Researchers from Harvard and the Instituto de Medicina Molecular (iMM) Lisboa have created a chimera virus that allows the study of molecules to treat cancers caused by human herpes virus infection in mice models of disease. The work was published yesterday in PLoS Pathogens.
There are a variety of herpesviruses and one of their main characteristics is their ability to infect their hosts for life and in some people ultimately lead to cancer. One way to eliminate cancer cells that were caused by the Herpesvirus Kaposi Sarcoma is to eliminate the virus. If the herpes virus is gone, the cancer cells could no longer proliferate.
The scientists—led by Pedro Simas, Ph.D., group leader at iMM, and Kenneth Kaye, M.D., associate professor at Harvard—found a protein called LANA, which is vital for the Kaposi virus to maintain infection. The team found that when LANA is cloned into a virus similar to Kaposi, but which infects mice instead of humans, it preserves its functionality. This finding came as a surprise since it was assumed that as a consequence of the evolutionary divergence between human and other animal viruses, the genes that code for LANA could not be switched.
However, in their current work, they showed that even though there are more than 60 million years of evolutive divergence between the human Kaposi sarcoma herpesvirus and its rodent homologue, LANA's functional mechanisms are preserved.
With these findings, the researchers were able to create a chimera virus—a mouse virus with a human viral gene that can be used to test molecules that inhibit human LANA protein in an animal model of disease, treating not only human herpes virus infection but also its associated cancers.
The scientists hope these molecules will be used in the future as drugs to treat Kaposi virus associated lymphomas.
Image: These are mice spleen cells (blue) infected with the chimera kaposi virus showing the LANA protein (red). Image courtesy of the Pedro Simas Lab at iMM Lisboa.