RESUMEN
This study focuses on the detection of chicken anemia virus (CAV) and avian gyrovirus 2 (AGV2) genomes in commercially available poultry vaccines. A duplex quantitative real-time PCR (dqPCR), capable of identifying genomes of both viruses in a single assay, was employed to determine the viral loads of these agents in commercially available vaccines. Thirty five vaccines from eight manufacturers (32 prepared with live and 3 with inactivated microorganisms) were examined. Genomes of CAV were detected as contaminants in 6/32 live vaccines and in 1/3 inactivated vaccines. The CAV genome loads ranged from 6.4 to 173.4 per 50 ng of vaccine DNA (equivalent to 0.07 to 0.69 genome copies per dose of vaccine). Likewise, AGV2 genomes were detected in 9/32 live vaccines, with viral loads ranging from 93 to 156,187 per 50 ng of vaccine DNA (equivalent to 0.28-9176 genome copies per dose of vaccine). These findings provide evidence for the possibility of contamination of poultry vaccines with CAV and AGV2 and they also emphasize the need of searching for these agents in vaccines in order to ensure the absence of such potential contaminants.
Asunto(s)
Virus de la Anemia del Pollo/inmunología , Infecciones por Circoviridae/inmunología , Contaminación de Medicamentos , Gyrovirus/inmunología , Vacunas/química , Secuencia de Aminoácidos , Animales , Pollos/virología , Clonación Molecular , ADN/química , ADN Viral/genética , Genoma Viral , Datos de Secuencia Molecular , Fenotipo , Reacción en Cadena de la Polimerasa/normas , Aves de Corral , Enfermedades de las Aves de Corral/virología , Control de Calidad , Reacción en Cadena en Tiempo Real de la Polimerasa , Vacunas Atenuadas , Carga ViralRESUMEN
The human gyrovirus-Apoptin (HGyv-Apoptin) is a protein that gained attention because it is selectively cytotoxic toward cancer cells. In this study, we have investigated the effect of HGyv-Apoptin on cell cycle progression of cancer cells. We also compared HGyv-Apoptin's action to its homologue chicken anemia virus Apoptin (CAV-Apoptin). We show that HGyv-Apoptin induces G2/M arrest in cancer cells. This is at least in part due to the fact that HGyv-Apoptin induces an abnormal spindle formation in mitotic cells that do not progress properly throughout the cell cycle. HGyv-Apoptin most likely inhibits APC function leading to a sustained cyclin-B1-expression. These results indicate that HGyv-Apoptin has a similar mechanism of action as its homolog CAV-Apoptin and further supports its cancer therapeutic potential.