These findings indicate that T and B cells can exert their full antiviral function independently of IFNAR stimulation and that during a highly inflammatory viral infection such as ECTV, Signal 3 may not be required or may be provided by alternative or redundant mechanisms, such as IL-2, IL-6, IL-12, IL-18 or IFN-γ. The gene discussed is IFNG; the disease is viral infectious disease.