RESUMO
Epizootics of a natural varicella-like disease occur in populations of nonhuman primates. Several primate herpesviruses have been isolated from these epizootics, but the relatedness of these isolates to each other is not well-defined. In this study, we demonstrated that the restriction endonuclease (REn) profiles of four epidemiologically distinct isolates were similar, although not identical, indicating that simian varicella epizootics are caused by various strains of simian varicella virus (SVV). The genetic variation among the isolates did not map to a specific region of the SVV genome and REn differences were detected within the SVV DNA long component and the inverted repeat region. Southern blot hybridization demonstrated that SVV is more closely related to varicella-zoster virus than to other primate herpesviruses. The study indicates that the current herpesvirus classification scheme should be changed to include SVV as a single taxonomic group within the Varicellovirus genus of alphaherpesviruses. In addition, REn profiles of SVV isolates, derived from primary and secondary episodes of simian varicella in the same monkey, were identical, providing evidence for SVV reactivation in a latently infected monkey.
Assuntos
Proteínas de Bactérias , Infecções por Herpesviridae/veterinária , Herpesvirus Cercopitecino 1/genética , Mapeamento por Restrição , Animais , Chlorocebus aethiops , Desoxirribonuclease BamHI/metabolismo , Desoxirribonuclease EcoRI/metabolismo , Desoxirribonucleases de Sítio Específico do Tipo II/metabolismo , Herpesviridae/classificação , Infecções por Herpesviridae/epidemiologia , Infecções por Herpesviridae/virologia , Herpesvirus Cercopitecino 1/classificação , Herpesvirus Cercopitecino 1/isolamento & purificação , Humanos , Doenças dos Primatas/virologia , Células VeroRESUMO
Simian varicella virus (SVV) causes a varicella-like disease in nonhuman primates. The DNA sequence and genetic organization of the inverted repeat region (RS) of the SVV genome was determined. The SVV RS is 7559 bp in size with 56% guanine+cytosine (G+C) content and includes 3 open reading frames (ORFs). The SVV RS1 ORF encodes a 1279 amino acid (aa) protein with 58 and 39% identity to the varicella-zoster virus (VZV) gene 62 and herpes simplex virus type 1 (HSV-1) ICP4 homologs, respectively. The predicted 261 aa SVV RS2 polypeptide possesses 52% identity with the VZV gene 63 homolog and 23% identity with the HSV-1 ICP22. The SVV RS3 encodes a 187 aa polypeptide with 56% and 28% identity to the VZV gene 64 and the HSV-1 US10 homologs, respectively, and includes an atypical zinc finger motif. A G+C-rich 16 base-pair (bp) sequence which is repeated 7 times and a putative SVV origin of replication were identified between the RS1 and RS2 ORFs. Comparison with the VZV RS indicates the SVV and VZV RS regions are similar in size and genetic organization.
Assuntos
DNA Viral , Herpesvirus Cercopitecino 1/genética , Herpesvirus Humano 3/genética , Sequências Repetitivas de Ácido Nucleico , Sequência de Aminoácidos , Animais , Sequência de Bases , Humanos , Dados de Sequência Molecular , Fases de Leitura Aberta , Homologia de Sequência de Aminoácidos , Homologia de Sequência do Ácido NucleicoRESUMO
The humoral immune response to simian varicella virus (SVV) was investigated following primary and secondary experimental infection of African green monkeys. Neutralization and immunoprecipitation assays were used to determine antibody titers to SVV throughout the course of infection. The immune response to specific viral polypeptides was analyzed by immunoprecipitation analysis. The results demonstrate that the simian varicella model offers a useful approach to investigate immune mechanisms in human varicella zoster virus (VZV) infections.
