Different theories have been hypothesized to explain the emergence of cancer in first place. Various studies have been conducted around these theories and we have managed to come up factors such drinking, smoking, gene mutations etc. that might increase one's susceptibility to cancer but no defined cause. One of the tangible cause we have so far are viruses.
Known to us since 1950s, Polyomaviruses are viruses that possess the ability to cause multiple (poly) tumors (-oma). These are close relatives of the Papillomaviruses that are known to cause warts or non cancerous tumours in humans. For quite some time, we knew of only two Polyomaviruses that could infect humans. But studies over the last five years or so have come across at least 8 more types of Polyomaviruses, taking the total known family count to 10. While much still remains unknown about them, here a few things that we found interesting about these cancer causing viruses.
1. JC Polyomavirus (JCPyV) was the first polyomavirus to be identified and is believed to be the causative agent of progressive damage of the white matter at multiple loci in the brain, medically known as progressive multifocal leukoencephalopathy (PML). Similarly, the other commonly known polyomavirus is the BK Polyomavirus (BKPyV) is the established causative agent of damage to the kidneys or nephropathy.
2. The incidence of polyomavirus related disease is very low globally. However, large percentage of the population has antibodies (cells capable of fighting invading organism) to the these viruses by the time they are 20 years of age. This means that infection by such viruses occur early in life and are effectively controlled by our immune system.
3. The viruses then manage to maintain a low profile in the body so as not to trigger the immune response. They swing back into action usually when an individual's immune system is weak, due to diseases such as AIDS or when it suppressed after a medical event such as organ transplant.
4. Each polyomavirus has its favorite set of cells in the human body where it likes to remain hidden from the immune system. e.g. inner root sheath cells of hair follicles or certain cells under the skin called Merkel cells. This 'latency' in the body allows the virus to survive for a longer period of time in the host.
|Merkel cell carcinoma. Gross pathology specimen. (Photo credit: Wikipedia)|
5. When the virus enters a healthy cell, it can either choose to use the cell to create other viruses or integrate its own genome in the DNA of the cell. This leads to formation of a 'transformed' cell, which could be cancerous in nature. Such transformation is seen in Merkel cell carcinoma, a cancer of skin, where 80% of cancerous cells are infected with Merkel Cell Virus (MCV) and genome of the virus is found integrated with the cell's own genome.
6. Also, scientists have found a specific mutation in the viral genome that is seen only in cancerous cells and not other infected cells, which might be the likely cause of the cancer.
7. Once integrated into the cell genome, the virus has no (known) way of extracting back its own genome from the host cell, meaning, it is a dead end for the virus and it cannot replicate ever again. 'Why would a virus, smart enough to maintain a low profile, integrate itself into the another cell's genome' is the questions scientists are looking to answer.
Only a few polyomaviruses have been discovered so far and we understand the exact roles of even fewer. If a large number of cancers are proven to be the result of infections, then we are in position to counter such cancerous infections through our expertise in molecular biology. Our understanding of these viruses will indeed pave way to the next generation of cancer treatments in the years to come.
- Identification of a Novel Human Polyomavirus in Organs of the Gastrointestinal Tract (plosone.org)
- Understanding Why Cancer Vaccines Fail (dailyfinance.com)
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