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A comparative study of surface membranes of human cell J-96 and J-48 cultures with different sensitivity to alpha/beta interferon (IF). Reduced sensitivity of J-41 cells to IF-alpha/beta was found to be accompanied by a loss of highly specific receptors for IF-alpha, the lack of changes in the cell surface structures upon treatment with IF-alpha/beta, reduced intensity of cell fusion upon successive treatment with IF and polyethylene glycol. The results are discussed in connection with the observed changes in the activity of superoxide dismutase in J-96 and J-41 cell lines after treatment with IF.

A study was made of histopathology of the organ cultures of the lung of 3 adult men infected with the FH, Erfurt and No. 13M. pneumoniae strains. Morphological changes in the infected tissue of the lung were characterized by affection of the cells of the alveolar lining and epithelium of the bronchi, moderate destruction of the interstitial tissue and formation of eosinophilic inclusions characteristic of M. pneumoniae infection. No. 13 strain caused a more intensive degeneration of the lung tissue than FH and Erfurt strains. The strains of M. pneumoniae under study reproduced in the organ culture of the human lung with sufficiently high titres (10(6)--10(8) colony-forming units/0.2 ml).

When Krebs-2 ascitic carcinoma is transplanted to mice, administration of interferon may produce either a stimulating or an inhibiting effect on replication of carcinoma cells in the peritoneal cavity depending on the responsiveness of mice (intact or vaccinated with Newcastle disease virus) and the state of the transplanted cells ("common" or "tolerant"). Parallelism was observed in changes of the intensity of cell multiplications and indices of their enzymatic activity under the influence of exogenic interferon.

The study was done with J-96 cell line sensitive to Coxsackie B3 virus and the subline J-41 derived from it and resistant to this virus. In order to determine the substrates responsible for the susceptibility or resistance of these cells to Coxsackie B3 virus, homogenates and filtrates of the susceptible cells were inoculated into resistant ones and vice versa. Inoculation of the resistant cell homogenates into the susceptible cells at various intervals after virus inoculation did not inhibit virus development. Inoculation of a filtrate of the susceptible cells into resistant ones followed by long-term cultivation resulted in restoration of the susceptibility. Reversion of susceptibility to Coxsackie B3 virus was gradual and accompanied by restoration in the cells of positive Homari test to alkaline phosphatase. The positive result was obtained twice in the absence of reversion in control cells not treated with the filtrate.

In the presence of serum from newborn mice the cells of newborn mice produce almost no interferon induced by Newcastle disease virus. When cultivated in a medium containing adult mouse serum, interferon production by the cells increases markedly reaching the level of interferon production by the cells of adult animals. It is suggested that there are factors present in mouse serum which are capable, depending on the age of the animals, either of inhibiting or stimulating the activation of lysosomal apparatus and interferon production.

Comparisons of native preparation of mouse interferons, "macrophage" and "Krebs" revealed some differences, Thus, the minimal time necessary for the development of resistance to vesicular stomatitis virus (VSV) in L cells treated with "macrophage" and "Krebs" interferon was 5 and 2 hours, respectively. The activity of the lysosomal enzyme of acid phosphatase was considerably higher in the cells treated with "Krebs" interferon and infected with VSV than with "macrophage" interferon. Differences in the antiviral and antioncogenic properties of fractions No. 1 and No. 5 of these interferons obtained in fractionation of native interferon preparations by the cryomethod were demonstrated. In particular, fraction No. 5 of "Krebs" interferon, in contrast to that of "macrophage" interferon, had no antioncogenic properties but did have antiviral properties. It is suggested that these differences are due to the presence in native preparations of different substances capable of exerting an effect on interferon.

Mice weighing 18--20 g were inoculated with herpes simplex virus type I. The rate of pathological changes in the myocardium was found to depend on the route of virus inoculation and the time of heart examinations in the infected animals. The development of myocardiopathies was not determined by the virus dose used in the test. An immunosuppressant drug, imurane, reduced the rate of heart affections. Pathomorphological changes in the heart were of parenchymatous-interstitial nature, with the leading role of lesions of myocardium muscle cells proper and secondary development of microcirculation disorders. The rate of heart lesions increased when herpes and influenza viruses were given to mice simultaneously; staphylococcus toxin had the same effect.

Among 28 strains of influenza A (H3N2) virus isolated from human patients 3 strains were found to be capable of replication in continuous monkey kidney cell cultures. When cells of different origins (PPO, chick embryo chorioallantio membrane, human nasal mucosa) were infected with the virus or when PPO were infected with allantoic or cultural virus strains, the pathological changes were of the same type. No specific inclusions were found in the cells. Adaptation of the virus to PPO cells resulted in inhibition of its hemagglutinating, neuraminidase and interferon-inducing activity and in decrease of thermostability, but the infectious and antgenic properties were retained unchanged.

The role of chromosomes 2, 5, 16, and 21 in production and effect of human interferon was checked in human diploid cells, human heteroploid cells J-96 and clone J-41 thereof. The J-41 cells were found to have a lower number of chromosomes 2 as compared to the other cells under study; J-41 cells produce less interferon than the other cells. Most J-41 cells lack chromosome 21. Unlike the other two cell cultures, these cells do not produce antivirus state after treatment with interferon. The number of chromosomes 16 is larger in J-96 cells than in diploid ones, and they are less sensitive to interferon than diploid cells. The experimental results confirm the importance of chromosome 2 for coding for interferon production, other chromosomes taking part in the regulation of this process. The gene of sensitivity to interferon is localized in chromosome 21, the regulator gene coding the production of repressor of sensitivity to interferon is in chromosome 16.

The study was done on a subline of cells reverting to sensitivity to Coxsackie B3 virus after treatment of J-41 cells resistant to this virus with a homogenate prepared from the sensitive J-96 cell culture. Cytogenetic examinations of this cell subline showed its karyological characteristics to approach those of the sensitive J-96 culture. The modal number of chromosomes and the number of chromosomes 2, 9, 11, 12, and 21 were completely restored and marker chromosomes typical of the sensitive culture appeared. In the reverted subline there was almost no marker chromosomes peculiar for the resistant J-41 culture. In addition, a decrease in the number of chromosomes 1 and 19 replicas as compared with J-96 and J-41 culture cells and the presence of marker chromosomes not found in the original cultures indicate that this subline has its own distinctive characteristics.

Cytoplasmic inclusion bodies corresponding in their tinctorial properties to Negri bodies were detected in TEp-2/2 and BHK-21/13S cell cultures chronically infected with fixed rabies virus. The number of cells containing the inclusions was always than that of the cells producing virus-specific antigen. Histological examinations of chronically infected cultures revealed considerable inhibition of the acid phosphatase activity, some weakening of the reaction to alkaline phosphatase, and a marked decline in the activity of succinate dehydrogenase. The intensity of reaction to RNA in chronically infected cultures was increased, particularly in those zones of the cells where RNA-containing inclusions were detected. The activity of the respiratory enzyme HAD-H2 tetrasolium reductase in HEp-2/2 cells was reduced and in BHK-21/13S cells increased as compared to the control.

Comparative characteristics of cytopathic changes in the cell cultures infected with adenovirus and with a biologically active preparation of adenovirus DNA are presented. The pathological process in the cells infected with the infectious DNA differs from that after virus infection by a shortened time of DNA penetration into the cell and a shortened latent period of infection development. The development of the pathological process in the cell cultures was accompanied by a complex of cytological changes with predominant affection of the nuclei and formation of intranuclear inclusions staining green with acridine orange. The distinctive feature of these changes was the time of their appearance: in cultures infected with the virus inclusions were formed within 12-48 hours, in those infected with DNA within 9-18 hours. The fluorescent antibdoy procedure revealed a virus antigen in these cultures induced by DNA preparationand by the virus, at different stages of its accumulation. The nucleoplasm was the site of specific antigens synthesis. The distribution of the virus antigen in the infected cells corresponds to the morphological pictures of intranuclear inclusions at later stages of infection which confirms the viral nature of the latter. The dynamics of the development of cytological changes and intranuclear inclusions in the infected cells as well as synthesis of a specific antigen in them are directly related to the quantitative accumulation of the virus.

A virus-carrier state was observed in the process of subcultivation of foot-and-mouth disease virus-infected calf kidney cell culture. Cytologically, the chronically infected culture differed from the control culture by the presence of a large number of syncytial cells which did not die in acute infection because of poor susceptibility to the virus. Chronic infection appeared to be maintained by occasionaly polygonal cells which retained the initial sesceptiblity to foot-and-mouth disease virus. The number of such cells did not exceed 1--4% and by the 9th passage they disappeared completely. At this time the experimental culture did not differ from control cytologically and cytochemically.