Study On Functions Of PRV Major Virulent Genes

Replication, pathogenicity, distribution and immunogenicity of the deletion mutant Pseudorabies virus (PRV) , absent of the major virulent genes, were studied in this paper with intention of the functions of TK, gI and gE genes with reverse methods.1 , TK gene The PRV D1 strain , absence of TK gene was sensitive to Vero, IBRS-2, Marc-145, MDBK and ST cells, this was similar to PRV Fa. Especially, Obvious CPE appeared in MDBK mono-cells post infection with the PRV Dl strain during 8-48h.The piglets infected by PRV Fa appeared pathological changes in Cerebrum, cerebellum, trigeminus, heart, lung, liver, kidney, lymphoid nodes and tonsilla, while those infected by Dl changed only in liver, kidney, lymphoid node and tonsilla. PRV could be detected in 10 tissues infected by PRV Fa, while those infected by Dl could not be detected in Cerebrum, cerebellum and lung. From above, we could draw the conclusion: (1)TK gene is non-essential gene to the replication of PRV, and the deletion of TK gene does not interfere PRV replication. (2)TK gene is the main virulent gene, TK deletion may remarkably lower or loss PRV virulence; TK gene is the major functional gene for PRV replication in central nerve system. TK gene is related to the local residence of PRV in Cerebrum, cerebellum, trigeminus, kidney and heart. (3)TK gene represent philic-nerves and its deletion enhances the ability of anti-latent infection.2. gE/gI gene The PRV D2 strain, absence of gE/gI gene, was sensitive to Vero, IBRS-2, Marc-145, MDBK and ST cells. Especially obvious CPE appeared in MDBK mono-cells post infection with the PRV D2 strain during 8-48h. However, the ability of D2 replication was lower than PRV Fa. The piglets infected by PRV Fa appeared pathological changes in Cerebrum, Cerebellum, Trigeminus, heart, lung, liver, kidney, lymphoid node and tonsilla, while those infected by D2 only changed in liver, lymphoid node and tonsilla. PRV could be detected in 10 tissues infected by PRV Fa, while D2 could not bedetected in Cerebrum and cerebellum. The results indicate that(l)gE/gI complex bind to the conjugation site, subsequently changed the conjugation sites, causing to inhibit the replication. gE/gl complex can promote cell fusion. (2) gE/gl are major virulent genes and correlate to the local residence in the lung. gE/gl deletion could lower virulence, replication, transmission and lethal of PRV. gE gene is the essential gene for PRV to invade from the trigeminal ganglion to center nerve system. The gE/gl deletion virus can only arrive at primary and second neuron, while the third neuron forbid.(3) gE/gl represent philic-nerves and its deletion enhances the ability of anti-latent infection.3. gE/gl/TK genes The PRV D3 strain, absence of gE/gl/TK genes, was sensitive toVero. IBRS-2> Marc-145> MDBK and ST cells. However, the ability of its replication was lower than PRV Fa. The piglets infected by PRV Fa appeared pathological changes in Cerebrum, cerebellum, trigeminus, heart, lung, liver, kidney, lymphoid node and tonsilla, while those infected by D3 changed only in liver, kidney and tonsilla. PRV could be detected in 10 tissues infected by PRV Fa, while D3 could not be detected in Cerebrum and cerebellum. The results indicate that(l) gl /gE together with TK enhance the PRV replication. (2)TK gene is main virulent gene, gl /gE are important virulent genes, the interaction among gl, gE and TK will help PRV residenting in lymphoid nodes, and in the mean time increasing toxicity to kidney. (3) gE/gl/TK genes represent philic-nerves, the deletion enhances the ability of anti-latent infection.4. The absence of PRV major virulent genes did not change the immunogenicity; these genes are non-antigenic genes.5. The pathogenic models in piglets infected by different virulent genes-deletion of PRV were established.6. Many empty capsids could be observed in nuclear of infected cells infected by Dl, D2 and D3, which delay the assembly of virus particles. Infection mechanism of PRV and powerful tropism to lung was discussed by different virulent gene mutant of PRV.