Molecular link between herpes and cancer
Lisbon/New York - A Portuguese-US research team has discovered a new molecular mechanism that enables gamma herpes viruses to chronically infect patients. Gamma herpes viruses infect white blood cells (B- or T-lymphocytes) remaining latent in the lymphoid tissues as an asymptomatic chronic infection. The results of the study, which were published online in the EMBO Journal, offer a greater understanding of why these patients are more likely to suffer from lymphocyte (white blood cell) cancer lymphoma immunodeficiency.
The researchers' findings demonstrate that a protein from the gamma herpes viruses, called ORF73, mimics the host´s molecular machinery to inhibit NF-kB on infected lymphocytes. NF-kB is a protein complex that acts as a transcription factor and is involved in cellular responses to various stimuli including death and proliferation. The researchers pointed out that the viral manipulation of the host molecular machinery wreaks havoc with the normal controls of the cells, which, in turn, raises the risk of cancer. If NF-kB inhibition in gamma herpes virus-infected patients with lymphomas is confirmed, drugs capable of saving the molecule could maybe decrease the chances of someone developing lymphomas.
Participating in the study were the Institutes of Microbiology and of Molecular Medicine at the University of Lisbon (Portugal), the Gulbenkian Science Institute (Portugal) and the Weill Medical College of Cornell University (US).