[Cryptosporidiosis: current views of its pathogenesis and resistance].

Cryptosporidiosis is a socially dangerous opportunistic infection that is intractable and, according to recent data, caused by a diversity of species of the genus Cryptosporidium, which are still recently considered to be nonpathogenic to a human being. The transmission of this infection is by the water route and the technology of water purification cannot be saved from the oocysts of Cryptosporidium. Therefore, the important line of investigations is to study the immunological aspects of the interaction of Cryptosporidia with the cells of a microorganism, the development of a pathological process, and the persistence of the pathogen. The review analyzes the factors providing the mobility of the pathogen, its attachment to and penetration into the cell. The inhibitory effect of a number of substances preventing the binding of sporozoites to the cell is described. It has been established that Cryptosporidia can control the apoptosis of the host's cells and affect different other parameters of cell functional activity. It is shown that infection resistance depends on many factors and it is studied on models with genome or immunity or artificially induced defects. Nitric oxide should be emphasized among the determinants of natural resistance to Cryptosporidia. gamma-IFN has a dominant role in infection control and the good response to infection is associated with the production of a number of cytokines mainly of the Th1 type. There is evidence that there is a relationship of the local immune response to the systemic one in cryptosporidiosis. It is noted that the loss of local immune reactions may cause severe sequels in patients with immunodeficiencies. The importance of nonspecific T-cell defense and antiparasitic antibodies in the control of the infection is demonstrated. It is concluded that the studies that give a better insight into the systemic mechanisms of infection protection should be conducted. In this direction, it is promising to construct models of cryptosporidiosis in the immunocompetent host and those of generalized infection, which will assist in studying the mechanisms that are responsible for the control of cryptosporidial dissemination in immunodeficiencies.