The appearance of nasopharyngeal carcinoma (NPC) cells in humans has been linked to the EBNA1 protein of the Epstein-Barr virus (EBV) by researchers at the University of Toronto. This is a major find, as the team has also figured out exactly how this happens. Apparently, the viral protein interferes in the natural cell processes, making them susceptible to mutating and generating cancerous cells.

 

EBV is not dangerous in its natural form. Its only manifestation is a form of herpes. The problem is that it binds with PML nuclear bodies and proteins in the cell. These cell parts control the replication of DNA strands and the cycle of life a cell undergoes regularly. In other words, they decide when the cell dies. But, in the presence of EBV, they are incapacitated and the cells can live longer than they’re supposed to. This is not as good as it may first seem, because the longer a cell lives, the stronger the possibility of it becoming infected with foreign bodies that can generate mutations. And mutations most often mean cancer.

 

Although it does not directly generate cancer, the EBNA1 protein acts “covertly” by disabling the natural cellular defense mechanisms. The result is multiplying broken-DNA cells that are no longer recognized by the organism, and are therefore considered to be part of some infection. The body then naturally tries to fight them off, but can't. This type of situation is extremely suited for the development of aggressive forms of cancer, which take advantage of the weak immune system in order to replicate.

 

NPC is responsible for large epidemics throughout the world, especially in third-world countries, where countless people have died because of it. Scientists are now trying to determine if EBV has the same effect on other types of cancer. The answer to this question could give them future windows of opportunities in successful cancer research.