Dorothy E. Fry

Effect of Avian Adeno-Associated Virus on Pathogenicity of Tipton Virus in Chicks

The avian adeno-associated virus (A-AV) reduced the pathogenicity of an adenovirus infection in vivo. Groups of chicks were infected with Tipton virus alone or in combination with high or low doses of A-AV. In both trials, the associated virus delayed and reduced chick mortality. This effect was dose-dependent and significant at the higher dose level.

Serological response of chickens exposed to a type 1 avian adenovirus alone or in combination with the adeno-associated virus.

The avian adenoviruses (AV) are common infectious agents of poultry and other avian species throughout the world (1,4,8). Limited observations suggest that the adeno-associated virus (A-AV) coinfects many of the chickens that carry AV (8). The presence and persistence of these infections in a flock is often determined by serological methods. In the current study, the immune response of chickens to type 1 AV alone and to a dual exposure, AV plus A-AV, was followed over a 12-week period with a variety of serological tests. The study also determined the duration of the viral infections.

Some observations of the propagation of infectious laryngotracheitis virus in tissue culture.

HE virus of infectious laryngotracheitis (LT) produced cytopathogenic effect (CPE) and plaques in chick-embryo fibroblast and respiratory epithelium.1 However, Buthala, et a.3 was unable to find CPE with LT virus in chick-embryo kidney cells, although the virus proliferated in the cell culture. The present study had three objectives: 1. to study the effect of LT virus in chick-embryo kidney cells and its ability to produce CPE and plaques, 2. to attempt the isolation of the virus by plaque method from chickens artificially or naturally infected with LT virus, 3. to study the differences between plaques formed by LT virus, chick-embryo-lethalorphan (CELO) virus and Newcastle disease (ND) virus.

Neutralizing antibodies to CELO and avian adenovirus-associated viruses in the albumen of chicken eggs.

Neutralizing antibodies to CELO virus and to avian adenovirus-associated virus (A-AV) were detected in the albumen of eggs from four hens inoculated with these viruses. The antibody concentrations of serum, yolk, and albumen were determined before inoculation and at various times postinoculation (PI) by enzyme-linked immunosorbent assay (ELISA) and virus-neutralization (VN) tests. The antibody concentration in albumen was 0.3% to 1.0% of that detected in serum and yolk. Uninoculated hens showed no detectable antibody in serum, yolk, or albumen. It is suggested that the presence of antibody in the egg albumen may play a role in egg-transmission of viruses.

Populations of infectious virus produced during avian adenovirus-associated virus infection.

Multiple rounds of infection in vitro or in vivo with avian adenovirus-associated virus (AvA-AV) and avian adenovirus (AvAV) result in production of both heavy (H) and light (L) infectious forms. In this study, the infectious AvA-AV progeny produced at different hours during recombined dual infection of cells with either H or L AvA-AV and AvAV was determined by equilibrium CSCl centrifugation and infectivity assay. In both types of infection, H virions were found early, both intra- and extracellularly, whereas L virions were found late. The data iondicate an H to L particle density shift during infection. Virus-specified cell-dependent factors mediated the process extracellularly, as activity was detected in infected cell-conditioned medium and in lysates of infected cells but not in medium or components of uninfected cells. The shift in density was accompanied by a conversion in particle type. H and L virions differed in size and conformation as evidenced by differences in serological cross-reactivity and physical-chemical stability during heat inactivation, ultrasonic disruption and DNA extraction.

Replication of a type I avian adenovirus (CELO) mutant in the chicken embryo

Replication of a CELO large plaque (LP) mutant and that of its wild type small plaque (SP) parent was studied in the chorioallantoic membrane (CAM) and in the amnion of 11-day-old embryos. Although both strains produced essentially the same amount of virus in the tissue fluids, they differed in their rates of replication. Replication of the SP parent was maximal in the CAM 24 to 48 hours before that of the LP mutant. Whereas inclusions were observed in SP inoculated CAM 48 hours PI and were present during the course of study; LP inclusions were rare at 72 hours PI and thereafter; LP inclusions were seen at 72 hours PI. Fewer SP than LP particles were required to produce inclusions. No inclusions were seen in sections of the trachea and liver removed at 96 hours PI from embryos inoculated via the amniotic sac with LP and SP virus.