‘I don’t normally point out funding press materials, preferring to focus on the other end of the research process, but this one, drawn to my attention by the Healthspan Campaign newsletter, contains a good overview of the current state of knowledge regarding the persistent herpesvirus called cytomegalovirus (CMV) and its role in immune aging. CMV is actually just about as innocuous and prevalent as herpesviruses get: most people are infected by the time they reach old age, and near all of them suffered no obvious and immediate consequences of that infection. Given the readership demographics here, I’d give even odds that you have CMV lurking in your tissues as you read this.
No obvious consequences is not the same as no consequences: the results of CMV infection are very real, just slow to appear. Like other herpesviruses, CMV can remain latent in the body and cannot be permanently cleared by the efforts of the immune system. One thesis on how it contributes to degeneration of the immune system is that ever more of the immune system’s limited cohort of cells become specialized to attack CMV, with no resulting gain in that unending fight, leaving ever fewer cells able to tackle all of the other necessary tasks. In effect this is a sort of progressive misconfiguration of a programmable system, and a problem that might in the near future be addressed by selectively destroying these specialized cells. Some experiments conducted in recent years strongly suggest that this will spur the generation of replacement immune cells, and consequently a restoration of some lost functionality in the immune system.
This is a pretty compelling hypothesis given the evidence to date, but as for so much of everything that involves the immune system it is yet to be proven beyond a doubt. As for many of these sorts of things my preferred approach to investigation would be to fix the damage, here meaning removal of the CMV-specialized memory T cells, such as by adopting one of the targeted cell destruction technologies in the late stages of development in the cancer research community, and see what happens afterwards in tissue and animal studies. That of course is not the way things are done in the mainstream of research, where the tendency is to be much more conservative in adopting hypotheses for experimentation, and the first focus is on developing as complete an understanding as possible before building potential treatments. That may all lead to the same place in the end, or it may not – we shall see.’