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B W Calnek

Publications and source records attributed to B W Calnek.

100 records · Page 6Linked to original sources
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Dose-dependent inhibition of virus rescue from lymphocytes latently infected with turkey herpesvirus or Marek's disease virus.

The number of plaque-forming units (PFU) of turkey herpesvirus (HVT) isolated per 10(6) latently infected splenic lymphocytes was determined by co-cultivation on permissive monolayer cultures in 35-mm-diameter Petri dishes. Doses of 1 x 10(6) spleen cells or less per culture gave uniform dose-related titers, whereas doses of 8 x 10(6) cells often yielded less than 1-2% of the expected number of PFU. Intermediate doses gave proportionally reduced virus yields. This dose-dependent inhibition was observed with spleen cells from birds within a week after infection and became more marked with time. A similar phenomenon occurred with a non-oncogenic Marek's disease virus (MDV) isolate (SB-1) but not with oncogenic MDV isolates (CU-2, JM-10, GA-5), except in genetically resistant birds. High numbers of uninfected spleen cells mixed with low numbers of HVT-infected cells during assay reduced titers only slightly. Immunosuppression by combined neonatal thymectomy and cyclophosphamide treatment before HVT infection prevented the inhibition, but embryonal bursectomy had no effect.

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Serological cross-reactivity of avian adenovirus serotypes in an enzyme-linked immunosorbent assay.

Fowl adenoviruses free of avian adenovirus-associated virus, representing 10 serotypes, were tested for cross-reactivity in an enzyme-linked immunosorbent assay (ELISA). All antigens and antisera prepared in chickens, along with uninfected control antigen and normal chicken serum, were reacted in a checkerboard pattern with ELISA. There was considerable cross-reactivity among all serotypes tested. Homologous reactions were generally, but not always, stronger than heterologous reactions. ELISA was about as sensitive as virus neutralization in detecting antibodies. The high sensitivity plus broad-spectrum reactivity should make ELISA a preferred test for the detection of adenovirus antibodies in poultry flocks.

Adenoviridae↗
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Field trials with a bivalent vaccine (HVT and SB-1) against Marek's disease.

White leghorn chickens on five farms were given a bivalent Marek's disease (MD) vaccine consisting of turkey herpesvirus (HVT) and SB-1 (a nononcogenic MD virus); other chickens received only HVT. The farms had histories of "vaccination failures," presumably owing to an exceptionally virulent challenge MD virus. The bivalent vaccine uniformly protected chickens better than HVT alone between 12 and 16-20 weeks of age, when serious MD losses occurred. During that period, total mortality in groups given both viruses ranged from 0.39 to 1.26% (mean 0.86%), whereas that in HVT-vaccinated groups not exposed to SB-1 varied from 1.92 to 7.44% (mean 3.43%). Chickens in pens or rows with close contact to those given bivalent vaccine also had low MD mortality rates (0.46-1.06%, mean 0.77%), probably from the spread of SB-1.

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Pathogenesis of reticuloendotheliosis virus infection in ducks.

A new isolate of reticuloendotheliosis virus (REV) from ducks, RU-1, was used to experimentally infect white pekin ducks. Embryonal or neonatal infection usually resulted in persistent viremias, no REV antibody development, and inability to mount antibody responses against bovine serum albumin (BSA) or sheep red blood cells (SRBC). In contrast, infection at 21 days of age resulted in transient viremias, which terminated coincident with REV antibody development. These ducks remained persistently infected, however, based on virus isolations from peripheral blood lymphocytes. Ducks infected at that age were immunologically competent against BSA and SRBC unless they had been embryonally bursectomized, in which case they behaved virologically and immunologically like those infected at an early age. Bursectomy by itself did not prevent responses against the antigens. Total mortality during 4- or 6-month experimental periods ranged from 80 to 100% in REV-infected groups, regardless of age at infection, route of exposure, or whether the ducks were intact or bursectomized. Most deaths were from non-neoplastic conditions (stunting, bacterial infections), but 17 of 69 (25%) infected ducks developed a variety of neoplasms, including lymphosarcomas, histiocytic sarcomas, and spindle-cell sarcomas.

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Marek's disease virus-induced tumor transplants: development and rejection in various genetic strains of chickens.

This study compares the ability of strains of chickens of varied genetic resistance to Marek's disease (MD) to resist or regress both local and general reactions to transplantable tumor cells induced by a variety of MD virus strains and to transmissible lymphoid tumor cells (Olson's TLT) induced by an avian leukosis-sarcoma retrovirus. Previous studies have dealt with only a single MD transplant. Three conclusions can be drawn from our data: 1) MD virus infection alone could induce progressive tumors at the site of inoculation. 2) Progression or regression of transplant tumors was independent of genetic susceptibility to MD. 3) Incidence of virus-induced host tumors was dependent upon genetic susceptibility to MD.

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Cytogenetic studies of cell lines derived from Marek's disease virus-induced local lesions.

Cytogenetic analysis of cell lines derived from Marek's disease virus (MDV) induced local lesions was performed to detect the presence of a chromosomal alteration found previously in cell lines derived from MDV-induced visceral tumors. This chromosomal alteration involves an amplified region on the short arm of chromosome 1. Trypsin G-binding was performed on 12 local-lesion cell lines having various T-cell receptor phenotypes. Eight of 12 cell lines had a diploid female karyotype, and four lines were diploid males. Ten of the cell lines showed a normal G-banding pattern; two lines, however, had the short arm amplification on chromosome 1 (1p+). Thus, the 1p+ alteration does not appear to be necessary for establishment of cell lines from local lesions. The occurrence of the 1p+ alteration in Marek's disease cell lines suggests a possible role for this alteration in late stages of multi-step viral oncogenesis.

Animals↗
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Interferon modulation of Marek's disease virus genome expression in chicken cell lines.

Lines of chicken lymphoblastoid cells were established from local lesions induced by simultaneous injection of Marek's disease virus and various stimulants of T-cell activation. Lines developed with regular medium had relatively high mean rates of spontaneous expression of viral internal antigen (6.2%). In contrast, lines developed and maintained with conditioned medium generated by mixed-lymphocyte reaction had a 62-fold reduction in the mean rate of viral internal antigen expression (0.1%). The expression rate could be modulated by the removal or re-addition of conditioned medium to the growth medium. Down regulation involved proteins classified as immediate-early (a 14-kDa polypeptide), early (a 38-kDa phosphoprotein), and late (glycoprotein B homologue) antigens, indicating that the block is very early in virus replication. Once initiated in a given cell, replication apparently proceeded unimpeded. Interferon was determined to be largely responsible for the suppressive activity of the conditioned medium, although involvement of other cytokines could not be ruled out. Also, chicken interferon from other sources, including recombinant interferon, was able to similarly suppress viral antigen expression.

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Relationship between the immunosuppressive potential and the pathotype of Marek's disease virus isolates.

Isolates of Marek's disease virus (MDV) representing three pathotypes of differing virulence were compared for relative immunosuppressive properties in genetically susceptible P2a-strain and genetically resistant N2a-strain chickens. Criteria of immunosuppression were 1) persistence of early cytolytic infection (i.e., a delay or failure to enter latency) in lymphoid organs, 2) atrophy of the bursa of Fabricius and thymus as measured by organ weight proportional to body weight at 8 and 14 days postinfection (DPI), and 3) histopathologic evidence of necrosis and atrophy in lymphoid organs. No significant differences in infection level were observed among the pathotypes during the early (4-5 DPI) period of infection. However, the extent of persistent cytolytic infection at 7-8 DPI, based on numbers of tissues positive and mean scores in immunofluorescence tests, was greater (P < 0.05) for three isolates (RK1, 584A, 648A) in the highest virulence pathotype (very virulent-plus MDV [vv + MDV]) than for two isolates (JM16, GA5) in a lower virulence (virulent MDV [vMDV]) pathotype. Results from two isolates (RB1B, Md5) classified in the intermediate very virulent pathotype (very virulent MDV [vvMDV]) fell between those from the other two pathotypes. Similarly, there was a stepwise effect of viral pathotype in which the vv + MDV isolates caused the most severe damage to lymphoid organs in terms of atrophy (relative organ weights) and histopathologic changes. Organs from chickens infected with vv + MDVs showed little recovery between 8 and 14 DPI. The vMDV isolates caused the least severe damage, and lymphoid organs showed a significant return toward normal by 14 DPI; vvMDV isolates induced intermediate degrees of atrophy and recovery. The same pattern of relationship between virulence pathotype and degree of bursal and thymic atrophy was also observed in genetically resistant N2a chickens. These results suggest that the degree of immunosuppression is linked to virulence and that a simple measure of atrophic changes (relative organ weights) in the bursa of Fabricius and thymus might be useful in determining the pathotype classification of new MDV isolates. The basis for differences in immunosuppressive potential of MDV isolates needs further clarification.

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Control of avian encephalomyelitis: a historical account.

Avian encephalomyelitis control methods were not developed until the 1950s although the disease had been discovered and described over 20 yr earlier. Inability to transmit the infection by other than intracerebral inoculation, lack of suitable immunologic methods, the unknowing use of immune chickens or embryos for experimental studies, and reliance on a highly adapted strain of virus rather than fresh field isolates were the main reasons for a general lack of progress. In the absence of supportive experimental data, at least two commercial breeding organizations turned to the use of a crude chicken brain-propagated virus for vaccination of breeder replacement flocks in the 1950s. This control procedure turned out to be practical and efficacious. Development of suitable embryo infection methods and immunologic tests and the chance finding that antibody-free flocks were essential for experimental studies led to the development of embryo-susceptibility tests to identify immune breeder flocks and formed the basis for another commercially applied control program, the testing and selection of only immune flocks for hatching purposes. The application of the new testing methods coupled with a switch from the adapted Van Roekel strain of virus to fresh field isolates for experimentation resulted in a rapid unraveling of the epizootiology and pathogenesis of the disease and also to the development of a safe and effective vaccine that was licensed for administration to breeder replacements in 1962.

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