Adenoviral infection is a serious human pathology leading to respiratory, gastrointestinal and ocular disorders and epidemic outbreaks, especially in children's groups. Here we present the results from an investigation of anti- adenoviral effect of 6-azacytidine (6-AC) both in vitro and in vivo. The selectivity index of 6-AC for adenovirus type 5 in HEp-2 cells was 374, the 50% effective concentration was 0.5 mg/ml. For in vivo investigations we developed a model of disseminated adenoviral infection in newborn Syrian hamsters. The infectious virus was recovered from the liver, kidney, lungs and heart. Application of 6-AC led to a reduced period of the virus presence (7 days in the liver and 4 days in the kidney and heart) and lowered virus titers on day 3 post-inoculation (p.i.) (liver - 2.7 and 4.1, heart - 0 and 3.2, kidney - 0 and 2.4 log(10 )CPD(50)/mg tissue weight, in the presence and absence of 6-AC, respectively). Application of 6-AC to newborn Syrian hamsters led to partial destruction of their splenocytes. The results obtained suggest that 6-AC or 6-ACbased drugs with lower toxicity or applied topically may be suitable for therapy and prevention of adenoviral infection in humans.

Two phase I strains of Coxiella burnetii of different virulence were injected into the yolk sacs of chicken embryos, and the yolk sacs and livers were examined at intervals by light, fluorescent, and electron microscopy. The high absorptive and digestive capacities of the yolk endoderm contributed to he entrance of the organisms into endodermal epithelial cells where C. burnetii multiplied. Organisms multiplied not only inside specific vacuoles originating from phagolysosomes but also in the cytoplasm itself. Lysis of the limiting membrane of some phagolysosomes, a normal function of endodermal cells, as well as rupture of vacuoles, provided the release of C. burnetii into the cytoplasm. The C. burnetii strain of greater virulence infected 100% of the endodermal cells, whereas the strain of lesser virulence infected only 60%. Budding of very small particles from the C. burnetii bodies was demonstrated. The particles were regarded as filterable forms of the organism. Despite the enormous multiplication of C. burnetii in the endodermal cells, organisms were only rarely detected in the vitelline blood vessels and liver sinusoids of the embryos. Peculiarities of the infectious process of C. burnetii in chicken embryos and possible mechanisms of limitation of spread of the infection are discussed.

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Acute and chronic pathological processes induced in murine lungs by influenza virus or intranasal administration of proteolytic enzymes chymotrypsin and proteinase K were compared. Histologic and electron microscopic analysis showed that a number of characteristics of these two processes were similar. These characteristics included serosanguineous lung edema on days 1-5 postinfection, infiltration of lung tissue with cell elements, metaplasia of bronchial epithelium, and presence of mycoplasma in chronic pneumonia foci. These parameters persisted during 150 days of the experiment without regression. The results suggest the key role of primary cell destruction and proteolytic activity enhancement in the development of chronic influenza-induced pneumonia.

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