-null viruses exhibit much lower viral genome copy numbers in comparison to wild type viruses when infecting 293T, HFF and HMVEC cells. The role of K8 in the early stage of de novo infection provides insights into the so-called
Viral replication following de novo infection leads to an increase in viral genome number and is important for establishment of KSHV latency. This proposal will investigate this less explored event during the early stages of KSHV infection. The results of the study would provide an insight into the mechanism of this mode of replication which will leads to new strategies and therapies against KSHV-mediated diseases.
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