Experimental infection of rabbits with a recombinant bovine herpesvirus type 5 (BoHV-5) gI, gE and US9-negative

Pesquisa Veterinária Brasileira

Alessandra D'avila Silva²  Ana Cláudia Franco¹  Paulo Augusto Esteves¹  Fernando Rosado Spilki¹  Paulo Michel Roehe² 

[1] ,Instituto de Pesquisas Veterinárias Desidério Finamor Equipe de Virologia Eldorado do Sul RS ,Brazil

关键词: Bovine herpesvirus type 5;    rabbits;    Herpesvírus bovino tipo 5;    BoHV-5 gI-/gE-/US9-;    coelhos;    neuropatogênese;   

DOI  :  10.1590/S0100-736X2009001100009

来源: SciELO

【 摘 要 】

Bovine herpesvirus type 5 (BoHV-5) is a major cause of viral meningoencephalitis in cattle. The expression of different viral proteins has been associated with BoHV-5 neuropathogenesis. Among these, gI, gE and US9 have been considered essential for the production of neurological disease in infected animals. To evaluate the role of gI, gE and US9 in neurovirulence, a recombinant from which the respective genes were deleted (BoHV-5 gI-/gE-/US9-) was constructed and inoculated in rabbits of two age groups (four and eight weeks-old). When the recombinant virus was inoculated through the paranasal sinuses of four weeks-old rabbits, neurological disease was observed and death was the outcome in 4 out of 13 (30.7 %) animals, whereas clinical signs and death were observed in 11/13 (84.6%) of rabbits infected with the parental virus. In eight weeks-old rabbits, the BoHV-5 gI-/gE-/US9- did not induce clinically apparent disease and could not be reactivated after dexamethasone administration, whereas wild type BoHV-5 caused disease in 55.5% of the animals and was reactivated. These findings reveal that the simultaneous deletion of gI, gE and US9 genes did reduce but did not completely abolish the neurovirulence of BoHV-5 in rabbits, indicating that other viral genes may also play a role in the induction of neurological disease.

【 授权许可】

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