The Relationship Between Viruses and Age-Related Immunosenescence is Complex
It is thought that the burden of infection is an important determinant of pace of the age-related decline of the immune system. This is particularly the case for persistent viral infections such as that caused by herpesviruses. There is plenty of evidence for cytomegalovirus infection to be a cause of immune dysfunction in later life, for example. In this open access paper, the author argues that the interaction between viruses and immune system in the context of aging is very complex and presently poorly understood. It certainly seems clear that some viruses are far worse than others when it comes to the damage done to the immune system.
Our body is in continuous contact with viruses and various defense mechanisms are used to prevent the entry or to eliminate the invader within the body. There is ample evidence demonstrating that the aging-associated decline of the immune system, i.e. immunosenescence, significantly weakens these mechanisms. This is often observed in the case of common viral pathogens, e.g. influenzavirus. On the other hand, it is known that at least some viruses may induce or modify immunosenescence and in this respect cytomegalovirus (CMV) is the classical and extensively investigated example.
However, there is now emerging evidence showing that the number of viruses or virus-like entities is much larger than expected. i) Next generation (NGS) RNA/DNA sequencing based approaches have shown that within our body there are large amounts of various viruses even without known clinical or biological significance, forming the virome, i.e. the classical concept about the "sterility" of the inner body should be rejected; ii) Our genome contains mobile genetic elements, retrotransposons, endogeneous retroviruses (HERV), some of which may still be active and might modify the immune system.
Analysis of the virome (including bacteriophages) is technically more challenging than that of the bacteriome, but the first virome analyses have now been published. It seems that the different compartments of the body harbor distinct viral communities. However, the total number of viruses is highly variable, 10^9 particles per gram in the intestinal content, 10^7/ml in the urine and 10^5/ml in the blood. Studies on gut virome have shown, that the most common viruses are not those infecting eukaryotic cells, but those infecting prokaryotic cells, bacteriophages, form a clear majority.
Thus far the relationship between virome composition and immunosenescence is not known. However, there are several reports demonstrating changes in the gut virome compostion in diseases of immunological nature, e.g. type I diabetes. Based on these, it could be expected that immunosenescence would have an influence on virome composition. However, its possible role in the aging-associated pathologies can presently only be speculated. Does the weaker immunity allow the presence of potentially pathogenic viruses in the blood of elderly individuals? It is also possible that this viral "normal flora" would have a protective effect, in analogy with the bacterial normal flora in several compartments of the human body.
The data shown here indicate that the relationship between viruses, virosphere, and immunosenescence is more complex than previously thought.
For a complex interaction I would expect to see a couple of viruses that have positive , even if marginally,
effect on lifespan either by keeping the immune system active or by tuning down the inflammatory responses or reducing the chances of cancer. Of course, if there is none, it means we can find a simple aggregate relationship between persistent infections and lifespan