(i) Type I and III IFNs (IFNB and IFNL) which increase transcription of interferon stimulated genes (ISGs) including IRF7 which fuels further IFN transcription [27], (ii) Proinflammatory cytokines TNF, IL-6 and IL-1β which prepare bystander immune cells to fight the infection and (iii) chemokines like CCL5 (RANTES) and CXCL10 (IP-10) to attract distal immune cells to the site of infection. The gene discussed is IFNB1; the disease is infection.