Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 14, 2014
Publication Date: February 6, 2014
Repository URL: http://handle.nal.usda.gov/10113/59018
Citation: Dunn, J.R., Auten, K.A., Heidari, M., Buscaglia, C. 2014. Correlation between Marek’s disease virus pathotype and replication. Avian Diseases. 58:287-292. Interpretive Summary: The traditional method of classifying Marek’s disease virus field isolates by pathotyping is an expensive and time-consuming process. This experiment evaluated the potential use of measuring virus replication rate as a faster and cheaper alternative for pathotyping. There are three levels that Marek’s disease virus strains are classified based on their virulence. We found that the lowest level could be distinguished from the higher two levels, but the highest two levels could not be distinguished from each other. As a result, we conclude that virus replication may be used as a threshold for choosing strains that are a certain level of virulence for pathotyping, but cannot be used as a stand alone alternative for classical pathotyping.
Technical Abstract: Marek’s disease virus (MDV) is an alphaherpesvirus that causes Marek’s disease (MD), a lymphoproliferative disease in chickens. Pathotyping has become an increasingly important assay for monitoring shifts in virulence of field strains, however, it is time-consuming and expensive and alternatives are needed to provide fast answers in the face of current outbreaks. The purpose of this study was to determine whether differences in virus replication between pathotypes that have been reported using a small number of virulent (v) and very virulent plus (vv+) MDV strains could be confirmed with a large collection of MD viruses. Based on pilot study data, bursa, brain and lung samples were collected at 9 and 11 days post-inoculation (dpi) from birds challenged with one of 15 MDV strains. The correlation between virus replication and virulence was confirmed between vMDV strains and higher virulent strains, but in most cases there was no significant difference between vv and vv+MDV groups. RNA expression of three MDV genes, Meq, pp38, and vIL8, was compared and quantities were higher in vv and vv+MDV pathotype groups compared to vMDV challenged groups, though most results were not significant due to high variability among samples. At both 9 and 11 dpi, chickens infected with vv and vv+MDV had significantly lower body weights and relative thymus and bursa weights compared to chickens challenged with vMDV. However, similar to virus quantity there was no significant difference between weights in birds challenged with vv or vv+MDV. No significant differences observed in ab- chickens carried over to ab+ chickens, demonstrating the requirement of ab- birds for this type of comparison. These data do not support the use of virus replication or organ weights as an alternative to pathotyping for discrimination between all three virulent MDV pathotypes, but may be useful for determining a virus replication threshold to choose which field strains meet a minimum virulence to be pathotyped by traditional methods.