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Trapping Cancer

by Kathleen Cason



In studying a contagious lung cancer in sheep, a research team led by University of Georgia scientists has discovered a naturally occurring mechanism that blocks a cancer-causing virus from exiting host cells and spreading. In the long run, these results could inform the design of new therapeutic strategies or drugs against retroviruses, which cause disease such as AIDS and certain leukemias.

This particular sheep cancer — ovine pulmonary adenocarcinoma — led to the death of Dolly, the first cloned mammal, and is a chronic problem for Europe’s sheep industry.

“The cancer is caused by a retrovirus that passes from sheep to sheep like any other virus, such as the flu,” said team leader Massimo Palmarini, a virologist in UGA’s College of Veterinary Medicine.

Like all viruses, retroviruses insert their genetic material into host cells and then force the host to copy it. But only retroviruses permanently insert their genes into the genomes of cells they invade.

If the cells happen to be reproductive cells, the retrovirus genes can be inherited by offspring and become a permanent feature of the host genome. These inheritable retrovirus genes rarely cause disease and may actually protect the host animal from infection by related disease-producing retroviruses.

For example, sheep carry in their genomes some 20 different retroviruses related to the lung-cancer-causing Jaagsiekte sheep retrovirus, or JSRV — the object of the Palmarini team’s study. The researchers discovered a member of that family, called enJS56A1, interferes with the ability of the retrovirus JSRV to exit host cells. It seems the infective JSRV retrovirus is forced to don a slightly defective protein coat and that traps it inside the host cell. The blocked escape route appears to result mainly from a single amino-acid substitution in a protein that constitutes the virus’s protective shell.

Understanding more completely how enJS56A1 functions could provide a model for designing new anti-retroviral therapies that work on already infected cells. Some common anti-retroviral drugs, such as reverse transcriptase inhibitors, function only immediately after the virus infects a new cell; but the Palmarini team’s findings are the first report of interference with retroviral replication late in the cycle — that is, after the retrovirus has inserted its genes into the host genome.

The team published its findings in the July 27, 2004, issue of the Proceedings of the National Academy of Sciences.

For more information, contact Massimo Palmarini at


Research Communications, Office of the VP for Research, UGA
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