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Primary Biliary Cirrhosis (cont.)

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What is the role of infection?

The possibility that PBC is caused by an infection with a virus, bacterium, or fungus has generated a number of studies. To date, none has shown conclusively that PBC is an infectious disease or even that it is triggered by a self-limited (nonpersistent) infection. Clearly, PBC is not associated with infection by any of the known hepatitis viruses. Furthermore, none of the new viruses that may cause liver diseases have been found preferentially or exclusively in patients with PBC.

Investigators are currently pursuing leads suggesting that the biliary epithelial cells of patients with PBC may contain an infectious virus that belongs to the class of viruses called retroviruses. (The human immunodeficiency virus, HIV, is an example of a retrovirus.) These studies have identified genetic fragments of a retrovirus in the biliary epithelial cells of patients with PBC. Nevertheless, further research is required to answer the important question of whether PBC is caused by a retroviral infection.

The possibility that PBC is caused by infection with bacteria has intrigued clinical investigators for decades. You see, the mitochondria in the cells of mammals were derived, during evolution, from bacteria. Thus, many bacteria contain antigens that react with the AMA found in patients with PBC. Some of these bacteria have been cultured from the urine of patients with PBC who have recurrent urinary tract infections. Interestingly enough, as discussed later, recurrent urinary tract infection has been recognized as a risk factor for developing PBC.

This association between urinary tract infection and PBC led to the speculation that a bacterial infection might trigger an immune response that developed into an autoimmune reaction. Although this speculation is plausible, there is currently no direct evidence that this sequence of events occurs in PBC. As a matter of fact, molecular techniques now exist to screen livers for the presence of any type of bacteria. So far, these kinds of studies have found no evidence of a chronic bacterial infection in PBC.

Another intriguing possibility is that an infection with a virus, bacterium, fungus or parasite might introduce foreign proteins that mimic the protein antigens of mitochondria. An immune response against these foreign proteins could develop antibodies and T lymphocytes that react with the mimicked self-proteins, thereby resulting in autoimmunity. In other words, the body's immune system responds to the foreign proteins but it reacts against its own mitochondrial proteins. This phenomenon is called molecular mimicry.

One of the best examples of molecular mimicry is found in rheumatic fever. This condition is an autoimmune reaction involving the skin, joints, and heart muscle, that is caused by an immune response to a streptococcal bacterial infection. Now, rheumatic fever is usually diagnosed within a few weeks of having strep throat. Physicians, therefore, recognized the relationship between the two events (streptococcal infection and rheumatic fever) before molecular mimicry was understood. PBC, however, is usually a more subtle condition that might not be diagnosed for many years. Therefore, if a transient infection were to trigger molecular mimicry in PBC, causing an autoimmune reaction, the relationship between the infection and the autoimmune disease might be easily missed.



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