[MOLECULAR BIOLOGY OF HEPATITIS B VIRUS AND IMMUNOPATHOGENESIS OF CHRONIC VIRAL HEPATITIS B].

Chronic hepatitis B belongs to a category of socially significant diseases due to its wide abundance in the world and high frequency of unfavourable outcomes of this disease. Features of interaction of hepatitis B virus with human immune system, accompanying development of mechanisms of escape from immunological control, is the basis of development of chronic hepatitis B. Molecular-biological features of hepatitis B virus are the basis of the indicated mechanisms, and the content of this review is their examination. Herewith, stages of immunopathogenesis of this disease is the basis of characteristics of interaction of viral proteins with cells of immune system, and isolation of those is accepted in contemporary foreign literature.

[MECHANISMS OF INTERACTION OF VIRAL CAUSATIVE AGENTS IN PATIENTS CO-INFECTED WITH HUMAN IMMUNODEFICIENCY AND HEPATITIS C VIRUSES].

In patients infected with human immunodeficiency virus (HIV) in 20 - 30% of cases co-in- fection with hepatitis C virus (HCV) is observed, that is associated with common routes of transmis- sion for these causative agents. The main cause of lethal outcome for co-infected patients is liver damage. Thus, analysis of mechanisms of mutual influence of HIV and HCV under the conditions of co-infection gains special attention, that can be examined from both standpoints of direct inter- molecular interaction of 2 viral causative agents, as well as from the position of their immune- mediated effect. Negative effect of HIV on the course of fibrosis process in liver during HCV infection is associated with the feature of this virus to cause deep alteration in the immune system by direct damage of CD4+ cells, disruption of mechanisms of immunological memory, suppression of functions of liver fraction of NK and NKT, as well as its ability of co-receptor interaction with hepatocytes and stellate cells, enhancing progress of fibrosis alterations and HCV replication in liver. HCV.is also established to effect replication of HIV, stimulate infection of macrophages with this virus. All these events facilitate the rise in lethality during HIV and HCV co-infection.

[Bronchial asthma pathogenesis and genetic prognosis development].

The review is dedicated to an actual problem--genetic prognosis of risk of bronchial asthma development that is quite a complex aspect of studies from a methodological viewpoint. Bronchial asthma--heterogeneous disease by both etiology and clinical characteristics. At the same time genetic prognosis is based on the unity of pathogenetic mechanisms of development, though in immunological reactions that are the base of this disease, alternative variants are possible. The aim of this review is carrying out parallels between modern achievements in the field of deciphering trigger mechanisms of bronchial asthma pathogenesis and object of genetic studies based on these mechanisms. Among the examined conceptions--role of epithelial tissue in trigger mechanisms of bronchial asthma, variants of key role of immune system cells, first of all, T-helpers of various types for further development of inflammatory-effector reactions with damage characteristic for this disease. Compliance of contemporary approaches of genetic studies and novel concepts of bronchial asthma pathogenesis is shown.

[Association between expression of lectin type receptors by natural killers and intensity of liver fibrosis during chronic hepatitis C].

AIM: To study functional activity of natural killers on different stages of fibrosis during chronic hepatitis C. MATERIALS AND METHODS: Functional activity of CD3-/CD56+/CD16+ lymphocytes measured as expression of natural killers receptors (NKR) and natural cytotoxicity receptors (NCR) was assessed by flow cytometry. RESULTS: At stage I of fibrosis, decrease of number of CD3-/CD56+/NKG2D+ cells was observed, whereas at precirrhotic stage III--sharp decrease of CD3-/CD56+/CD94+ and CD3-/ CD56+/NKG2D+ populations, and at cirrhotic stage--decrease of number of CD3-/CD56+/ NKG2D+ cells and increase of cytolytic activity of natural killers carrying CD107a marker compared to precirrhotic stage. CONCLUSION: Obtained data demonstrate that natural killers during chronic hepatitis C receive regulatory signals mainly through lectin type receptors (CD94 and NKG2D).

[Hepatitis B virus: biology, immunopathogenesis, NK/NKT system in viral persistence].

In this review, the problem of hepatitis B is considered as related to the recent data on the biology of the viral agent, on the pathogenesis of disturbances that it causes in an organism as well as on accompanying deviations in its immune system. Special attention is paid to mechanisms of hepatitis B virus (HBV) persistence and the role of regulatory lymphocytes of NK/NKT system in this process. Some problems in further studies are specified.

[Hepatitis C virus: biology, immunopathogenesis, and NK/NKT cells during viral persistence].

Data on immunological changes that accompanied HCV infection are analyzed. Role of various viral proteins in induction of immune alterations leading to HCV persistence is reviewed. Possibility of association between pathogenic mechanisms (and outcomes) of hepatitis C and alteration of aminergic regulation mechanisms in the immune system as well as perspectives of further studies assessing the role NK and NKT cell in this process.