SUMMARYWhen mice were inoculated intravenously with Newcastle disease virus, interferon was formed, and the mice were protected against the lethal effects of a subsequent intravenous injection of a toxic strain of influenza A virus. Mice were similarly protected when injected intravenously with a suspension of mouse macrophages which had been stimulated to produce interferon by treatment in vitro with Newcastle disease virus. It is known that the reticuloendothelial system has a role in the production of interferon and in the development of non-specific resistance to virus infections. When this system was blocked completely by a thorotrast injection, or partially as the result of splenectomy, there was a sharp decrease both in the amounts of interferon formed in mice in response to an injection of Newcastle disease virus and in their resistance to the toxic effects of influenza virus.
The authors propose classification of placental insufficiency, based on the fact that the placenta, as a provisory organ, has an exclusive ability to develop compensatory processes to be present during the whole pregnancy. The authors established the role of placental barriers, in particular the syncytiocapillary membranes, in developing placental insufficiency. The Immunohistochemical methods allow us to detect the presence of antigens and different classes of immunoglobulins on the membranes. Dystrophic and necrobiotic changes in the syncytiocapillary membranes increase the permeability of the placental barrier and contribute to the penetration of specific antibodies and pathogenic antigens to foetal organs. The risk of intrauterine infections of the foetus increases sharply if the woman has suffered a respiratory infection during pregnancy.
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