Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. I. Rapid evolution of encephalomyocarditis virus infection.

Abstract

The role of interferon in the pathogenesis of encephalomyocarditis (EMC) virus infection was determined by treating mice with potent, partially purified sheep anti-mouse interferon globulin. In control mice, EMC, virus was present in low titers in various visceral organs, but attained high titers in the brain towards the 4th-5th day, at which time mice died with signs of CNS disease. In mice treated with anti-mouse interferon globulin, virus was present in high titer in visceral organs 24-36 h after viral inoculation, and virtually all mice were dead by 48 h. This rapid evolution of EMC virus infection was not observed in mice treated with the globulin fraction prepared from a normal sheep, from a sheep exhibiting a low anti-mouse interferon-neutralizing titer, or from a sheep having a high titer of antibody to human leukocyte interferon. Anti-interferon globulin apparently neutralized the interferon liberated by virus-infected cells, thus permitting extensive virus multiplication in several visceral organs. Interferon is an important early component of host resistance to this virus infection.