In a study conducted by Temple University, researchers connected a common childhood virus and certain types of pediatric brain tumors. This information may provide scientists with a missing link that would bring them closer to understanding what causes these tumors.
The group’s findings were released in the report “Expression of Human Polyomavirus JCV Late Gene Product Agnoprotein in Human Medulloblastoma,” in the Feb. 20 issue of the Journal of the National Cancer Institute.
Luis Del Valle, M.D. and Kamel Khalili, Ph.D., of Temple’s Center for Neurovirology and Cancer Biology led the study. The group discovered viral components of the JC Virus, which affects more than 70 percent of the entire human population during early childhood, present in samples of pediatric brain tumors.
Khalili, a professor and director of Temple’s neurovirology center, said the JC Virus often displays the same set of chromosomes, or genome, as the medulloblastoma tumor. This type of tumor is highly malignant and accounts for 20 percent of all pediatric brain tumors.
T-antigen, which has the potential to cause tumors, was among the JC Virus components detected in the tumor’s genome. Another, called agnoprotein, has not been determined to be a factor in the formation of brain tumors, although its interaction with T-antigen is suggested to have an effect on cell growth.
Khalili said the two proteins were found simultaneously in almost 50 percent of the brain tumor samples examined in the study.
“That the JC Virus early genome can cause medulloblastoma tumors in animals has been established,” Khalili said. “The fact that it’s a human virus, and has oncogenic (cancer-causing) potential, seriously necessitates the need for the development of a vaccine.”
The JC Virus is believed to enter the body through the upper respiratory tract and remain dormant in most cases throughout a person’s lifetime, causing only infrequent and minor health problems. The effects of the JC Virus are detailed in Khalili’s book Polyomaviruses: Molecular and Clinical Perspectives, which was published late last year.
In cases of people who have a significant decrease in immune function, such as organ transplant or AIDS patients, however, the virus can become active and cause Progressive Multifocal Leukoencephalopathy, a disease which depletes the brain’s myelin, a fatty substance that protects the neurons.
“About 4-8 percent of AIDS patients develop PML, even when treated with highly active anti-retroviral therapy,” said Khalili. PML usually results in death within five months of onset.
Khalili said that other possible relationships between the virus and the tumors cannot be completely dismissed at this point.
“We still need to further determine whether the JC Virus is acting mainly as either a co-factor, a cause, or whether another factor caused the tumors, and a gene expression is leading us to believe that the virus is the culprit,” he said.
Addressing the remaining uncertainty about the causal relation between the JC Virus and the medulloblastoma tumors, Khalili said more tests need to be done to make a determination.
“Obviously we cannot inject humans with the virus. More studies with primates will give us a better clue about the relationship between the JC Virus and the genesis of the tumors,” he said.
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