Furthermore, reactivation and dissemination of the EBV infection presumably lead to enhanced expression of the lytic cycle viral IL10 homologue (vIL10) that (similar to human IL10) inhibits the synthesis of IFNγ and suppresses CTL activity and upregulation of MHC-I [58], which may contribute to the impaired cytokine response observed here. The gene discussed is IL10; the disease is Epstein-Barr virus infection.