Development Of Antiviral State Research Articles

Characterization of Lymphocyte Interferons with Different Species Specificities From Normal and Genetically Dystrophic Chickens

Lymphocytes from thymus and spleen of normal (Line 412) and genetically dystrophic (Line 413) chickens produce two types of interferons (IFNs) with different host cell specificities. The first type, referred to as ChIFN-alpha, demonstrates antiviral activity on primary normal chicken embryo (CE) cells. This activity is stable at 60 degrees C for 1 h and, in this respect, ChIFN-alpha is similar to the standard ChIFN-beta. In contrast, the second type, referred to as ChIFN-alpha 1, demonstrates antiviral activity in human and simian cells but not in primary CE cells. This activity is labile at 60 degrees C for 1 h. The amount of these two types of IFNs produced in lymphocytes from the spleen of dystrophic chickens was fourfold greater than that produced from normal chickens under similar experimental conditions. In contrast to the lymphocytes from thymus and spleen, the lymphocytes from the bursa of both the normal and dystrophic chickens produced only one type of IFN, namely ChIFN-alpha 1. The development of antiviral state in human cells by ChIFN-alpha 1 requires host RNA synthesis. Although ChIFN-alpha 1 has antiviral properties similar to HuIFN-alpha in human cells, the two IFNs are not antigenically related.

Interaction of interferon with cells: characteristic of the induction of interferon uptake in relation to interferon antiviral activity

A study of the factors influencing the development of an interferon-induced antiviral state indicated that the induction phase of the interferon "uptake" system was dependent on interferon concentration and exposure time of cells to interferon. The same parameters were found to affect the development of antiviral activity when a greater concentration of interferon was applied to cells which had been induced. Low pH was found to affect, adversely, the development of an antiviral state in cells exposed to interferon. This effect was at the induction rather than the uptake level of interferon action.