Conversely, infection of cells with a mutant HCMV lacking pUL31 expression resulted in a significant upregulation of type I IFN, as well as downstream antiviral genes, including IFNB1, RANTES, and IL6. Supporting pUL31′s role in countering the antiviral response, lytic infection of fibroblasts with the UL31-deletion mutant results in attenuated viral growth, when compared to wild type infection; a phenotype that is reversed by infection of cells devoid of cGAS [98]. The gene discussed is CCL5; the disease is infection.