The Virology of Hepatitis Pathology
Hepatitis virale is an infection of the liver brought on by a virus that has made its way into the bloodstream. Hepatitis A, B, C, D, and E are just a few examples of the viruses that could infect a person. Within three to ten days of a virus’s first infection, symptoms typically begin to manifest. It’s around this time when jaundice sets in and the urine turns a darker color.
When your body’s immune system detects foreign substances, such as viruses, germs, or irritants, it mounts an attack known as inflammation. It aids in eradicating the source of the harm, getting rid of damaged or dead cells, and beginning the healing process.
Macrophages, dendritic cells, histiocytes, and Kupffer cells are resident immune cells that play key roles in regulating the inflammatory response. PAMPs, or pathogen-associated molecular patterns, and DAMPs, or damage-associated molecular patterns, are molecular patterns that these cells recognize and bind (DAMPs).
Chronic inflammation causes liver cell loss and scar tissue, which alters normal hepatic lobule architecture.Bridging necrosis occurs when the dead cells join together to produce stripes between the marginal zones of two different lobules. Panlobular infiltration of mononuclear cells and rounded acidophil (Councilman) bodies are two further histological characteristics of hepatic damage.
Hepatocytes experience extensive cellular and DNA damage from chronic hepatitis B (HBV) infection.
This involves cellular inflammation and proliferation, chromosomal instability, and recombination-dependent DNA damage repair.
DNA damages are abnormal chemical and structural alterations in the DNA that can lead to disease, as opposed to mutations, which entail the regular four bases in a different configuration. Single-strand breaks, inter-strand cross-links, and insertional mutagenesis are all examples.
Prolonged exposure to these cellular and DNA damages can lead to fibrosis. Loss of liver function is another possible consequence of this fibrosis.
Having certain strains of the hepatitis virus and your geographic location are two factors that affect your chance of developing HCC. The risk of HCC is highest in Asia-Pacific and Sub-Saharan Africa, and lowest in the rest of the world.
When cells have served their purpose or reached the end of their lifespan, they undergo a process called apoptosis and die. It is essential for cell growth and has vital functions in immunity.
When cells die by apoptosis, they change significantly in shape. Condensation of chromatin (forming a crescent or ring-like structure at the nuclear membrane’s perimeter), loss of cell connections, and shrinkage of the cell are all symptoms of this (pyknosis).
After chromatin condensation, the nucleus breaks apart apoptotically, releasing the DNA and allowing it to be phosphorylated. Apoptotic bodies, which are made up of dehydrated cytoplasm, protrude out of the cell in a way that looks like bubbles.
Phagocytic cells are capable of recognizing apoptotic bodies and ingesting them. Apoptosis is complete, and dead cells are removed in this step.
When damaged or diseased, the liver is one of the few organs that can repair itself. New hepatocytes and other cell types can be generated through either mitotic division of liver cells or activation of stem/progenitor cells during the regeneration process.
In the field of hepatology, research into healing is essential. Diseases that lead to liver death or degeneration, such as cirrhosis and hepatocellular carcinoma, have researchers searching for ways to tap into the liver’s regenerative potential as a cure (HCC).
There are a number of different processes that work together to regulate liver regeneration. Regeneration relies on uPA, growth factors, cytokines, and endothelial cells, among other things.
