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Pathomorphology of Viral Hepatitis B

*Hepatitis viralis B*

For medical students2 min readUpdated 2026-10-10

Viral hepatitis B is accompanied by prominent changes in the liver parenchyma, including various types of necrosis, hepatocyte degeneration, and apoptosis. A classic histological marker of viral injury is the Councilman body, while macroscopically the organ appears as a 'big red liver'.

Gross Specimen'Big red liver' — the organ is significantly enlarged in size and congested with blood.

Apoptosis MarkerCouncilman bodies (clearly identified on hematoxylin and eosin staining).

InfiltratePredominantly lymphocytes and macrophages localized within the hepatic acini.

Severe FormFulminant hepatitis is accompanied by submassive and massive necrosis.

Gross Appearance and Parenchymal Cellular Reaction

Upon visual assessment of the gross specimen, the affected organ is described by the classic term 'big red liver'.

At the microscopic level, the main pathological processes unfold within the hepatic lobules (acini). There is abundant inflammatory infiltration of the parenchyma. The cellular composition of the infiltrate is specific: it is represented predominantly by lymphocytes and macrophages, whereas the admixture of standard leukocytes remains small.

Stellate reticuloendothelial cells (Kupffer cells) play an important role in the local reaction. In response to viral aggression, they undergo marked hyperplasia and focal proliferation. Along with injury, signs of repair—regenerating hepatocytes—can be found in microsections. An additional microscopic sign is frequently intrahepatic cholestasis (cholestasis).

Hepatocyte Degeneration and Necrosis

Viral infection leads to profound metabolic disorders in liver cells, which morphologically manifest as degenerative changes. Histological preparations reveal two main types of degeneration: ballooning and hydropic (the latter is visualized in especially high detail using electron microscopy).

The extreme degree of cell damage is cell death. Viral hepatitis B is characterized by a wide spectrum of necrotic hepatocyte changes, which are classified by prevalence and localization:

Spotty necrosis — small foci of liver cell death accompanied by local lymphomacrophagic infiltration.
Periportal and centrilobular necrosis — localized in the corresponding zones of the hepatic acinus.
Bridging necrosis — forms strands of dead tissue between various lobular structures.
Submassive and massive necrosis — indicate extremely severe organ damage.

Apoptosis and Specific Markers

In addition to necrosis, hepatocyte death actively occurs via apoptosis. The primary histological marker of this process in viral infection is the formation of Councilman bodies.

These structures represent shrunken apoptotic bodies that are detected using standard hematoxylin and eosin staining of microsections. The detection of Councilman bodies is a critical diagnostic criterion confirming the viral etiology of the liver injury.

Fulminant Form and Severe Complications

In some cases, viral hepatitis B takes on a rapidly progressive (fulminant) course. Clinically, this condition manifests as acute liver failure. The morphological substrate of this pathology is the development of extensive submassive and massive necrosis of the parenchyma.

The severe course of the disease and its progression to cirrhosis lead to life-threatening complications:

Neurological: hepatic encephalopathy.
Hemorrhagic: bleeding from esophageal varices, as well as gastrointestinal and hemorrhoidal bleeding.
Infectious: secondary flora superinfection leading to sepsis, intestinal phlegmon, or spontaneous bacterial peritonitis (ascites-peritonitis).

Prevention Principles

To prevent the spread of infection, comprehensive prevention strategies are applied, aimed at interrupting the natural and artificial transmission routes of the virus.

Vaccination is recognized as the primary method for controlling the epidemic process. Plasma-derived and recombinant DNA vaccines are used for immunization. Vaccination is included in childhood immunization schedules and is mandatory for high-risk groups.

Mnemonic

To remember the types of necrosis in order of increasing severity, use the chain: Spotty → Periportal / Centrilobular → Bridging → Submassive → Massive. The apoptosis marker is easy to remember: the virus destroys the cell, leaving behind a Councilman body.

Frequently asked questions

How does the liver look macroscopically in acute versus chronic viral hepatitis B?

The macroscopic appearance of the liver depends on the form and stage of the disease. In the acute course, the organ appears as a 'big red liver'. In the fulminant form (yellow dystrophy stage), the liver is flaccid, reduced in size, with a wrinkled capsule, and on cross-section the tissue has a variegated, predominantly yellow color. In the chronic course progressing to post-necrotic cirrhosis, the liver is shrunken, firm, with a macronodular surface. On cross-section, the parenchyma is represented by nodules greater than 3 mm in diameter separated by broad, firm, grayish connective tissue septa.

What specific marker cells are identified in the parenchyma in chronic viral hepatitis B?

In chronic viral hepatitis B, specific altered cells serving as morphological markers of infection are identified in the liver parenchyma. These include:

Ground-glass hepatocytes — cells with a specific alteration of the cytoplasm resembling ground glass, caused by the accumulation of HBsAg in the endoplasmic reticulum.
Hepatocytes with 'sanded' nuclei — cells containing HBcAg in their nuclei in the form of vacuoles with small eosinophilic inclusions.

What morphological criteria are used to evaluate the histological activity index (HAI) in hepatitis?

The histological activity index (HAI) in chronic hepatitis is evaluated using a semi-quantitative scoring analysis of biopsy specimens. The following morphological criteria are used to calculate the index:

Periportal and bridging necrosis — scored from 0 to 10.
Intralobular focal necrosis and hepatocyte degeneration — scored from 0 to 4.
Inflammatory infiltrate — severity of portal tract infiltration (scored from 0 to 4).
Fibrosis — stage of connective tissue proliferation (scored from 0 to 4).

What stages of liver fibrosis are distinguished during the progression of viral hepatitis B?

During the progression of chronic viral hepatitis B, fibrosis stages are evaluated using the METAVIR scoring system. The following stages are distinguished:

F0 — no fibrosis.
F1 (mild fibrosis) — portal fibrosis without septa.
F2 (moderate fibrosis) — portal fibrosis with rare portoportal septa.
F3 (severe fibrosis) — numerous portocentral septa without cirrhosis.
F4 — cirrhosis.

Which cells predominate in the inflammatory infiltrate in hepatitis B?

The infiltrate within the acini consists predominantly of lymphocytes and macrophages. The admixture of standard leukocytes within it is insignificant.

What are Councilman bodies and how are they detected?

These are specific apoptotic bodies formed during hepatocyte death. They serve as a marker of viral injury and are clearly visible in microsections using standard hematoxylin and eosin staining.

What morphological substrate is characteristic of fulminant hepatitis?

The rapidly progressive form leading to acute liver failure is based on extensive submassive and massive necrosis of the liver parenchyma.

How do Kupffer cells react to viral injury?

Stellate reticuloendothelial cells (Kupffer cells) respond to injury with marked hyperplasia and focal proliferation.

Go deeper

Chronic hepatitis B (CHB): morphological features.
Interaction of viral hepatitis B with delta infection (HDV).
Vaccine prophylaxis: types of plasma-derived and recombinant vaccines.
Pathogenesis of hepatic encephalopathy in severe disease.
Mechanisms of bleeding from esophageal varices.