Study proposes new theory of how viruses may contribute to cancer

Oct 24, 2007

A new study suggests that viruses may contribute to cancer by causing excessive death to normal cells while promoting the growth of surviving cells with cancerous traits. Viruses may act as forces of natural selection by wiping out normal cells that support the replication of viruses and leaving behind those cells that have acquired defects in their circuitry.

When this process is repeated over and over, cancer can develop say study authors, led by Preet M. Chaudhary, M.D., Ph.D., professor of medicine at the University of Pittsburgh School of Medicine. Their findings are published by Public Library of Science in the Oct. 24 issue of PLoS ONE.

Infection with viruses has been linked to many human cancers, including some forms of Hodgkin’s and non-Hodgkin’s lymphomas, sarcomas and cancers of the throat and liver. Over the years, scientists have proposed a number of mechanisms to explain this link. One commonly held belief is that when a virus infects a cell, its genetic material alters the cell, making it grow uncontrollably, eventually leading to cancer. Some viruses also are thought to promote cancer by causing chronic inflammation. In his study, Dr. Chaudhary proposes that viruses also can lead to cancer in a less direct manner.

“We believe a separate mechanism may be at play in which a cellular insult, such as infection with a virus, selects a few pre-existing mutated clones of cells, promotes their further growth and multiplication, eventually leading to the emergence of fully cancerous cells. Consequently, similar to the role played by natural selection during evolution, excessive cell death, rather than its absence, may be a defining force that drives the initial emergence of cancer,” said Dr. Chaudhary. He named this model the Phoenix Paradigm in which cancer theoretically arises out of the ashes of dead cells.

The paradigm was developed based on a study of cells infected with the Kaposi’s sarcoma associated herpesvirus, or KSHV, also known as human herpesvirus 8 (HHV-8). The researchers examined a gene called K13 that activates a pathway previously implicated in cancer development. Cells with low K13 expression allowed KSHV to replicate, and these cells subsequently died off, the researchers noted. Cells with higher expression of K13 emerged after KSHV replication and showed defective expression of two key proteins that are known to promote cancer.

“This paradigm, if validated by further studies, has implications not only for an improved understanding of the processes involved in cancer, but also for the development of effective strategies for its prevention and treatment,” said Dr. Chaudhary.

Source: University of Pittsburgh

Explore further: Targeted MRI / ultrasound beats standard biopsy to detect high-risk prostate cancer

add to favorites email to friend print save as pdf

Related Stories

Using viruses to find the cellular Achilles heel

Jan 22, 2015

Back-to-back studies from researchers at the Gladstone Institutes have exposed new battle tactics employed by two deadly viruses: hepatitis C (HCV) and the Kaposi's sarcoma-associated herpesvirus (KSHV). Published in the ...

Locking mechanism found for 'scissors' that cut DNA

Dec 24, 2014

Researchers at Johns Hopkins have discovered what keeps an enzyme from becoming overzealous in its clipping of DNA. Since controlled clipping is required for the production of specialized immune system proteins, ...

Research reveals structure of key CRISPR complex

Dec 10, 2014

Using a gene-editing system originally developed to delete specific genes, MIT researchers have now shown that they can reliably turn on any gene of their choosing in living cells.

Recommended for you

Inhibiting CDK6 prevents leukemic relapse

4 hours ago

Despite enormous progress in cancer therapy, many patients still relapse because their treatment addresses the symptoms of the disease rather than the cause, the so-called stem cells. Work in the group of ...

User comments : 0

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.