Reactivation and lytic replication of KSHV

Abstract

Overview: goals of lytic replication Herpesviruses are extremely successful pathogens that have coevolved with their mammalian hosts over the past 60–80 million years (McGeoch and Davison, 1999). This success likely is attributable to the ability of the Herpesviridae to establish lifelong latent infections of their host. Latently infected cells provide a perpetual reservoir from which progeny viruses can be amplified for dissemination within the host and transmission between hosts. Herpesvirologists have traditionally used the term “lytic reactivation” to describe the biological events that begin with emergence of a virus from latency and end with lysis of the host cell and release of progeny virions. Clinico-epidemiologic studies suggest that lytic reactivation of KSHV is an essential pathogenic step in multiple human diseases. The goal of this chapter is to review the host–virus interactions that are critical for regulating induction of KSHV from latency, subsequent progression through the lytic cycle, replication of the viral genome, and assembly of mature viral particles. Lytic reactivation of KSHV is a critical pathogenic step in development of KS and other human diseases Numerous epidemiologic studies unanimously agree that reactivation of KSHV from latency is a critical pathogenic step during the progression to KS. Serologic assays (Gao et al ., 1996a; Kedes et al ., 1996; Martin et al ., 1998; Simpson et al ., 1996) demonstrate that primary infection by KSHV typically occurs at least 10 years prior to clinically apparent KS in AIDS patients (Martin et al ., 1998).