The viral life cycle of KSHV: Kaposi sarcoma herpesvirus (KSHV) virion binds to receptors present on the cell surface (such as integrins, the cystine–glutamate transporter (xCT), CD98 and heparan sulfate) via glycoproteins (such as gpK8.1, gB, gM–gN and gH–gL) on its envelope; this binding, in most cases, results in the endocytosis of the virion into the cell. The virion uncoats itself in the cell cytoplasm, and the capsid containing the viral genome traverses to the nucleus. The viral genome enters the nucleus, where it can remain latent as a circular episome tethered to host chromosomes via its latency-associated nuclear protein (LANA), or it can enter the lytic cycle where the viral genomes are replicated and new virions are produced through a complex mechanism of envelopment and ultimately released from the cell via budding. Note that KSHV proteins can increase host signalling through the phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signalling pathways. RTA, replication and transcription activator. | Cesarman, E., Damania, B., Krown, S. E., Martin, J., Bower, M., & Whitby, D. (2019). Kaposi sarcoma. Nature Reviews. Disease Primers, 5(1), 9.

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