Abstract
Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are two oncogenic human γ-herpesviruses that are each associated with 1-2% of human tumors. They encode bona fide oncogenes that they express during latent infection to amplify their host cells and themselves within these. In contrast, lytic virus particle producing infection has been considered to destroy host cells and might be even induced to therapeutically eliminate EBV and KSHV associated tumors. However, it has become apparent in recent years that early lytic replication supports tumorigenesis by these two human oncogenic viruses. This review will discuss the evidence for this paradigm change and how lytic gene products might condition the microenvironment to facilitate EBV and KSHV associated tumorigenesis.
Highlights
ON EBV AND KSHV INFECTION AND TUMORIGENESISEpstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are the two human gherpesviruses (Ehlers et al, 2010)
In healthy virus carriers a large proportion of the cytotoxic CD8+ T cell response is dedicated to the recognition of early lytic KSHV and EBV antigens, probably more than to their latent antigens (Long et al, 2019)
Most EBV specific vaccination approaches have so far focused on latent antigens to elicit protective T cells and late lytic antigens to induce antibodies (Taylor et al, 2004; Smith et al, 2006; Moutschen et al, 2007; Gurer et al, 2008; Ruiss et al, 2011; Meixlsperger et al, 2013; Kanekiyo et al, 2015; van Zyl et al, 2018; Rühl et al, 2019; Bu et al, 2019). From these studies the latent EBV antigens EBNA1, LMP1 and LMP2 have emerged as protective antigens (Rühl et al, 2020)
Summary
Epstein Barr virus (EBV) and Kaposi sarcoma associated herpesvirus (KSHV) are two oncogenic human g-herpesviruses that are each associated with 1-2% of human tumors. They encode bona fide oncogenes that they express during latent infection to amplify their host cells and themselves within these. Lytic virus particle producing infection has been considered to destroy host cells and might be even induced to therapeutically eliminate EBV and KSHV associated tumors. It has become apparent in recent years that early lytic replication supports tumorigenesis by these two human oncogenic viruses.
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