A reassortant between influenza A viruses (H7N2) synthesizing an enzymatically inactive neuraminidase at 40 degrees which is not incorporated into infectious particles.

Cells infected with a reassortant (113/Ho, H7N2) between A/fowl plague/Rostock/34 (FPV, H7N1) and A/Hong Kong/1/68 (H3N2) carrying RNA segments 1 and 6 of the Hong Kong virus and the residual genes of FPV, synthesized at 40 degrees a neuraminidase (NA) which is enzymatically not active and which is not incorporated into infectious particles. At 40 degrees NA accumulates in the rough endoplasmic reticulum. It contains mainly carbohydrate side chains of the mannose type, and fucose is only scarcely incorporated. At 33 degrees NA of the reassortant is overproduced, and at least some of it is active and is incorporated into viral particles. Under nonreducing conditions during PAGE its NA migrates to the same position as after heating with mercaptoethanol, in contrast to the Hong Kong parent virus. It is speculated that at 40 degrees the tetramerization of the NA in the rough endoplasmic reticulum does not function, and in this way its migration to the cytoplasmic membrane and its incorporation into infectious particles does not occur. Since 113/Ho is as pathogenic for the chicken (body temperature of 41 degrees) as is FPV, the question arises which role the NA plays in virus replication and spread in the infected organism.