Chicken infectious anemia virus (CIAV) is known to infect and replicate in various Marek's disease chicken cell lines (MDCCs) derived from Marek's disease (MD) tumors. One line, MDCC-MSB1, has been the substrate used in most studies. We compared a total of 26 MDCCs, including two sublines of MDCC-MSB1, MSB1 (L) and MSB1 (S), four other MD tumor-derived lines, and 20 lines derived from MD virus-induced local lesions, for susceptibility to the Cux-1 and CIA-1 strains of CIAV. The cell lines represented six phenotypic groups of T cells based on the expression of CD4, CD8, and TCR-2 and -3 surface markers. Susceptibility was measured by the number of cells positive for viral antigen in immunofluorescence (IF) tests at 3-10 days postinfection. No clear-cut differences were found in susceptibility related to phenotype, although CD4-/8+ lines and CD4-/8- lines might be more susceptible than CD4+/8- lines. However, several individual lines were more susceptible to Cux-1 than the two MSB1 sublines tested. Contrary to an earlier report, cells of MDCC-CU147, a CD8+, TCR3+, local-lesion derived line, were found to be susceptible to CIA-1. In fact, CU147 was distinguished by very high susceptibility to both CIAV strains. In direct comparisons with MSB1, CU147 detected approximately 10-fold lower doses of virus. Also, virus spread was faster (P < 0.05) in CU147 than in MSB1 and other lines. Results from polymerase chain reaction (PCR) tests to detect infection in titrations were in general agreement with IF test results although PCR detected infection in a few terminal dilution cultures that were negative by IF.

Animals↗

PubMedDate not supplied

Adenoviruses of chickens: serologic groups.

By literature review and experimental studies, 57 adenovirus isolants from chickens were grouped into 10 distinct serotypes. In plaque-reduction tests, 20 antibody units were reacted with 32-320 plaque-forming units of virus. Viruses that were neutralized (80% or greater reduction in titer) by a given serum were considered to belong to that serotype. Used to distinguish among serotypes were their antisera. One-way neutralization occurred in only two instances; in both cases it was traced to contamination of the virus inocula used to induce specific antiserum. Recloning corrected the problem. Of the 10 serotypes described, all are known to exist in the United States, 7 were found in Northern Ireland, and at least 6 have been shown to occur in Japan.

Adenoviridae↗

PubMedDate not supplied

Stable transfection of reticuloendotheliosis virus-transformed lymphoblastoid cell lines.

Lymphoblastoid T cell lines were established by infection of chicken splenocytes with reticuloendotheliosis virus (REV). The target cells first were cultured in interleukin-containing conditioned medium or were stimulated by concanavalin A, or both. Most cell lines were T cells expressing CD3 and one of the T cell receptors, and all cell lines were positive for major histocompatibility complex (MHC) class II antigens. Several REV-transformed cell lines were stably transfected using electroporation with a selectable plasmid, pNL1, containing the neor gene. Transfected cell lines were selected using G418 and were maintained for periods up to 137 days. Transfected cell lines were susceptible to MHC class-I restricted lysis by cytotoxic T lymphocytes from REV-infected chickens.

Animals↗

PubMedDate not supplied

Pathologic and serologic characterization of a variant of duck hepatitis type I virus.

A duck hepatitis virus (DHV), isolated from ducks on a farm in Virginia in 1963, was shown to be only partially related to DHV type I (DHV-I) in cross-neutralization and in cross-protection tests. The virus, named DHV-Ia, apparently is a serologic variant of DHV-I; both viruses are serologically distinct from DHV type III. Pathologic responses to DHV-Ia were similar to those described for DHV-I infection.

Age Factors↗

PubMedDate not supplied

Experimental egg-transmission of avian reovirus.

Two experiments with an avian reovirus (FDO isolant), serologically identical to the Fahey-Crawley and WVU 2937 isolants, provided conclusive proof that egg-transmission can occur. In the first experiment, 4-day-old chicken embryos were inoculated into the yolk sac with serial dilutions of virus and subsequently hatched. High virus doses killed all embryos, whereas low doses (14 or less plaque-forming units) allowed some embryos to hatch normally although infected. In the second experiment, virus was administered by the nasal, esophageal, and tracheal routes to twenty 15-month-old breeders. Eggs from -6 to 21 days and 58 to 64 days postinoculation were incubated. Three newly hatched chicks from eggs laid on successive days (17, 18, and 19 days postinoculation) and one infertile egg (61 days postinoculation) were found infected. Active infection, as judged by virus isolations from cloacal swabs, was over by the 17th day postinoculation.

Administration, Intranasal↗

PubMedDate not supplied

Localization of avian reovirus (FDO isolant) in tissues of mature chickens.

Mature hens were exposed to a reovirus (FDO isolant) serologically related to the viral arthritis agent. Examination of 23 tissues from the respiratory, alimentary, and reproductive tracts and tendons from the hock joint revealed widespread infection 4 days after inoculation via the respiratory and alimentary tracts. By 14-15 days, infection had largely subsided but was still detectable in the tendons, oviduct, and alimentary tract of some birds. No infection was found at 30 days. Virus isolation attempts in chick kidney cultures were more reliable than fluorescent-antibody tests for detecting infection. None of 156 chicks hatched from eggs laid between 12 and 33 days postinoculation were infected.

Administration, Intranasal↗

PubMedDate not supplied

Proliferation of chicken lymphoblastoid cells after in vitro infection with Marek's disease virus.

Activated, thymus-derived (T) lymphoblasts were exposed to Marek's disease virus and cultivated in attempts to induce in vitro transformation. After 9 to 15 days, colonies or small clusters of proliferating lymphoblasts were observed in cultures from three of a total of 122 attempts. These developed into proliferating cell cultures that resembled conventional Marek's disease (MD) lymphoblastoid cell lines in terms of growth characteristics and morphology. All proliferative cultures were unusual in that 1) the expression of viral internal antigens consistently or periodically was very high (up to 30% of all cells) and 2) the cells deteriorated and/or proliferation ceased in all cases after culture periods of 45-176 days. The proliferative cultures were all characterized as CD2+ and CD3+, Ia-bearing T cells; one was CD4+/CD8- and TCR2+, the other two were CD4-/CD8- and TCR1+. The latter two are the only cultures of MD-infected cells known to be TCR1+.

Animals↗

PubMedDate not supplied

Rous sarcoma regression in chickens resistant or susceptible to Marek's disease.

In 4 experiments, strains of chickens relatively susceptible (S-strain, P-line) or resistant (N-line, PDRC) to Marek's disease (MD) were challenged with Rous sarcoma virus (RSV) at 6-8 weeks old. RSV tumors occurred in 94-100% of the birds in each strain, but the number with tumors that regressed during the 40-46-day experiment varied from 7% (S-strain) to 91% (PDRC). The N-line and P-line birds, derived from a random-bred flock with selection only for susceptibility or resistance to MD, regressed their tumors at about equal rates (respectively 59 and 65%). Thus, although the genetic strains differed in ability to regress RSV tumors, the difference was not necessarily related to genetic resistance or susceptibility to MD. Other birds in 2 of the experiments, infected 2-4 weeks earlier with JM or GA isolants of MD virus, had significantly (P less than 0.01) lower incidence of RSV tumor regression than did controls provided that they developed gross lesions of MD.

Animals↗

PubMedDate not supplied

Pathogenicity of low-virulence Marek's disease viruses in normal versus immunologically compromised chickens.

To learn whether "low virulence" isolants of Marek's disease (MD) virus have a low inherent oncogenic potential, 3 isolants (CU-1, CU-2, S-11) were given to genetically susceptible S-strain or P-line birds with or without immunosuppressive treatments. Based on lesion incidence and type during an 8-10-week experimental period, embryonal (17-day) bursectomy and neonatal cyclophosphamide (CY) treatment were without effect on CU-1 and CU-2 infections in P-lines. S-11 virus was virulent for P-lines, and CY treatment reduced MD incidence as reported by others for virulent virus infections. Neonatal thymectomy or infection in ovo (at 8 days of incubation) or use of the more susceptible S-strain chicks all increased the incidence of MD induced by CU-1 and CU-2 viruses. It was concluded that the "low virulence" of these viruses is a reflection of an adequate immune response by the host.

Animals↗