Functional defects of fowl plague virus temperature-sensitive mutant having mutation in the neuraminidase

Abstract

A fowl plague virus (FPV) temperature-sensitive mutant ts 5 having mutation lesions in the gene coding for the neuraminidase has been obtained. The mutant induced synthesis of cRNA, vRNA and proteins in cells under non-permissive conditions, but formation of virions including non-infectious ones was defective. The neuraminidase and haemagglutinin synthesized under non-permissive conditions possessed functional activity and could migrate from the rough endoplasmic reticulum into plasma membranes; however, cleavage of the haemagglutinin was reduced. In ts 5-infected cells under non-permissive conditions the synthesis of segments 5 and 8 of cRNA and vRNA was predominant both early and late in the reproduction cycle, and the synthesis of P1, P2, P3, HA and M proteins was reduced after approximately 3 hours. The data obtained suggest that involvement of the neuraminidase in the formation of infectious virions may have no direct association with the enzymatic activity of this protein, and that the mutation in the neuraminidase may affect regulation of replication and transcription processes.

Studies of a Recombinant which Inherited the Haemagglutinin from the Human Influenza Virus A/Hong Kong/1/68 (H3N2) and Other Genes from Influenza Virus A/duck/Ukraine/1/63 (H3N8)

“…When one of the FPV genes was substituted in these recombinants by a corresponding gene of A/Krasnodar/101/59 virus, they did not lose their ability to reproduce and form plaques in CEF cultures provided that these substitutions involved genes 1,2, 3, 5, 6, 7 or 8 (Ghendon et al, , 1983Lisovskaya et al, 1981). At the same time as the FPV gene coding for the haemagglutinin was substituted by a corresponding gene of A/Krasnodar/101/59, the recombinant entirely lost its ability to form plaques in CEF cultures (Ghendon et al, 1979).…”

Characterization of a temperature-sensitive influenza B virus mutant defective in neuraminidase

“…The function of NA in replication of influenza A viruses, including human and avian viruses, has been studied extensively, and several roles for it have been proposed. (i) NA assists in releasing progeny viruses by cleaving neuraminic acid from cell receptors and from HA (20); (ii) NA modifies HA carbohydrate side chains to allow proteolytic cleavage of HA (22), and through this mechanism, it is implicated in aiding viral neurovirulence (27); and (iii) NA contributes to the regulation of both RNA and protein synthesis and virus morphogenesis (8). Evidence has also been presented, however, that NA function is not required for the production of infectious virus (3,4).…”