Purpose of this review: Human gammaherpesviruses have complex lifecycles that drive their pathogenesis. KSHV and EBV are the etiological agents of multiple cancers worldwide. There is no FDA-approved vaccine for either KSHV or EBV. This review will describe recent progress in understanding EBV and KSHV lifecycles during infection.
Recent findings: Determining how latency is established, particularly how non-coding RNAs influence latent and lytic infection, is a rapidly growing area of investigation into how gammaherpesviruses successfully persist in the human population. Many factors have been identified as restrictors of reactivation from latency, especially innate immune antagonism. Finally, new host proteins that play a role in lytic replication have been identified.
Summary: In this review we discuss recent findings over the last 5 years on both host and viral factors that are involved in EBV and KSHV pathogenesis.
Keywords: EBV; KSHV; Latency; Lytic; Reactivation; Tropism.