Discussion in 'Other Health News and Research' started by Christopher, Feb 3, 2014.
02 February 2014
I've asked oncologists how often cells with neoplastic potential arise and are eliminated by active immune response in healthy people. The answers I get basically indicate that they don't know because it isn't cancer until it proliferates. Some have added that immune function is not compromised until late in the disease.
This is true for general immune function, but understanding of specific immune compromise, as in the case of those subsets of T-cells which perform this function against a particular pathogen, is still very poor. We saw evidence that highly specific immune dysfunction is possible in ME/CFS patients in recent research by Carmen Scheibenbogen's group in Berlin. The most striking aspect had to do with a missing response to EBNA-1, a protein produced at the very beginning of the replication cycle.
As I understand things, (and this is a limited understanding,) LMP1 is formed fairly late in the sequence of events leading to EBV replication. Expression of this, and especially some mutant forms of the gene, seems to be connected with metastasis. It appears to perform dual, opposing roles: first, it signals on cell membranes that a cell is actively infected, enabling immune response to eliminate those cells; second, it interferes with the ability of the cell to adhere to membranes. Once cells with oncogenic properties cease to be confined to membranes they are much more likely to become metastatic. This is the point at which it becomes much, much harder to control or eliminate a neoplasm.
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