Cellular Suicide: How HCV Destroys The Liver

Apoptosis. That’s the medical term. More commonly, it is known as cellular suicide. It’s the process or mechanism by which liver cells, or hepatocytes, meet their end. The death of liver cells create non-functioning areas in the liver. This leads to a buildup of collagen, better known as scarring. Scarring causes fibrosis, then cirrhosis, and finally, necrosis, which can result in hepatocellular carcinoma (HCC) – liver cancer. The liver is equipped with a mechanism of regeneration. Though amazing, it is massive regeneration that causes HCC.

In the body of a healthy person, the lymph nodes watch over cellular regeneration. They capture and destroy abnormal cells. When disease suppresses the immune system, lymph nodes can fall down on the job. When liver cells die, its regenerative properties go into overdrive, in an attempt to replace the dead hepatocytes with new ones. The more new cells the liver has to make, the greater the chance of it spinning off abnormal cells. It takes only one cell missed by the lymphatic system to start the trouble. Usually, the liver must be in an advanced state of disease or over-burdened with toxins for this to happen.

Hepatitis C doesn’t kill liver cells by design. When HCV enters a hepatocyte, it follows programmed instructions contained within viral RNA. The virion makes itself at home, unpacks itself, and then turns the liver cell into a viral replication factory. The goal of any successful virus it to keep its host alive for as long as possible – a crucial element of survival. Viruses that quickly kill their hosts usually burn themselves out, as with Ebola. But in the case of HCV, we know that the virus is in for the long haul. Many folks discover they’ve had the virus for decades before they start showing signs and symptoms. Hep C can operate under the radar for many years; its actions are, in the beginning, sub-microscopic, and the liver is still healthy enough to keep up with dying cells through regeneration, but not yet on a cancer-causing scale.

As soon as the virus starts making baby virions, it feeds on the cell’s natural resources – primarily, oxygen, contained within the powerhouses of cells – the mitochondria. When HCV makes physical contact with a mitochondrion, it damages that cell organ, causing oxygen to spill into the cell. Too much oxygen in a cell causes oxidative stress. At this point, the cell knows it’s in trouble, and begins writing its own suicide note. Eventually, the excess oxygen damages the cell nucleus, which causes degrading of cell DNA. Although the mechanism is not completely understood, we know that AIF (apoptosis-inducing factor) resides within the double wall of the hepatocyte. A signal is sent to this factor, telling it to kill the cell. It calls upon other factors, mainly TNF alpha (TNF=Tumor Necrosis Factor), to finish off the cell. The hepatocyte has killed itself. When the cell is dead, it is not removed from the liver. It remains in place, doing nothing. Too many dead liver cells in close proximity to each other will create a scar, just like damaged skin cells.

Curing hepatitis C as early as possible is the best way to stop cellular suicide. In early stages of infection, this process goes on painlessly, without any alarming symptoms. It’s easy – too easy to ignore the urgency for treatment.

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