Suppressed Response to Interferon Induction in Mice Infected with Encephalomyocarditis Virus, Semliki Forest Virus, Influenza A2 Virus, Herpesvirus hominis Type 2, or Murine Cytomegalovirus

Abstract

Mice infected with encephalomyocarditis virus, Semliki Forest virus, influenza A2 virus, Herpesvirus hominis type 2 or murine cytomegalovirus developed hyporeactivity to interferon induction. In general, the capacity of infected animals to produce interferon in response to inducers became progressively impaired during the course of infection. The severity and time of onset of hyporeactivity were dependent on the inducer and the nature of the viral infection. During viral infections associated with generalized hyporesponsiveness, a factor that could inhibit interferon production by murine [fibroblast L] cells in culture was identified in the serum. This serum hyporeactive factor may have mediated the development of hyporeactivity in vivo. Hyporeactivity of the host''s interferon response was associated with progression of viral infection and may be partially responsible for the limited effectiveness of interferon inducers in the modification of viral infections, when administered after onset of symptoms. [This study was done to investigate the variable time course effectiveness of interferon therapy in human viral infection. Inducers used were tilorone hydrochloride, poly I:poly C, Newcastle disease virus and Rochester mouse virus.].