Defective interfering type A equine influenza virus (H3N8) protects mice from morbidity and mortality caused by homologous and heterologous subtypes of influenza A virus.

Intranasal administration of defective interfering A/equine/Newmarket/7339/79 (H3N8) influenza virus (DI EQV) protected mice from otherwise lethal intranasal infection with homologous virus (EQV) or with the heterologous subtypes A/WSN (H1N1) or A/PR/8/34 (H1N1). Such protected mice showed little or no sign of clinical disease. Disease with only low mortality resulting from a 'low' dose of WSN was completely prevented with a 100-fold lower dose of DI EQV (4 haemagglutinating units/ml or 12 ng virus/mouse), indicating that there was a roughly proportional relationship between the protective dose of DI virus and the infecting inoculum. DI EQV-protected mice continued to gain weight at the normal rate, whereas those treated with inactivated DI EQV ceased putting on weight for about 7 days and were still underweight nearly 3 weeks later. Unlike DI WSN, DI EQV inhibited multiplication of infectious WSN in the lungs by 20 to 60-fold. Intranasal DI EQV on its own gave little protection to mice challenged 24 days later with EQV suggesting that it was only weakly immunogenic. DI EQV afforded significant protection when given up to 5 days before live virus challenge indicating that the DI genome remained active in the respiratory tract for this period of time.