Wagner et al. (2015) have demonstrated that PKs are cleaved by HIV-1 PR expressed by proviral genes after integration and not by the PRs brought in by the incoming viruses during early infection. This could possibly explain that non-PR mediated mechanisms are responsible for IFN suppression in acute productive infection while PR plays a role in IFN suppression in latently infected cells. Rigogliuso et al. (2019) have demonstrated the expression of PR in cells containing proviral genomes of Human endogenous retroviruses (HERVs) and its ability to cleave several cellular proteins. The gene discussed is WNK3; the disease is infection.