Search PubMed⌕ Search

Biomedical subjects

J M Sharma

Publications and source records attributed to J M Sharma.

At least 91 records · Page 5Linked to original sources

Replication of Marek's disease virus in cell cultures derived from genetically resistant chickens.

Various parameters of replication of Marek's disease virus (MDV) were studied in cells derived from genetically resistant (line 6) and susceptible (line 7) chickens. Cell-free and cell-associated preparations of three strains of pathogenic MDV (JM, GA, and Id-1) replicated equally well in cells of resistant and susceptible chickens. There were no demonstrable differences between the two genetic sources of cells for the chronological appearance and type of cytopathic effects and for the type of virus-induced antigens detectable by immunofluorescent and agar-gel precipitin tests. MDV propagated for about 4 weeks in cells of resistant line 6 chickens remained nonvirulent for line 6 and fully virulent for line 7 chickens. The lack of expression of genetic resistance to Marek's disease at cellular level contrasts the infection mechanisms of MDV from those of viruses associated with lymphoid leukosis in chickens.

Animals↗

Pathogenesis of Marek's disease in old chickens: lesion regression as the basis for age-related resistance.

Chickens of various age levels, free from prior infection, were simultaneously exposed to Marek's disease virus, and the response of each age group was recorded. Four- and 20-week-old chickens of lines 15x7 and CM (commercial source) had substantial resistance to mortality and gross lesions. In contrast, in line 7, which was tested at 1-day, 2-, 4-, 8-, 12- and 16-week age levels, 4-week-old chickens were fully susceptible to clinical Marek's disease (MD), although resistance was demonstrated at 8-week and older age levels. Genetically resistant chickens of line 6 maintained their resistance at all age levels tested. Pathogenesis of MD was compared in 12-week-old and 1-day-old chickens of line 15x7. Within the 1-day-old group, 23% of the chickens died because of MD, whereas there were no deaths in the 12-week-old group. Both groups developed viremia although duration, incidence, and levels of virus in the 1-day-old group were higher than in the 12-week-old group. Although initially the 12-week-old group responded by producing higher levels of antibody, the long term incidence of agar gel precipitin, immunofluorescent, and virus neutralization antibody in the two groups was similar. Gross and microscopic lesions of MD developed in both groups, but lesions regressed in the 12-week-old group and persisted in the 1-day-old group. It was concluded that age resistance to MD was expressed through lesion regression.

Age Factors↗

Blastogenic response of whole blood cells of turkeys to a T-cell mitogen.

Cellular immune mechanisms in the turkey are not well understood because adequately standardized, reproducible in vitro assays to measure cellular immunity are not available. Our purpose was to optimize conditions for a whole blood mitogenic assay that would facilitate quantitative assessment of the ability of circulating T cells of turkeys to respond to Con A. Heparinized peripheral blood from normal turkeys was examined. Data indicated that diluting the blood 1:20 or 1:40 and incubating the test cultures at 39 degrees C or 41 degrees C gave the best mitogenic stimulation. Presence of 7.5% turkey serum but not chicken or fetal bovine serum in the culture medium substantially enhanced the blastogenic response. Ontogeny of the whole blood mitogenic response was examined by repeat observations on a group of turkeys at various age levels starting at 1 week of age. Whole blood cells from 1-week-old turkeys responded poorly to Con A, although by 2 weeks of age, the response was well developed. Tests at subsequent ages revealed variable levels of activity. There was a considerable individual variation in the level of blastogenic response of turkeys within the same age group.

Animals↗