MORPHOLOGICAL CHANGES AT THE HEPATOCYTE LEVEL IN PATIENTS WITH CHRONIC HEPATITIS B AND C

Аннотация

Chronic hepatitis B and C infections remain among the most pressing global public health challenges due to their widespread prevalence, silent progression, and potential to cause irreversible liver damage. The hepatotropic nature of HBV and HCV leads to persistent inflammation, immune-mediated injury, and significant morphological alterations at the hepatocyte level, ultimately resulting in fibrosis, cirrhosis, and hepatocellular carcinoma. This study aims to comprehensively evaluate and characterize the cellular and subcellular morphological changes in hepatocytes in patients with chronic viral hepatitis B and C. Emphasis is placed on cytoplasmic vacuolization, nuclear polymorphism, ballooning degeneration, apoptotic and necrotic changes, Mallory-Denk bodies, and mitochondrial dysfunction. By integrating histopathological findings with current virological and immunological data, the study highlights the mechanisms by which chronic infection alters liver architecture and function. The analysis also underscores the role of liver biopsy and advanced imaging techniques in detecting these morphological patterns and supports the development of targeted therapeutic strategies. These insights are critical for improving early diagnosis, patient stratification, and long-term clinical outcomes in individuals affected by chronic viral hepatitis. Keywords: Chronic hepatitis B, chronic hepatitis C, hepatocyte injury, morphological changes, histopathology, liver biopsy, viral hepatitis, ballooning degeneration, Mallory-Denk bodies, hepatic fibrosis, hepatocellular carcinoma. Chronic viral hepatitis, particularly infections caused by hepatitis B virus (HBV) and hepatitis C virus (HCV), represents a major public health concern globally due to its high prevalence, long-term asymptomatic progression, and significant risk of severe complications such as liver cirrhosis and hepatocellular carcinoma (HCC). As reported by the World Health Organization (WHO), an estimated 296 million individuals were living with chronic HBV and approximately 58 million with chronic HCV worldwide as of 2022, with over 1.1 million deaths annually attributed to related liver diseases. Despite advances in vaccination programs for HBV and the availability of direct-acting antiviral agents (DAAs) for HCV, the global burden remains significant, especially in regions with limited access to diagnostic tools and treatment. The liver, being a vital metabolic and detoxifying organ, is particularly susceptible to viral aggression, with hepatocytes as the primary targets of infection and immune-mediated injury. Chronic infection with HBV or HCV initiates a cascade of pathogenic processes including persistent inflammation, oxidative stress, mitochondrial dysfunction, and immunological disturbances, all of which culminate in structural and functional alterations of hepatocytes. These morphological changes— ranging from cellular ballooning and hydropic degeneration to the formation of Mallory-Denk bodies, apoptotic bodies, and nuclear polymorphism—are crucial histopathological hallmarks of ongoing liver injury. 5 5 International scientific journal ISSN: 2181-3906 «MODERN SCIENCE АND RESEARCH» 2025 VOLUME 4 / ISSUE 8 / UIF:8.2 / MODERNSCIENCE.UZ They provide essential insights into disease severity, stage, and progression and serve as a basis for therapeutic decision-making. A comprehensive evaluation of these cellular alterations, combined with virological and immunohistochemical profiling, offers a deeper understanding of the mechanisms underlying chronic viral hepatitis and informs clinical strategies aimed at early detection, risk stratification, and personalized treatment. The objective of this study is to systematically examine the morphological manifestations of hepatocyte injury in chronic HBV and HCV infections and to elucidate their clinical and prognostic significance within the broader context of liver pathology. Pathophysiology of hepatocyte injury in chronic HBV and HCV infections The pathophysiological mechanisms underlying hepatocyte injury in chronic hepatitis B and C infections are complex and multifactorial, involving direct viral effects, host immune responses, and chronic inflammation-driven cellular stress. Hepatitis B virus (HBV), a partially double-stranded DNA virus, and hepatitis C virus (HCV), a single-stranded RNA virus, differ in their replication strategies and interaction with the host immune system; however, both ultimately lead to chronic liver damage through sustained immune-mediated cytotoxicity and hepatocellular degeneration. Upon infection, HBV does not exert direct cytopathic effects in most cases; instead, liver damage is largely a consequence of cytotoxic T lymphocyte (CTL)- mediated lysis of infected hepatocytes as part of the host's antiviral immune defense. HCV, on the other hand, has more direct cytopathic properties and can also provoke endoplasmic reticulum (ER) stress, oxidative stress, and mitochondrial dysfunction