Incomplete avian influenza virus contains a defective non-interfering component.
Incomplete avian influenza (fowl plague) virus derived by undiluted egg passage, displayed an increased capacity to promote the synthesis of intracellular virus-specific proteins when compared with standard virus. The in vitro virion-bound RNA polymerase activity of incomplete virus was also greater than could be explained by the presence of residual infectious virus. When the titres of infectious and interfering virus species were determined directly, they did not account for all the virus present. The existence of defective non-interfering (DNI) virus, even in standard virus preparations, was inferred. DNI virus is capable of initiating infection, synthesis of mRNA and proteins but cannot complete a productive replication cycle, and does not interfere with multiplication of standard virus. Such DNI virus could exaggerate the true extent of DI virus formation by lowering the PFU:HAU ratio and  so account for the failure to correlate infectivity with RNA composition or RNA polymerase activity.
D000818:Animals; D002478:Cells, Cultured; D002642:Chick Embryo; D003673:Defective Viruses / Q000378:metabolism / Q000502:physiology*; D009980:Influenza A virus / Q000378:metabolism / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D012367:RNA, Viral / Q000032:analysis / Q000096:biosynthesis; D014762:Viral Interference; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D012333:RNA, Messenger; D012367:RNA, Viral; D014764:Viral Proteins