Hypoxia and HIF-1 alpha promote lytic de novo KSHV infection

The impact of different stress conditions on the oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) primary infection that can occur in vivo remains largely unknown. We hypothesized that KSHV can establish latency or lytic cycle following de novo infection depending on the conditions of the cellular environment. Previous studies showed that hypoxia is a natural stress condition that promotes lytic reactivation and contributes to KSHV pathogenesis, but its effect on de novo KSHV infection is unknown. To test the effect of hypoxia on KSHV infection, we infected SLK cells in normoxia and hypoxia (1% O2), and performed a comparative analysis of viral gene expression, viral replication, and tested chromatinization of the KSHV genome during infection.