Abstract
Introduction. The study of HCV + HBV mixed hepatitis is a serious problem due to the varied and more severe clinical picture compared to mono-infection, as well as the presence of seronegative variants of HBV infection. In addition, mixed infection is characterized by a more rapid progression of the pathological process to cirrhosis of the liver. The frequency of mixed infection detection has been increasing in recent years. Aim of the research. To study the structural and functional characteristics of the liver in mixed infection with HCV + HBV. Materials and methods. A comprehensive clinical and pathomorphological study of HCV + HBV mixed infection was carried out, which included 112 patients with markers of chronic hepatitis C and B. The age of the patients ranged from 16 to 69 years, 68 men and 44 women. In a clinical study, in addition to a detailed study of the anamnesis, blood biochemical parameters were tested: the level of aminotransferases (AlAT and AST), alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGTP), bilirubin, total protein, albumin, cholesterol, glucose. The system of hemostasis was studied: prothrombin time, prothrombin index; peripheral blood parameters were determined — hemoglobin, erythrocytes, platelets, leukocytes, ESR. Results. With a high activity of the infectious process, a tendency was found to increase in the surface density of the granular cytoplasmic reticulum in comparison with low activity indicators, which led to rather high ratio of organelles of the protein-synthesizing compartment and mitochondria to the cytoplasm of hepatocytes. In addition, with a high degree of mixed hepatitis activity, a slightly higher structural density of lipid inclusions and a lower volumetric density of cytoplasm devastation zones were found. In general, most of the main cytoplasmic organelles of hepatocytes in chronic HCV + HBV mixed infection had similar indicators of structural density, regardless of the process activity. Conclusion. Mixed HCV + HBV infection is characterized by phenotypic heterogeneity of the hepatocyte population associated with a variety of cytopathic effects caused by complex viral exposure. Hepatitis C RNA virus attacks predominantly cytoplasmic organelles while preserving the nucleus, hepatitis B DNA virus causes degradation of the nuclear compartment with the formation of a ring-shaped nucle cricoid that can be detected by light-optics. The combination of RNA and DNA hepatitis C and B viruses caused phenotypic heterogeneity of the hepatocyte population. Hepatitis C RNA virus caused the degradation of the cytoplasmic compartment of the cell, hepatitis B DNA virus, first of all, caused the modification of the nucleus.
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